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wdr5  (MedChemExpress)


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    MedChemExpress wdr5
    Wdr5, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/wdr5+inhibitor/WDR5-0103/10__1172_slash_jci203565-223-27-31
    Average 94 stars, based on 3 article reviews
    wdr5 - by Bioz Stars, 2026-10
    94/100 stars

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    Related Articles

    Quantitative RT-PCR:

    Article Title: WDR5 remodels NANOG condensates to drive transcriptional programs and sustain stem cell identity.
    Article Snippet: The recipient mice, at 8-weeks old, underwent sublethal irradiation (4.5 Gy) and were then transplanted with 1 × 105 BM cells via tail vein injection.The recipient mice, at 8-weeks old, underwent sublethal irradiation (4.5 Gy) and were then transplanted with 1 × 105 BM cells via tail vein injection.. The WDR5 inhibitor, C16 (WDR5-IN-1, HY-133121, MedChemExpress) was prepared as a 2 mg/mL solution in 20% 2-(hydroxypropyl)-β-cyclodextrin (HP-β-CD, HY-101103, MedChemExpress) in ddH2O.. The Menin inhibitor, Revumenib was dissolved in PBS to 2 mg/mL.The Menin inhibitor, Revumenib was dissolved in PBS to 2 mg/mL.

    Article Title: Kinesin family member 23, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway.
    Article Snippet: FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA). .. T

    Article Title: Kinesin family member 23, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway
    Article Snippet: FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA). .. T

    Article Title: Mitotic kinesin-like protein 1, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway
    Article Snippet: Chromatin immunoprecipitation assay (ChIP) ChIP assays were performed using chromatin immunoprecipitation kits (17–371, EZ-ChIP, Millipore) according to the manufacturer’s instructions as in previous reports [37].Chromatin immunoprecipitation assay (ChIP) ChIP assays were performed using chromatin immunoprecipitation kits (17–371, EZ-ChIP, Millipore) according to the manufacturer’s instructions as in previous reports [37].. Chemical reagents Page 5/17 FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA).. The regents were dissolved in dimethyl sulfoxide (DMSO) to generate the stock solution.The regents were dissolved in dimethyl sulfoxide (DMSO) to generate the stock solution.

    Expressing:

    Article Title: WDR5 remodels NANOG condensates to drive transcriptional programs and sustain stem cell identity.
    Article Snippet: The recipient mice, at 8-weeks old, underwent sublethal irradiation (4.5 Gy) and were then transplanted with 1 × 105 BM cells via tail vein injection.The recipient mice, at 8-weeks old, underwent sublethal irradiation (4.5 Gy) and were then transplanted with 1 × 105 BM cells via tail vein injection.. The WDR5 inhibitor, C16 (WDR5-IN-1, HY-133121, MedChemExpress) was prepared as a 2 mg/mL solution in 20% 2-(hydroxypropyl)-β-cyclodextrin (HP-β-CD, HY-101103, MedChemExpress) in ddH2O.. The Menin inhibitor, Revumenib was dissolved in PBS to 2 mg/mL.The Menin inhibitor, Revumenib was dissolved in PBS to 2 mg/mL.

    Article Title: Kinesin family member 23, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway.
    Article Snippet: FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA). .. T

    Article Title: Kinesin family member 23, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway
    Article Snippet: FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA). .. T

    Article Title: Mitotic kinesin-like protein 1, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway
    Article Snippet: Chromatin immunoprecipitation assay (ChIP) ChIP assays were performed using chromatin immunoprecipitation kits (17–371, EZ-ChIP, Millipore) according to the manufacturer’s instructions as in previous reports [37].Chromatin immunoprecipitation assay (ChIP) ChIP assays were performed using chromatin immunoprecipitation kits (17–371, EZ-ChIP, Millipore) according to the manufacturer’s instructions as in previous reports [37].. Chemical reagents Page 5/17 FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA).. The regents were dissolved in dimethyl sulfoxide (DMSO) to generate the stock solution.The regents were dissolved in dimethyl sulfoxide (DMSO) to generate the stock solution.

    Transfection:

    Article Title: WDR5 remodels NANOG condensates to drive transcriptional programs and sustain stem cell identity.
    Article Snippet: The recipient mice, at 8-weeks old, underwent sublethal irradiation (4.5 Gy) and were then transplanted with 1 × 105 BM cells via tail vein injection.The recipient mice, at 8-weeks old, underwent sublethal irradiation (4.5 Gy) and were then transplanted with 1 × 105 BM cells via tail vein injection.. The WDR5 inhibitor, C16 (WDR5-IN-1, HY-133121, MedChemExpress) was prepared as a 2 mg/mL solution in 20% 2-(hydroxypropyl)-β-cyclodextrin (HP-β-CD, HY-101103, MedChemExpress) in ddH2O.. The Menin inhibitor, Revumenib was dissolved in PBS to 2 mg/mL.The Menin inhibitor, Revumenib was dissolved in PBS to 2 mg/mL.

    Article Title: Kinesin family member 23, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway.
    Article Snippet: FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA). .. T

    Article Title: Kinesin family member 23, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway
    Article Snippet: FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA). .. T

    Article Title: Mitotic kinesin-like protein 1, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway
    Article Snippet: Chromatin immunoprecipitation assay (ChIP) ChIP assays were performed using chromatin immunoprecipitation kits (17–371, EZ-ChIP, Millipore) according to the manufacturer’s instructions as in previous reports [37].Chromatin immunoprecipitation assay (ChIP) ChIP assays were performed using chromatin immunoprecipitation kits (17–371, EZ-ChIP, Millipore) according to the manufacturer’s instructions as in previous reports [37].. Chemical reagents Page 5/17 FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA).. The regents were dissolved in dimethyl sulfoxide (DMSO) to generate the stock solution.The regents were dissolved in dimethyl sulfoxide (DMSO) to generate the stock solution.

    Western Blot:

    Article Title: WDR5 remodels NANOG condensates to drive transcriptional programs and sustain stem cell identity.
    Article Snippet: The recipient mice, at 8-weeks old, underwent sublethal irradiation (4.5 Gy) and were then transplanted with 1 × 105 BM cells via tail vein injection.The recipient mice, at 8-weeks old, underwent sublethal irradiation (4.5 Gy) and were then transplanted with 1 × 105 BM cells via tail vein injection.. The WDR5 inhibitor, C16 (WDR5-IN-1, HY-133121, MedChemExpress) was prepared as a 2 mg/mL solution in 20% 2-(hydroxypropyl)-β-cyclodextrin (HP-β-CD, HY-101103, MedChemExpress) in ddH2O.. The Menin inhibitor, Revumenib was dissolved in PBS to 2 mg/mL.The Menin inhibitor, Revumenib was dissolved in PBS to 2 mg/mL.

    Article Title: Kinesin family member 23, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway.
    Article Snippet: FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA). .. T

    Article Title: Kinesin family member 23, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway
    Article Snippet: FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA). .. T

    Article Title: Mitotic kinesin-like protein 1, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway
    Article Snippet: Chromatin immunoprecipitation assay (ChIP) ChIP assays were performed using chromatin immunoprecipitation kits (17–371, EZ-ChIP, Millipore) according to the manufacturer’s instructions as in previous reports [37].Chromatin immunoprecipitation assay (ChIP) ChIP assays were performed using chromatin immunoprecipitation kits (17–371, EZ-ChIP, Millipore) according to the manufacturer’s instructions as in previous reports [37].. Chemical reagents Page 5/17 FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA).. The regents were dissolved in dimethyl sulfoxide (DMSO) to generate the stock solution.The regents were dissolved in dimethyl sulfoxide (DMSO) to generate the stock solution.

