wdr5 in 4 Search Results


wdr5 inhibitor wdr5  (MedChemExpress)
92
MedChemExpress wdr5 inhibitor wdr5
(A–D) Wild-type (WT) T cells were labeled with CFSE and activated in the presence of MM-401, <t>WDR5-IN-4,</t> or DMSO. After 4 days, cells were analyzed by flow cytometry to assess the effects of MM-401 (A) and <t>WDR5-IN-4</t> (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.
Wdr5 Inhibitor Wdr5, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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wdr5 inhibitor wdr5 - by Bioz Stars, 2026-05
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wdr5 in 4  (TargetMol)
94
TargetMol wdr5 in 4
a, Growth curves of SU-DIPGXIII cells transduced with shRNAs to knockdown both KAT2A and KAT2B, showing significantly reduced growth compared to control shRNA-transduced cells. b, Number of live SU-DIPGXIII+Cas9 cells expressing a control plasmid (HA/flag-GFP) or sgRNAs to KO SAGA-associated acetyltransferase activity ( TADA2B sgRNAs), or de-ubiquitinase activity ( ENY2 sgRNA). c, Schematic illustrating inhibition of histone-modifying modules of SAGA/ATAC complexes using chemical probes to target SAGA/ATAC-dependent histone acetylation (GSK4027, CPTH2, garcinol), SAGA-dependent H2A/H2B de-ubiquitination (USP22si-02), or <t>WDR5-mediated</t> H3K4me3 methylation (OICR-9529, WM856, <t>WDR5-IN-4,</t> and WDR5-IN-6). d, Average normalized cell viability from CellTiter-Glo assays conducted seven days after starting treatment of H3K27M mutant cells (teal curves) or non-transformed, H3 wildtype, control cells (black curves) with increasing doses of the KAT2A/2B bromodomain-targeting acetyltransferase inhibitor, GSK4027. e, Immunoblots confirming that treatment of BT245 cells with GSK4027 reduced H3K9ac in a dose-dependent manner, but not total H3 or SGF29 protein abundance. f-h, Dose response curves showing inhibition of H3K27M mutant DMG cell viability, but no effect on control H3 wild-type cells (black curves) following seven days of treatment with the DUB inhibitor, USP22i-S02 ( f, yellow curves), the WDR5 WIN site inhibitor, WDR5-IN-4 ( g, blue curves), or the WDR5 WBM site inhibitor, WDR5-IN-6 ( h, blue curves). i-j Average number of live SU-DIPGXIIIP*+ZsG/luc cells ( i ), and average BT245 ( j ) cell viability (CellTiter-Glo) following treatment with combinations of GSK4027 and USP22si-02 to simultaneously target both SAGA/ATAC-dependent histone acetyltransferase activity and SAGA-dependent H2A/H2B de-ubiquitination. k-l, BLISS synergy plots showing a combined effect of GSK4027 and WDR5-IN-6 treatment in reducing SU-DIPGXIIIP*+ZsG/luc growth ( k, **p<1.74×10 -3 ), and a combined effect of GSK4027 and WDR5-IN-4 treatment in reducing BT245 cell growth ( l , ****p<2.5×10 -10 ).
Wdr5 In 4, supplied by TargetMol, 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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Average 94 stars, based on 1 article reviews
wdr5 in 4 - by Bioz Stars, 2026-05
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wdr5-in-4 tfa  (Aladdin Scientific Corporation)
N/A
WDR5-IN-4 TFA is an inhibitor of the WIN site of chromatin-associated WD repeat-containing protein 5 (WDR5), with a Kd of 0.1 nM. WDR5-IN-4 TFA displaces WDR5 from chromatin and decreases the expression of associated genes,
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wdr5-in-4 tfa  (TargetMol)
N/A
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wdr5-in-4  (MedChemExpress)
N/A
WDR5-IN-4 (Compound C6) is a WIN site inhibitor of chromatin-associated WD repeat domain 5 protein (WDR5), Kd The value is 0.1 nM. WDR5-IN-4 is able to displace WDR5 from chromatin and reduce the expression of
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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, Growth curves of SU-DIPGXIII cells transduced with shRNAs to knockdown both KAT2A and KAT2B, showing significantly reduced growth compared to control shRNA-transduced cells. b, Number of live SU-DIPGXIII+Cas9 cells expressing a control plasmid (HA/flag-GFP) or sgRNAs to KO SAGA-associated acetyltransferase activity ( TADA2B sgRNAs), or de-ubiquitinase activity ( ENY2 sgRNA). c, Schematic illustrating inhibition of histone-modifying modules of SAGA/ATAC complexes using chemical probes to target SAGA/ATAC-dependent histone acetylation (GSK4027, CPTH2, garcinol), SAGA-dependent H2A/H2B de-ubiquitination (USP22si-02), or WDR5-mediated H3K4me3 methylation (OICR-9529, WM856, WDR5-IN-4, and WDR5-IN-6). d, Average normalized cell viability from CellTiter-Glo assays conducted seven days after starting treatment of H3K27M mutant cells (teal curves) or non-transformed, H3 wildtype, control cells (black curves) with increasing doses of the KAT2A/2B bromodomain-targeting acetyltransferase inhibitor, GSK4027. e, Immunoblots confirming that treatment of BT245 cells with GSK4027 reduced H3K9ac in a dose-dependent manner, but not total H3 or SGF29 protein abundance. f-h, Dose response curves showing inhibition of H3K27M mutant DMG cell viability, but no effect on control H3 wild-type cells (black curves) following seven days of treatment with the DUB inhibitor, USP22i-S02 ( f, yellow curves), the WDR5 WIN site inhibitor, WDR5-IN-4 ( g, blue curves), or the WDR5 WBM site inhibitor, WDR5-IN-6 ( h, blue curves). i-j Average number of live SU-DIPGXIIIP*+ZsG/luc cells ( i ), and average BT245 ( j ) cell viability (CellTiter-Glo) following treatment with combinations of GSK4027 and USP22si-02 to simultaneously target both SAGA/ATAC-dependent histone acetyltransferase activity and SAGA-dependent H2A/H2B de-ubiquitination. k-l, BLISS synergy plots showing a combined effect of GSK4027 and WDR5-IN-6 treatment in reducing SU-DIPGXIIIP*+ZsG/luc growth ( k, **p<1.74×10 -3 ), and a combined effect of GSK4027 and WDR5-IN-4 treatment in reducing BT245 cell growth ( l , ****p<2.5×10 -10 ).

Journal: bioRxiv

Article Title: SAGA/ATAC complexes sustain aberrant chromatin regulation and promote tumorigenesis in diffuse midline glioma

doi: 10.64898/2026.01.22.701194

Figure Lengend Snippet: a, Growth curves of SU-DIPGXIII cells transduced with shRNAs to knockdown both KAT2A and KAT2B, showing significantly reduced growth compared to control shRNA-transduced cells. b, Number of live SU-DIPGXIII+Cas9 cells expressing a control plasmid (HA/flag-GFP) or sgRNAs to KO SAGA-associated acetyltransferase activity ( TADA2B sgRNAs), or de-ubiquitinase activity ( ENY2 sgRNA). c, Schematic illustrating inhibition of histone-modifying modules of SAGA/ATAC complexes