    CCK-8 Assay:

    Article Title: WDR5 remodels NANOG condensates to drive transcriptional programs and sustain stem cell identity.
    Article Snippet: The recipient mice, at 8-weeks old, underwent sublethal irradiation (4.5 Gy) and were then transplanted with 1 × 105 BM cells via tail vein injection.The recipient mice, at 8-weeks old, underwent sublethal irradiation (4.5 Gy) and were then transplanted with 1 × 105 BM cells via tail vein injection.. The WDR5 inhibitor, C16 (WDR5-IN-1, HY-133121, MedChemExpress) was prepared as a 2 mg/mL solution in 20% 2-(hydroxypropyl)-β-cyclodextrin (HP-β-CD, HY-101103, MedChemExpress) in ddH2O.. The Menin inhibitor, Revumenib was dissolved in PBS to 2 mg/mL.The Menin inhibitor, Revumenib was dissolved in PBS to 2 mg/mL.

    Article Title: Kinesin family member 23, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway.
    Article Snippet: FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA). .. T

    Article Title: Kinesin family member 23, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway
    Article Snippet: FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA). .. T

    Article Title: Mitotic kinesin-like protein 1, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway
    Article Snippet: Chromatin immunoprecipitation assay (ChIP) ChIP assays were performed using chromatin immunoprecipitation kits (17–371, EZ-ChIP, Millipore) according to the manufacturer’s instructions as in previous reports [37].Chromatin immunoprecipitation assay (ChIP) ChIP assays were performed using chromatin immunoprecipitation kits (17–371, EZ-ChIP, Millipore) according to the manufacturer’s instructions as in previous reports [37].. Chemical reagents Page 5/17 FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA).. The regents were dissolved in dimethyl sulfoxide (DMSO) to generate the stock solution.The regents were dissolved in dimethyl sulfoxide (DMSO) to generate the stock solution.

    Knockdown:

    Article Title: WDR5 remodels NANOG condensates to drive transcriptional programs and sustain stem cell identity.
    Article Snippet: The recipient mice, at 8-weeks old, underwent sublethal irradiation (4.5 Gy) and were then transplanted with 1 × 105 BM cells via tail vein injection.The recipient mice, at 8-weeks old, underwent sublethal irradiation (4.5 Gy) and were then transplanted with 1 × 105 BM cells via tail vein injection.. The WDR5 inhibitor, C16 (WDR5-IN-1, HY-133121, MedChemExpress) was prepared as a 2 mg/mL solution in 20% 2-(hydroxypropyl)-β-cyclodextrin (HP-β-CD, HY-101103, MedChemExpress) in ddH2O.. The Menin inhibitor, Revumenib was dissolved in PBS to 2 mg/mL.The Menin inhibitor, Revumenib was dissolved in PBS to 2 mg/mL.

    Article Title: Kinesin family member 23, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway.
    Article Snippet: FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA). .. T

    Article Title: Kinesin family member 23, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway
    Article Snippet: FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA). .. T

    Article Title: Mitotic kinesin-like protein 1, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway
    Article Snippet: Chromatin immunoprecipitation assay (ChIP) ChIP assays were performed using chromatin immunoprecipitation kits (17–371, EZ-ChIP, Millipore) according to the manufacturer’s instructions as in previous reports [37].Chromatin immunoprecipitation assay (ChIP) ChIP assays were performed using chromatin immunoprecipitation kits (17–371, EZ-ChIP, Millipore) according to the manufacturer’s instructions as in previous reports [37].. Chemical reagents Page 5/17 FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA).. The regents were dissolved in dimethyl sulfoxide (DMSO) to generate the stock solution.The regents were dissolved in dimethyl sulfoxide (DMSO) to generate the stock solution.

    Over Expression:

    Article Title: WDR5 remodels NANOG condensates to drive transcriptional programs and sustain stem cell identity.
    Article Snippet: The recipient mice, at 8-weeks old, underwent sublethal irradiation (4.5 Gy) and were then transplanted with 1 × 105 BM cells via tail vein injection.The recipient mice, at 8-weeks old, underwent sublethal irradiation (4.5 Gy) and were then transplanted with 1 × 105 BM cells via tail vein injection.. The WDR5 inhibitor, C16 (WDR5-IN-1, HY-133121, MedChemExpress) was prepared as a 2 mg/mL solution in 20% 2-(hydroxypropyl)-β-cyclodextrin (HP-β-CD, HY-101103, MedChemExpress) in ddH2O.. The Menin inhibitor, Revumenib was dissolved in PBS to 2 mg/mL.The Menin inhibitor, Revumenib was dissolved in PBS to 2 mg/mL.

    Article Title: Kinesin family member 23, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway.
    Article Snippet: FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA). .. T

    Article Title: Kinesin family member 23, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway
    Article Snippet: FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA). .. T

    Article Title: Mitotic kinesin-like protein 1, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway
    Article Snippet: Chromatin immunoprecipitation assay (ChIP) ChIP assays were performed using chromatin immunoprecipitation kits (17–371, EZ-ChIP, Millipore) according to the manufacturer’s instructions as in previous reports [37].Chromatin immunoprecipitation assay (ChIP) ChIP assays were performed using chromatin immunoprecipitation kits (17–371, EZ-ChIP, Millipore) according to the manufacturer’s instructions as in previous reports [37].. Chemical reagents Page 5/17 FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA).. The regents were dissolved in dimethyl sulfoxide (DMSO) to generate the stock solution.The regents were dissolved in dimethyl sulfoxide (DMSO) to generate the stock solution.

    Migration:

    Article Title: WDR5 remodels NANOG condensates to drive transcriptional programs and sustain stem cell identity.
    Article Snippet: The recipient mice, at 8-weeks old, underwent sublethal irradiation (4.5 Gy) and were then transplanted with 1 × 105 BM cells via tail vein injection.The recipient mice, at 8-weeks old, underwent sublethal irradiation (4.5 Gy) and were then transplanted with 1 × 105 BM cells via tail vein injection.. The WDR5 inhibitor, C16 (WDR5-IN-1, HY-133121, MedChemExpress) was prepared as a 2 mg/mL solution in 20% 2-(hydroxypropyl)-β-cyclodextrin (HP-β-CD, HY-101103, MedChemExpress) in ddH2O.. The Menin inhibitor, Revumenib was dissolved in PBS to 2 mg/mL.The Menin inhibitor, Revumenib was dissolved in PBS to 2 mg/mL.

    Article Title: Kinesin family member 23, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway.
    Article Snippet: FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA). .. T

    Article Title: Kinesin family member 23, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway
    Article Snippet: FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA). .. T

    Article Title: Mitotic kinesin-like protein 1, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway
    Article Snippet: Chromatin immunoprecipitation assay (ChIP) ChIP assays were performed using chromatin immunoprecipitation kits (17–371, EZ-ChIP, Millipore) according to the manufacturer’s instructions as in previous reports [37].Chromatin immunoprecipitation assay (ChIP) ChIP assays were performed using chromatin immunoprecipitation kits (17–371, EZ-ChIP, Millipore) according to the manufacturer’s instructions as in previous reports [37].. Chemical reagents Page 5/17 FOXM1 inhibitor (Thiostrepton) and WDR5 inhibitor (OICR-9429) were purchased from MedChemexpress (Monmouth Junction, NJ, USA).. The regents were dissolved in dimethyl sulfoxide (DMSO) to generate the stock solution.The regents were dissolved in dimethyl sulfoxide (DMSO) to generate the stock solution.



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    MedChemExpress wdr5 inhibitor
    Hypoxia-induced epigenetic regulation contributes to increased OPN expression. (A) Western blotting showing the levels of HIF-1α, H3K4me3, H3K9me3, H3K27me3, and H3 in THP-1 and U937 cells exposed to 1% O 2 for the indicated durations. (B) IF staining showing the levels of HIF-1α, H3K4me3, H3K9me3, and H3K27me3 in THP-1 cells exposed to 1% O 2 for the indicated durations. The target proteins are shown in green. DAPI was used to stain the nuclei, and F-actin was labeled to delineate the cytoplasmic region (scale bar = 40 μm). (C) qPCR analysis of H3K4me3 enrichment at SPP1 promoter area in THP-1 cells under indicated treatment conditions ( n = 3 per group; normoxia, normoxic culture for 24 h; hypoxia, hypoxic culture for 24 h; H + siCtrl, hypoxic culture for 24 h together with transfection of the negative control siRNA; H + siWDR5-2, hypoxic culture for 24 h together with <t>WDR5</t> knockdown; H + DMSO, hypoxic culture for 24 h together with DMSO treatment; H + <t>OICR-9429,</t> hypoxic culture for 24 h together with OICR-9429 treatment). (D) qPCR analysis of WDR5 enrichment at SPP1 promoter area in THP-1 cells under indicated treatment conditions ( n = 3 per group). (E) Agarose gel electrophoresis assays showing ChIP-PCR (SPP1 promoter sequence) products from THP-1 cells immunoprecipitated with anti-H3K4me3, anti-WDR5, and IgG antibodies under indicated treatment conditions. (F) qPCR analysis of H3K4me3 enrichment at SPP1 promoter area in U937 cells under indicated treatment conditions ( n = 3 per group). (G) qPCR analysis of WDR5 enrichment at SPP1 promoter area in U937 cells under indicated treatment conditions ( n = 3 per group). (H) Agarose gel electrophoresis assays showing ChIP-PCR (SPP1 promoter sequence) products from U937 cells immunoprecipitated with anti-H3K4me3, anti-WDR5, and IgG antibodies under indicated treatment conditions. (I and J) qPCR analysis of SPP1 expression in THP-1 (I) and U937 (J) cells under indicated treatment conditions ( n = 3 per group). (K) Western blotting showing OPN expression in THP-1 and U937 cells subjected to the indicated treatments. The data are presented as the means ± SD; * P < 0.05, ** P < 0.01, and *** P < 0.001. HIF-1α, hypoxia-inducible factor α; H3K4me3, histone 3 lysine 4 trimethylation; H3K9me3, histone 3 lysine 9 trimethylation; H3K27me3, histone 3 lysine 27 trimethylation; IF, immunofluorescence; ChIP, chromatin immunoprecipitation; WDR5, WD40 repeat-containing protein 5; SPP1, secreted phosphoprotein 1; OPN, osteopontin; DMSO, dimethyl sulfoxide; qPCR, quantitative real-time PCR; SD, standard deviation; kDa, kilodaltons.
    Wdr5 Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    wdr5 inhibitor  (Selleck Chemicals)
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    Mediation of Setd5 regulation by ANKRD11 through <t>WDR5-KMT2</t> (A) Proteins identified to interact with ANKRD11 via immunoprecipitation followed by mass spectrometry (IP-MS) in HeLa cells, data sourced from Hein et al. (B) Lysates prepared from Neuro-2a cells transfected with expression plasmid for 3xFLAG-ANKRD11-3xHA were subjected to immunoprecipitation (IP) with FLAG antibody and the resulting precipitates as well as original cell lysates were subjected to immunoblot analysis (IB) with indicated antibodies. (C) ChIP-qPCR analysis using FLAG antibody on Setd5 promoter, enhancer and intron 2 (control) in wild type (WT) and Ankrd11 -disrupted Neuro-2a cells expressing <t>FLAG-WDR5.</t> Vector-transfected cells also served as controls. Data are means ± SEM ( n = 3 independent experiments). ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). Immunoblot analysis (IB) confirmed comparable expression of FLAG-WDR5 in WT and Ankrd11 -disrupted Neuro-2a cells (inset). (D) ChIP-qPCR analysis using H3K4me3 antibody on Setd5 promoter, enhancer and intron 2 (control) in wild-type (WT) and Ankrd11 -disrupted Neuro-2a cells. Normal rabbit IgG was used as a control. Data are means ± SEM ( n = 4 independent experiments). ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). (E) RT-qPCR analysis of Setd5 mRNA levels in Neuro-2a cells treated with WDR5 inhibitor OICR9429 at the indicated concentrations for 5 days. Data are means ± SEM ( n = 3 for each genotype). ∗∗ p < 0.01, ∗∗∗ p < 0.005, and ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). (F) Schematic representation of Setd5 regulation by ANKRD11 through WDR5 and KMT2-mediated H3K4 trimethylation on Setd5 promoter. See also and .
    Wdr5 Inhibitor, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    reversible inhibitors of the wdr5-myc interaction  (Novartis)
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    Novartis reversible inhibitors of the wdr5-myc interaction
    Mediation of Setd5 regulation by ANKRD11 through <t>WDR5-KMT2</t> (A) Proteins identified to interact with ANKRD11 via immunoprecipitation followed by mass spectrometry (IP-MS) in HeLa cells, data sourced from Hein et al. (B) Lysates prepared from Neuro-2a cells transfected with expression plasmid for 3xFLAG-ANKRD11-3xHA were subjected to immunoprecipitation (IP) with FLAG antibody and the resulting precipitates as well as original cell lysates were subjected to immunoblot analysis (IB) with indicated antibodies. (C) ChIP-qPCR analysis using FLAG antibody on Setd5 promoter, enhancer and intron 2 (control) in wild type (WT) and Ankrd11 -disrupted Neuro-2a cells expressing <t>FLAG-WDR5.</t> Vector-transfected cells also served as controls. Data are means ± SEM ( n = 3 independent experiments). ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). Immunoblot analysis (IB) confirmed comparable expression of FLAG-WDR5 in WT and Ankrd11 -disrupted Neuro-2a cells (inset). (D) ChIP-qPCR analysis using H3K4me3 antibody on Setd5 promoter, enhancer and intron 2 (control) in wild-type (WT) and Ankrd11 -disrupted Neuro-2a cells. Normal rabbit IgG was used as a control. Data are means ± SEM ( n = 4 independent experiments). ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). (E) RT-qPCR analysis of Setd5 mRNA levels in Neuro-2a cells treated with WDR5 inhibitor OICR9429 at the indicated concentrations for 5 days. Data are means ± SEM ( n = 3 for each genotype). ∗∗ p < 0.01, ∗∗∗ p < 0.005, and ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). (F) Schematic representation of Setd5 regulation by ANKRD11 through WDR5 and KMT2-mediated H3K4 trimethylation on Setd5 promoter. See also and .
    Reversible Inhibitors Of The Wdr5 Myc Interaction, supplied by Novartis, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    wdr5 inhibitors  (Celgene)
    90
    Celgene wdr5 inhibitors
    Mediation of Setd5 regulation by ANKRD11 through <t>WDR5-KMT2</t> (A) Proteins identified to interact with ANKRD11 via immunoprecipitation followed by mass spectrometry (IP-MS) in HeLa cells, data sourced from Hein et al. (B) Lysates prepared from Neuro-2a cells transfected with expression plasmid for 3xFLAG-ANKRD11-3xHA were subjected to immunoprecipitation (IP) with FLAG antibody and the resulting precipitates as well as original cell lysates were subjected to immunoblot analysis (IB) with indicated antibodies. (C) ChIP-qPCR analysis using FLAG antibody on Setd5 promoter, enhancer and intron 2 (control) in wild type (WT) and Ankrd11 -disrupted Neuro-2a cells expressing <t>FLAG-WDR5.</t> Vector-transfected cells also served as controls. Data are means ± SEM ( n = 3 independent experiments). ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). Immunoblot analysis (IB) confirmed comparable expression of FLAG-WDR5 in WT and Ankrd11 -disrupted Neuro-2a cells (inset). (D) ChIP-qPCR analysis using H3K4me3 antibody on Setd5 promoter, enhancer and intron 2 (control) in wild-type (WT) and Ankrd11 -disrupted Neuro-2a cells. Normal rabbit IgG was used as a control. Data are means ± SEM ( n = 4 independent experiments). ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). (E) RT-qPCR analysis of Setd5 mRNA levels in Neuro-2a cells treated with WDR5 inhibitor OICR9429 at the indicated concentrations for 5 days. Data are means ± SEM ( n = 3 for each genotype). ∗∗ p < 0.01, ∗∗∗ p < 0.005, and ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). (F) Schematic representation of Setd5 regulation by ANKRD11 through WDR5 and KMT2-mediated H3K4 trimethylation on Setd5 promoter. See also and .
    Wdr5 Inhibitors, supplied by Celgene, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    wdr5 inhibitor campaign  (Triphase Accelerator)
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    Mediation of Setd5 regulation by ANKRD11 through <t>WDR5-KMT2</t> (A) Proteins identified to interact with ANKRD11 via immunoprecipitation followed by mass spectrometry (IP-MS) in HeLa cells, data sourced from Hein et al. (B) Lysates prepared from Neuro-2a cells transfected with expression plasmid for 3xFLAG-ANKRD11-3xHA were subjected to immunoprecipitation (IP) with FLAG antibody and the resulting precipitates as well as original cell lysates were subjected to immunoblot analysis (IB) with indicated antibodies. (C) ChIP-qPCR analysis using FLAG antibody on Setd5 promoter, enhancer and intron 2 (control) in wild type (WT) and Ankrd11 -disrupted Neuro-2a cells expressing <t>FLAG-WDR5.</t> Vector-transfected cells also served as controls. Data are means ± SEM ( n = 3 independent experiments). ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). Immunoblot analysis (IB) confirmed comparable expression of FLAG-WDR5 in WT and Ankrd11 -disrupted Neuro-2a cells (inset). (D) ChIP-qPCR analysis using H3K4me3 antibody on Setd5 promoter, enhancer and intron 2 (control) in wild-type (WT) and Ankrd11 -disrupted Neuro-2a cells. Normal rabbit IgG was used as a control. Data are means ± SEM ( n = 4 independent experiments). ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). (E) RT-qPCR analysis of Setd5 mRNA levels in Neuro-2a cells treated with WDR5 inhibitor OICR9429 at the indicated concentrations for 5 days. Data are means ± SEM ( n = 3 for each genotype). ∗∗ p < 0.01, ∗∗∗ p < 0.005, and ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). (F) Schematic representation of Setd5 regulation by ANKRD11 through WDR5 and KMT2-mediated H3K4 trimethylation on Setd5 promoter. See also and .
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    Image Search Results


    (A–D) Wild-type (WT) T cells were labeled with CFSE and activated in the presence of MM-401, WDR5-IN-4, or DMSO. After 4 days, cells were analyzed by flow cytometry to assess the effects of MM-401 (A) and WDR5-IN-4 (B) on cell division (CFSE dilution), and by RT-PCR to determine the effects of these inhibitors on Sell (C) and Tcf7 (D) transcription. Data are representative of two independent experiments. (E, F) Naïve CD8⁺ T cells were isolated from WT mice and activated in vitro for 4 days to generate activated T cells. Naïve and activated T cells were compared for Tcf7 expression by RT-PCR (E) and for H3K4me3 enrichment at the Tcf7 locus by ChIP-PCR (F). Data are representative of two independent experiments. (G, H) Mll1KO and WT T cells were activated in vitro and analyzed after 4 days for Tcf7 transcription by RT-PCR (G) and H3K4me3 enrichment at the Tcf7 locus by ChIP-PCR (H). Data are representative of three independent experiments. (I, J) Thymocytes and B cells were isolated from WT mice and compared for Tcf7 transcription by RT-PCR (I) and H3K4me3 enrichment at the Tcf7 locus by ChIP-PCR (J). Data are representative of two independent experiments.

    Journal: bioRxiv

    Article Title: The MLL1–MENIN complex preserves CD8 T cell memory through a TOX–BTLA-TCF1 axis

    doi: 10.64898/2026.04.03.715913

    Figure Lengend Snippet: (A–D) Wild-type (WT) T cells were labeled with CFSE and activated in the presence of MM-401, WDR5-IN-4, or DMSO. After 4 days, cells were analyzed by flow cytometry to assess the effects of MM-401 (A) and WDR5-IN-4 (B) on cell division (CFSE dilution), and by RT-PCR to determine the effects of these inhibitors on Sell (C) and Tcf7 (D) transcription. Data are representative of two independent experiments. (E, F) Naïve CD8⁺ T cells were isolated from WT mice and activated in vitro for 4 days to generate activated T cells. Naïve and activated T cells were compared for Tcf7 expression by RT-PCR (E) and for H3K4me3 enrichment at the Tcf7 locus by ChIP-PCR (F). Data are representative of two independent experiments. (G, H) Mll1KO and WT T cells were activated in vitro and analyzed after 4 days for Tcf7 transcription by RT-PCR (G) and H3K4me3 enrichment at the Tcf7 locus by ChIP-PCR (H). Data are representative of three independent experiments. (I, J) Thymocytes and B cells were isolated from WT mice and compared for Tcf7 transcription by RT-PCR (I) and H3K4me3 enrichment at the Tcf7 locus by ChIP-PCR (J). Data are representative of two independent experiments.

    Article Snippet: Small-molecule inhibitors used included AKT inhibitor MK-2206 (selleckchem) used at 0.05uM, AKT inhibitor AKTi-1/2 (selleckchem) used at 0.5uM, Menin inhibitor MI-3454 used at 0.25uM, Wdr5 inhibitor WDR5-IN-4 (Medchemexpress) used at 2.5uM, Wdr5 inhibitor MM-401 (invivochem) used at 25uM, Thymidine (for S-phase arrest) used at 2mM (sigma-aldrich), Nocodazole (for mitotic arrest) used at 0.5uM (selleckchem).

    Techniques: Labeling, Flow Cytometry, Reverse Transcription Polymerase Chain Reaction, Isolation, In Vitro, Expressing

    (A) Wild-type (WT) T cells were activated in the presence of WDR5-IN-4, MM-401, or DMSO. After 4 days, cells were collected and analyzed for Tox expression by RT-PCR. Data are representative of two independent experiments. (B, E) T cells from Mll1KO mice and their WT littermates were activated in vitro. After 4 days, cells were collected and analyzed for H3K4me3 (B) and H4K16ac (E) enrichment at the Tox locus by ChIP-PCR. Data are representative of three independent experiments. (C, D, F) Thymocytes and B cells were isolated from WT mice and compared for Tox expression by RT-PCR (C), and for H3K4me3 (D) and H4K16ac (F) enrichment at the Tox locus by ChIP-PCR. Data are representative of two independent experiments. (G, H) T cells from Mll1KO mice and their WT littermates were activated in the presence of MI-3454 or DMSO. After 4 days, cells were collected and analyzed for Tox (G) and Btla (H) expression by RT-PCR. Data are representative of two independent experiments.

    Journal: bioRxiv

    Article Title: The MLL1–MENIN complex preserves CD8 T cell memory through a TOX–BTLA-TCF1 axis

    doi: 10.64898/2026.04.03.715913

    Figure Lengend Snippet: (A) Wild-type (WT) T cells were activated in the presence of WDR5-IN-4, MM-401, or DMSO. After 4 days, cells were collected and analyzed for Tox expression by RT-PCR. Data are representative of two independent experiments. (B, E) T cells from Mll1KO mice and their WT littermates were activated in vitro. After 4 days, cells were collected and analyzed for H3K4me3 (B) and H4K16ac (E) enrichment at the Tox locus by ChIP-PCR. Data are representative of three independent experiments. (C, D, F) Thymocytes and B cells were isolated from WT mice and compared for Tox expression by RT-PCR (C), and for H3K4me3 (D) and H4K16ac (F) enrichment at the Tox locus by ChIP-PCR. Data are representative of two independent experiments. (G, H) T cells from Mll1KO mice and their WT littermates were activated in the presence of MI-3454 or DMSO. After 4 days, cells were collected and analyzed for Tox (G) and Btla (H) expression by RT-PCR. Data are representative of two independent experiments.

    Article Snippet: Small-molecule inhibitors used included AKT inhibitor MK-2206 (selleckchem) used at 0.05uM, AKT inhibitor AKTi-1/2 (selleckchem) used at 0.5uM, Menin inhibitor MI-3454 used at 0.25uM, Wdr5 inhibitor WDR5-IN-4 (Medchemexpress) used at 2.5uM, Wdr5 inhibitor MM-401 (invivochem) used at 25uM, Thymidine (for S-phase arrest) used at 2mM (sigma-aldrich), Nocodazole (for mitotic arrest) used at 0.5uM (selleckchem).

    Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, In Vitro, Isolation

    (A–D) Wild-type (WT) T cells were labeled with CFSE and activated in the presence of MM-401, WDR5-IN-4, or DMSO. After 4 days, cells were analyzed by flow cytometry to assess the effects of MM-401 (A) and WDR5-IN-4 (B) on cell division (CFSE dilution), and by RT-PCR to determine the effects of these inhibitors on Sell (C) and Tcf7 (D) transcription. Data are representative of two independent experiments. (E, F) Naïve CD8⁺ T cells were isolated from WT mice and activated in vitro for 4 days to generate activated T cells. Naïve and activated T cells were compared for Tcf7 expression by RT-PCR (E) and for H3K4me3 enrichment at the Tcf7 locus by ChIP-PCR (F). Data are representative of two independent experiments. (G, H) Mll1KO and WT T cells were activated in vitro and analyzed after 4 days for Tcf7 transcription by RT-PCR (G) and H3K4me3 enrichment at the Tcf7 locus by ChIP-PCR (H). Data are representative of three independent experiments. (I, J) Thymocytes and B cells were isolated from WT mice and compared for Tcf7 transcription by RT-PCR (I) and H3K4me3 enrichment at the Tcf7 locus by ChIP-PCR (J). Data are representative of two independent experiments.

    Journal: bioRxiv

    Article Title: The MLL1–MENIN complex preserves CD8 T cell memory through a TOX–BTLA-TCF1 axis

    doi: 10.64898/2026.04.03.715913

    Figure Lengend Snippet: (A–D) Wild-type (WT) T cells were labeled with CFSE and activated in the presence of MM-401, WDR5-IN-4, or DMSO. After 4 days, cells were analyzed by flow cytometry to assess the effects of MM-401 (A) and WDR5-IN-4 (B) on cell division (CFSE dilution), and by RT-PCR to determine the effects of these inhibitors on Sell (C) and Tcf7 (D) transcription. Data are representative of two independent experiments. (E, F) Naïve CD8⁺ T cells were isolated from WT mice and activated in vitro for 4 days to generate activated T cells. Naïve and activated T cells were compared for Tcf7 expression by RT-PCR (E) and for H3K4me3 enrichment at the Tcf7 locus by ChIP-PCR (F). Data are representative of two independent experiments. (G, H) Mll1KO and WT T cells were activated in vitro and analyzed after 4 days for Tcf7 transcription by RT-PCR (G) and H3K4me3 enrichment at the Tcf7 locus by ChIP-PCR (H). Data are representative of three independent experiments. (I, J) Thymocytes and B cells were isolated from WT mice and compared for Tcf7 transcription by RT-PCR (I) and H3K4me3 enrichment at the Tcf7 locus by ChIP-PCR (J). Data are representative of two independent experiments.

    Article Snippet: Small-molecule inhibitors used included AKT inhibitor MK-2206 (selleckchem) used at 0.05uM, AKT inhibitor AKTi-1/2 (selleckchem) used at 0.5uM, Menin inhibitor MI-3454 used at 0.25uM, Wdr5 inhibitor WDR5-IN-4 (Medchemexpress) used at 2.5uM, Wdr5 inhibitor MM-401 (invivochem) used at 25uM, Thymidine (for S-phase arrest) used at 2mM (sigma-aldrich), Nocodazole (for mitotic arrest) used at 0.5uM (selleckchem).

    Techniques: Labeling, Flow Cytometry, Reverse Transcription Polymerase Chain Reaction, Isolation, In Vitro, Expressing

    (A) Wild-type (WT) T cells were activated in the presence of WDR5-IN-4, MM-401, or DMSO. After 4 days, cells were collected and analyzed for Tox expression by RT-PCR. Data are representative of two independent experiments. (B, E) T cells from Mll1KO mice and their WT littermates were activated in vitro. After 4 days, cells were collected and analyzed for H3K4me3 (B) and H4K16ac (E) enrichment at the Tox locus by ChIP-PCR. Data are representative of three independent experiments. (C, D, F) Thymocytes and B cells were isolated from WT mice and compared for Tox expression by RT-PCR (C), and for H3K4me3 (D) and H4K16ac (F) enrichment at the Tox locus by ChIP-PCR. Data are representative of two independent experiments. (G, H) T cells from Mll1KO mice and their WT littermates were activated in the presence of MI-3454 or DMSO. After 4 days, cells were collected and analyzed for Tox (G) and Btla (H) expression by RT-PCR. Data are representative of two independent experiments.

    Journal: bioRxiv

    Article Title: The MLL1–MENIN complex preserves CD8 T cell memory through a TOX–BTLA-TCF1 axis

    doi: 10.64898/2026.04.03.715913

    Figure Lengend Snippet: (A) Wild-type (WT) T cells were activated in the presence of WDR5-IN-4, MM-401, or DMSO. After 4 days, cells were collected and analyzed for Tox expression by RT-PCR. Data are representative of two independent experiments. (B, E) T cells from Mll1KO mice and their WT littermates were activated in vitro. After 4 days, cells were collected and analyzed for H3K4me3 (B) and H4K16ac (E) enrichment at the Tox locus by ChIP-PCR. Data are representative of three independent experiments. (C, D, F) Thymocytes and B cells were isolated from WT mice and compared for Tox expression by RT-PCR (C), and for H3K4me3 (D) and H4K16ac (F) enrichment at the Tox locus by ChIP-PCR. Data are representative of two independent experiments. (G, H) T cells from Mll1KO mice and their WT littermates were activated in the presence of MI-3454 or DMSO. After 4 days, cells were collected and analyzed for Tox (G) and Btla (H) expression by RT-PCR. Data are representative of two independent experiments.

    Article Snippet: Small-molecule inhibitors used included AKT inhibitor MK-2206 (selleckchem) used at 0.05uM, AKT inhibitor AKTi-1/2 (selleckchem) used at 0.5uM, Menin inhibitor MI-3454 used at 0.25uM, Wdr5 inhibitor WDR5-IN-4 (Medchemexpress) used at 2.5uM, Wdr5 inhibitor MM-401 (invivochem) used at 25uM, Thymidine (for S-phase arrest) used at 2mM (sigma-aldrich), Nocodazole (for mitotic arrest) used at 0.5uM (selleckchem).

    Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, In Vitro, Isolation

    Hypoxia-induced epigenetic regulation contributes to increased OPN expression. (A) Western blotting showing the levels of HIF-1α, H3K4me3, H3K9me3, H3K27me3, and H3 in THP-1 and U937 cells exposed to 1% O 2 for the indicated durations. (B) IF staining showing the levels of HIF-1α, H3K4me3, H3K9me3, and H3K27me3 in THP-1 cells exposed to 1% O 2 for the indicated durations. The target proteins are shown in green. DAPI was used to stain the nuclei, and F-actin was labeled to delineate the cytoplasmic region (scale bar = 40 μm). (C) qPCR analysis of H3K4me3 enrichment at SPP1 promoter area in THP-1 cells under indicated treatment conditions ( n = 3 per group; normoxia, normoxic culture for 24 h; hypoxia, hypoxic culture for 24 h; H + siCtrl, hypoxic culture for 24 h together with transfection of the negative control siRNA; H + siWDR5-2, hypoxic culture for 24 h together with WDR5 knockdown; H + DMSO, hypoxic culture for 24 h together with DMSO treatment; H + OICR-9429, hypoxic culture for 24 h together with OICR-9429 treatment). (D) qPCR analysis of WDR5 enrichment at SPP1 promoter area in THP-1 cells under indicated treatment conditions ( n = 3 per group). (E) Agarose gel electrophoresis assays showing ChIP-PCR (SPP1 promoter sequence) products from THP-1 cells immunoprecipitated with anti-H3K4me3, anti-WDR5, and IgG antibodies under indicated treatment conditions. (F) qPCR analysis of H3K4me3 enrichment at SPP1 promoter area in U937 cells under indicated treatment conditions ( n = 3 per group). (G) qPCR analysis of WDR5 enrichment at SPP1 promoter area in U937 cells under indicated treatment conditions ( n = 3 per group). (H) Agarose gel electrophoresis assays showing ChIP-PCR (SPP1 promoter sequence) products from U937 cells immunoprecipitated with anti-H3K4me3, anti-WDR5, and IgG antibodies under indicated treatment conditions. (I and J) qPCR analysis of SPP1 expression in THP-1 (I) and U937 (J) cells under indicated treatment conditions ( n = 3 per group). (K) Western blotting showing OPN expression in THP-1 and U937 cells subjected to the indicated treatments. The data are presented as the means ± SD; * P < 0.05, ** P < 0.01, and *** P < 0.001. HIF-1α, hypoxia-inducible factor α; H3K4me3, histone 3 lysine 4 trimethylation; H3K9me3, histone 3 lysine 9 trimethylation; H3K27me3, histone 3 lysine 27 trimethylation; IF, immunofluorescence; ChIP, chromatin immunoprecipitation; WDR5, WD40 repeat-containing protein 5; SPP1, secreted phosphoprotein 1; OPN, osteopontin; DMSO, dimethyl sulfoxide; qPCR, quantitative real-time PCR; SD, standard deviation; kDa, kilodaltons.

    Journal: Cancer Communications

    Article Title: Hypoxia-Induced Osteopontin-Positive Glioma-Associated Macrophages Facilitate Glioma Mesenchymal Transition via NF-κB Pathway Activation

    doi: 10.34133/cancomm.0007

    Figure Lengend Snippet: Hypoxia-induced epigenetic regulation contributes to increased OPN expression. (A) Western blotting showing the levels of HIF-1α, H3K4me3, H3K9me3, H3K27me3, and H3 in THP-1 and U937 cells exposed to 1% O 2 for the indicated durations. (B) IF staining showing the levels of HIF-1α, H3K4me3, H3K9me3, and H3K27me3 in THP-1 cells exposed to 1% O 2 for the indicated durations. The target proteins are shown in green. DAPI was used to stain the nuclei, and F-actin was labeled to delineate the cytoplasmic region (scale bar = 40 μm). (C) qPCR analysis of H3K4me3 enrichment at SPP1 promoter area in THP-1 cells under indicated treatment conditions ( n = 3 per group; normoxia, normoxic culture for 24 h; hypoxia, hypoxic culture for 24 h; H + siCtrl, hypoxic culture for 24 h together with transfection of the negative control siRNA; H + siWDR5-2, hypoxic culture for 24 h together with WDR5 knockdown; H + DMSO, hypoxic culture for 24 h together with DMSO treatment; H + OICR-9429, hypoxic culture for 24 h together with OICR-9429 treatment). (D) qPCR analysis of WDR5 enrichment at SPP1 promoter area in THP-1 cells under indicated treatment conditions ( n = 3 per group). (E) Agarose gel electrophoresis assays showing ChIP-PCR (SPP1 promoter sequence) products from THP-1 cells immunoprecipitated with anti-H3K4me3, anti-WDR5, and IgG antibodies under indicated treatment conditions. (F) qPCR analysis of H3K4me3 enrichment at SPP1 promoter area in U937 cells under indicated treatment conditions ( n = 3 per group). (G) qPCR analysis of WDR5 enrichment at SPP1 promoter area in U937 cells under indicated treatment conditions ( n = 3 per group). (H) Agarose gel electrophoresis assays showing ChIP-PCR (SPP1 promoter sequence) products from U937 cells immunoprecipitated with anti-H3K4me3, anti-WDR5, and IgG antibodies under indicated treatment conditions. (I and J) qPCR analysis of SPP1 expression in THP-1 (I) and U937 (J) cells under indicated treatment conditions ( n = 3 per group). (K) Western blotting showing OPN expression in THP-1 and U937 cells subjected to the indicated treatments. The data are presented as the means ± SD; * P < 0.05, ** P < 0.01, and *** P < 0.001. HIF-1α, hypoxia-inducible factor α; H3K4me3, histone 3 lysine 4 trimethylation; H3K9me3, histone 3 lysine 9 trimethylation; H3K27me3, histone 3 lysine 27 trimethylation; IF, immunofluorescence; ChIP, chromatin immunoprecipitation; WDR5, WD40 repeat-containing protein 5; SPP1, secreted phosphoprotein 1; OPN, osteopontin; DMSO, dimethyl sulfoxide; qPCR, quantitative real-time PCR; SD, standard deviation; kDa, kilodaltons.

    Article Snippet: THP-1 and U937 cells were treated with the WD40 repeat-containing protein 5 (WDR5) inhibitor OICR-9429 (20 μM, catalog no. HY-16993, MedChemExpress) for 24 h during hypoxic culture.

    Techniques: Expressing, Western Blot, Staining, Labeling, Transfection, Negative Control, Knockdown, Agarose Gel Electrophoresis, Sequencing, Immunoprecipitation, Immunofluorescence, Chromatin Immunoprecipitation, Real-time Polymerase Chain Reaction, Standard Deviation

    Targeting OPN increases the therapeutic effectiveness of TMZ in a C57BL/6J in vivo glioma model. (A) Schematic illustration of the in vivo experimental design in C57BL/6J mice. The blue arrow represents intracranial implantation; the red arrows represent treatments (control, treatment with PBS; OPNi-1, treatment with OPNi-1 alone; TMZ, treatment with TMZ alone; TMZ + OPNi-1, combined treatment with TMZ and OPNi-1); the green arrows represent MRI scans. (B) Representative MR images showing the intracranial tumor burden in C57BL/6J mice from the indicated treatment groups. (C) Quantification of the tumor volume in C57BL/6J mice from the indicated groups on days 0, 7, and 14 since initial treatment ( n = 7 mice per group). (D) Kaplan–Meier survival curves of glioma-bearing mice receiving the indicated treatments ( n = 7 mice per group). (E) Representative mIHC images of glioma tissues from mouse brain sections. Eight markers were divided into 2 staining panels and applied to serial tumor sections to preserve spatial consistency. Panel 1 includes PD-L1, F4/80, CD163, and OPN, and panel 2 includes CD20, NK1.1, CD8a, and CD4. Images for both panels were acquired from matched anatomical regions on adjacent serial sections. (F) Quantification of PD-L1 positivity based on mIHC staining ( n = 3 per group). (G) Quantification of macrophage (F4/80 + cells) proportion based on mIHC staining ( n = 3 per group). (H) Quantification of GAM (CD163 + F4/80 + cells) proportion based on mIHC staining ( n = 3 per group). (I) Quantification of OPN + GAM (OPN + CD163 + F4/80 + cells) proportion based on mIHC staining ( n = 3 per group). (J) Quantification of B cell (CD20 + cells) proportion based on mIHC staining ( n = 3 per group). (K) Quantification of NK cell (NK1.1 + cells) proportion based on mIHC staining ( n = 3 per group). (L) Quantification of CD8 + T cell (CD8a + cells) proportion based on mIHC staining ( n = 3 per group). (M) Quantification of CD4 + T cell (CD4 + cells) proportion based on mIHC staining ( n = 3 per group). Data are presented as the mean ± SD; * P < 0.05, ** P < 0.01. PD-L1, programmed cell death ligand 1; F4/80, mouse EGF-like module-containing mucin-like hormone receptor-like 1; CD163, cluster of differentiation 163; OPN, osteopontin; GAM, glioma-associated macrophage; OPN + GAM, osteopontin positive glioma-associated macrophage; NK, natural killer; CD20, cluster of differentiation 20; SD, standard deviation. Hypoxia induces the emergence of OPN + GAMs through the epigenetic activation of the H3K4me3-WDR5 axis. The secreted OPN promotes the mesenchymal transition and PD-L1 expression in glioma cells via CD44-mediated activation of the NF-κB signaling pathway.

    Journal: Cancer Communications

    Article Title: Hypoxia-Induced Osteopontin-Positive Glioma-Associated Macrophages Facilitate Glioma Mesenchymal Transition via NF-κB Pathway Activation

    doi: 10.34133/cancomm.0007

    Figure Lengend Snippet: Targeting OPN increases the therapeutic effectiveness of TMZ in a C57BL/6J in vivo glioma model. (A) Schematic illustration of the in vivo experimental design in C57BL/6J mice. The blue arrow represents intracranial implantation; the red arrows represent treatments (control, treatment with PBS; OPNi-1, treatment with OPNi-1 alone; TMZ, treatment with TMZ alone; TMZ + OPNi-1, combined treatment with TMZ and OPNi-1); the green arrows represent MRI scans. (B) Representative MR images showing the intracranial tumor burden in C57BL/6J mice from the indicated treatment groups. (C) Quantification of the tumor volume in C57BL/6J mice from the indicated groups on days 0, 7, and 14 since initial treatment ( n = 7 mice per group). (D) Kaplan–Meier survival curves of glioma-bearing mice receiving the indicated treatments ( n = 7 mice per group). (E) Representative mIHC images of glioma tissues from mouse brain sections. Eight markers were divided into 2 staining panels and applied to serial tumor sections to preserve spatial consistency. Panel 1 includes PD-L1, F4/80, CD163, and OPN, and panel 2 includes CD20, NK1.1, CD8a, and CD4. Images for both panels were acquired from matched anatomical regions on adjacent serial sections. (F) Quantification of PD-L1 positivity based on mIHC staining ( n = 3 per group). (G) Quantification of macrophage (F4/80 + cells) proportion based on mIHC staining ( n = 3 per group). (H) Quantification of GAM (CD163 + F4/80 + cells) proportion based on mIHC staining ( n = 3 per group). (I) Quantification of OPN + GAM (OPN + CD163 + F4/80 + cells) proportion based on mIHC staining ( n = 3 per group). (J) Quantification of B cell (CD20 + cells) proportion based on mIHC staining ( n = 3 per group). (K) Quantification of NK cell (NK1.1 + cells) proportion based on mIHC staining ( n = 3 per group). (L) Quantification of CD8 + T cell (CD8a + cells) proportion based on mIHC staining ( n = 3 per group). (M) Quantification of CD4 + T cell (CD4 + cells) proportion based on mIHC staining ( n = 3 per group). Data are presented as the mean ± SD; * P < 0.05, ** P < 0.01. PD-L1, programmed cell death ligand 1; F4/80, mouse EGF-like module-containing mucin-like hormone receptor-like 1; CD163, cluster of differentiation 163; OPN, osteopontin; GAM, glioma-associated macrophage; OPN + GAM, osteopontin positive glioma-associated macrophage; NK, natural killer; CD20, cluster of differentiation 20; SD, standard deviation. Hypoxia induces the emergence of OPN + GAMs through the epigenetic activation of the H3K4me3-WDR5 axis. The secreted OPN promotes the mesenchymal transition and PD-L1 expression in glioma cells via CD44-mediated activation of the NF-κB signaling pathway.

    Article Snippet: THP-1 and U937 cells were treated with the WD40 repeat-containing protein 5 (WDR5) inhibitor OICR-9429 (20 μM, catalog no. HY-16993, MedChemExpress) for 24 h during hypoxic culture.

    Techniques: In Vivo, Control, Staining, Standard Deviation, Activation Assay, Expressing

    Schematic diagram showing mechanistic summary of OPN + GAM promoting mesenchymal transition of glioma cells under hypoxic conditions. Hypoxia induces the emergence of OPN + GAMs through the epigenetic activation of the H3K4me3-WDR5 axis. The secreted OPN promotes mesenchymal transition and PD-L1 expression in glioma cell axis. The secreted OPN promotes the mesenchymal transition and PD-L1 expression in glioma cells via CD44-mediated activation of the NF-κB signaling pathway. PD-L1, programmed cell death ligand 1; OPN, osteopontin; GAM, glioma-associated macrophage; H3K4me3, histone 3 lysine 4 trimethylation; MES, mesenchymal; PN, proneural; GBM, glioblastoma.

    Journal: Cancer Communications

    Article Title: Hypoxia-Induced Osteopontin-Positive Glioma-Associated Macrophages Facilitate Glioma Mesenchymal Transition via NF-κB Pathway Activation

    doi: 10.34133/cancomm.0007

    Figure Lengend Snippet: Schematic diagram showing mechanistic summary of OPN + GAM promoting mesenchymal transition of glioma cells under hypoxic conditions. Hypoxia induces the emergence of OPN + GAMs through the epigenetic activation of the H3K4me3-WDR5 axis. The secreted OPN promotes mesenchymal transition and PD-L1 expression in glioma cell axis. The secreted OPN promotes the mesenchymal transition and PD-L1 expression in glioma cells via CD44-mediated activation of the NF-κB signaling pathway. PD-L1, programmed cell death ligand 1; OPN, osteopontin; GAM, glioma-associated macrophage; H3K4me3, histone 3 lysine 4 trimethylation; MES, mesenchymal; PN, proneural; GBM, glioblastoma.

    Article Snippet: THP-1 and U937 cells were treated with the WD40 repeat-containing protein 5 (WDR5) inhibitor OICR-9429 (20 μM, catalog no. HY-16993, MedChemExpress) for 24 h during hypoxic culture.

    Techniques: Activation Assay, Expressing

    Mediation of Setd5 regulation by ANKRD11 through WDR5-KMT2 (A) Proteins identified to interact with ANKRD11 via immunoprecipitation followed by mass spectrometry (IP-MS) in HeLa cells, data sourced from Hein et al. (B) Lysates prepared from Neuro-2a cells transfected with expression plasmid for 3xFLAG-ANKRD11-3xHA were subjected to immunoprecipitation (IP) with FLAG antibody and the resulting precipitates as well as original cell lysates were subjected to immunoblot analysis (IB) with indicated antibodies. (C) ChIP-qPCR analysis using FLAG antibody on Setd5 promoter, enhancer and intron 2 (control) in wild type (WT) and Ankrd11 -disrupted Neuro-2a cells expressing FLAG-WDR5. Vector-transfected cells also served as controls. Data are means ± SEM ( n = 3 independent experiments). ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). Immunoblot analysis (IB) confirmed comparable expression of FLAG-WDR5 in WT and Ankrd11 -disrupted Neuro-2a cells (inset). (D) ChIP-qPCR analysis using H3K4me3 antibody on Setd5 promoter, enhancer and intron 2 (control) in wild-type (WT) and Ankrd11 -disrupted Neuro-2a cells. Normal rabbit IgG was used as a control. Data are means ± SEM ( n = 4 independent experiments). ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). (E) RT-qPCR analysis of Setd5 mRNA levels in Neuro-2a cells treated with WDR5 inhibitor OICR9429 at the indicated concentrations for 5 days. Data are means ± SEM ( n = 3 for each genotype). ∗∗ p < 0.01, ∗∗∗ p < 0.005, and ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). (F) Schematic representation of Setd5 regulation by ANKRD11 through WDR5 and KMT2-mediated H3K4 trimethylation on Setd5 promoter. See also and .

    Journal: iScience

    Article Title: KBG syndrome-associated protein ANKRD11 regulates SETD5 expression to modulate rRNA levels and translation

    doi: 10.1016/j.isci.2025.112699

    Figure Lengend Snippet: Mediation of Setd5 regulation by ANKRD11 through WDR5-KMT2 (A) Proteins identified to interact with ANKRD11 via immunoprecipitation followed by mass spectrometry (IP-MS) in HeLa cells, data sourced from Hein et al. (B) Lysates prepared from Neuro-2a cells transfected with expression plasmid for 3xFLAG-ANKRD11-3xHA were subjected to immunoprecipitation (IP) with FLAG antibody and the resulting precipitates as well as original cell lysates were subjected to immunoblot analysis (IB) with indicated antibodies. (C) ChIP-qPCR analysis using FLAG antibody on Setd5 promoter, enhancer and intron 2 (control) in wild type (WT) and Ankrd11 -disrupted Neuro-2a cells expressing FLAG-WDR5. Vector-transfected cells also served as controls. Data are means ± SEM ( n = 3 independent experiments). ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). Immunoblot analysis (IB) confirmed comparable expression of FLAG-WDR5 in WT and Ankrd11 -disrupted Neuro-2a cells (inset). (D) ChIP-qPCR analysis using H3K4me3 antibody on Setd5 promoter, enhancer and intron 2 (control) in wild-type (WT) and Ankrd11 -disrupted Neuro-2a cells. Normal rabbit IgG was used as a control. Data are means ± SEM ( n = 4 independent experiments). ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). (E) RT-qPCR analysis of Setd5 mRNA levels in Neuro-2a cells treated with WDR5 inhibitor OICR9429 at the indicated concentrations for 5 days. Data are means ± SEM ( n = 3 for each genotype). ∗∗ p < 0.01, ∗∗∗ p < 0.005, and ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). (F) Schematic representation of Setd5 regulation by ANKRD11 through WDR5 and KMT2-mediated H3K4 trimethylation on Setd5 promoter. See also and .

    Article Snippet: OICR-9429, WDR5 inhibitor , Selleck , S7833; CAS: 1801787-56-3.

    Techniques: Immunoprecipitation, Mass Spectrometry, Protein-Protein interactions, Transfection, Expressing, Plasmid Preparation, Western Blot, ChIP-qPCR, Control, Quantitative RT-PCR

    Correlated expression of ANKRD11 and SETD5 in human cells (A) Expression levels of ANKRD11 mRNA (x axis) and SETD5 mRNA (y axis) across 1,479 human cell lines from the DepMap project, depicted as log2(TPM+1). Pearson correlation coefficient (r) and p value (Pearson’s correlation test) are provided. (B) Expression levels of ANKRD11 mRNA ( x axis) and SETD5 mRNA ( y axis) across 33 human neuroblastoma cell lines from the DepMap project, depicted as log2(TPM+1). Pearson correlation coefficient (r) and p value (Pearson’s correlation test) are provided. (C) RT-qPCR analysis of ANKRD11 mRNA levels in SH-SY5Y cells transfected with Cas9 targeting ANKRD11 exon 5 or control vector. Data are means ± SEM ( n = 3 for each treatment). ∗∗ p < 0.01 (one-way ANOVA followed by Tukey’s test). (D) RT-qPCR analysis of SETD5 mRNA levels in SH-SY5Y cells transfected with Cas9 targeting ANKRD11 exon 5 or control vector. Data are means ± SEM ( n = 3 for each treatment). ∗ p < 0.05 and ∗∗ p < 0.01 (one-way ANOVA followed by Tukey’s test). (E) RT-qPCR analysis of pre-rRNA levels in SH-SY5Y cells transfected with Cas9 targeting ANKRD11 exon 5 or control vector. Data are means ± SEM ( n = 3 for each treatment). ∗ p < 0.05 and ∗∗ p < 0.01 (one-way ANOVA followed by Tukey’s test). (F) Immunoblot analysis (IB) of puromycin-incorporated newly synthesized proteins, ANKRD11, SETD5, and DDB1 (loading control) in SH-SY5Y cells transfected with Cas9 targeting ANKRD11 exon 5 or control vector. (G) Relative translational activity measured as in F. Data are means ± SEM ( n = 3 for each treatment). ∗ p < 0.05 (one-way ANOVA followed by Tukey’s test). (H) ChIP-qPCR analysis using FLAG antibody on SETD5 promoter, enhancer and intron 2 (control) in wild-type (WT) and Ankrd11 -disrupted SH-SY5Y cells expressing FLAG-WDR5 in response to doxycycline (1 μg/mL for WT and 2 μg/mL for Ankrd11 -disrupted SH-SY5Y cells) for 3 days. Doxycycline-untreated cells served as controls. Data are means ± SEM ( n = 3 independent experiments). ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). Immunoblot analysis (IB) confirmed comparable expression of FLAG-WDR5 in WT and Ankrd11 -disrupted SH-SY5Y cells (inset). (I) ChIP-qPCR analysis using H3K4me3 antibody on SETD5 promoter, enhancer and intron 2 (control) in wild-type (WT) and Ankrd11 -disrupted SH-SY5Y cells. Normal rabbit IgG was used as a control. Data are means ± SEM ( n = 3 independent experiments). ∗∗∗ p < 0.005 and ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). See also .

    Journal: iScience

    Article Title: KBG syndrome-associated protein ANKRD11 regulates SETD5 expression to modulate rRNA levels and translation

    doi: 10.1016/j.isci.2025.112699

    Figure Lengend Snippet: Correlated expression of ANKRD11 and SETD5 in human cells (A) Expression levels of ANKRD11 mRNA (x axis) and SETD5 mRNA (y axis) across 1,479 human cell lines from the DepMap project, depicted as log2(TPM+1). Pearson correlation coefficient (r) and p value (Pearson’s correlation test) are provided. (B) Expression levels of ANKRD11 mRNA ( x axis) and SETD5 mRNA ( y axis) across 33 human neuroblastoma cell lines from the DepMap project, depicted as log2(TPM+1). Pearson correlation coefficient (r) and p value (Pearson’s correlation test) are provided. (C) RT-qPCR analysis of ANKRD11 mRNA levels in SH-SY5Y cells transfected with Cas9 targeting ANKRD11 exon 5 or control vector. Data are means ± SEM ( n = 3 for each treatment). ∗∗ p < 0.01 (one-way ANOVA followed by Tukey’s test). (D) RT-qPCR analysis of SETD5 mRNA levels in SH-SY5Y cells transfected with Cas9 targeting ANKRD11 exon 5 or control vector. Data are means ± SEM ( n = 3 for each treatment). ∗ p < 0.05 and ∗∗ p < 0.01 (one-way ANOVA followed by Tukey’s test). (E) RT-qPCR analysis of pre-rRNA levels in SH-SY5Y cells transfected with Cas9 targeting ANKRD11 exon 5 or control vector. Data are means ± SEM ( n = 3 for each treatment). ∗ p < 0.05 and ∗∗ p < 0.01 (one-way ANOVA followed by Tukey’s test). (F) Immunoblot analysis (IB) of puromycin-incorporated newly synthesized proteins, ANKRD11, SETD5, and DDB1 (loading control) in SH-SY5Y cells transfected with Cas9 targeting ANKRD11 exon 5 or control vector. (G) Relative translational activity measured as in F. Data are means ± SEM ( n = 3 for each treatment). ∗ p < 0.05 (one-way ANOVA followed by Tukey’s test). (H) ChIP-qPCR analysis using FLAG antibody on SETD5 promoter, enhancer and intron 2 (control) in wild-type (WT) and Ankrd11 -disrupted SH-SY5Y cells expressing FLAG-WDR5 in response to doxycycline (1 μg/mL for WT and 2 μg/mL for Ankrd11 -disrupted SH-SY5Y cells) for 3 days. Doxycycline-untreated cells served as controls. Data are means ± SEM ( n = 3 independent experiments). ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). Immunoblot analysis (IB) confirmed comparable expression of FLAG-WDR5 in WT and Ankrd11 -disrupted SH-SY5Y cells (inset). (I) ChIP-qPCR analysis using H3K4me3 antibody on SETD5 promoter, enhancer and intron 2 (control) in wild-type (WT) and Ankrd11 -disrupted SH-SY5Y cells. Normal rabbit IgG was used as a control. Data are means ± SEM ( n = 3 independent experiments). ∗∗∗ p < 0.005 and ∗∗∗∗ p < 0.001 (one-way ANOVA followed by Tukey’s test). See also .

    Article Snippet: OICR-9429, WDR5 inhibitor , Selleck , S7833; CAS: 1801787-56-3.

    Techniques: Expressing, Quantitative RT-PCR, Transfection, Control, Plasmid Preparation, Western Blot, Synthesized, Activity Assay, ChIP-qPCR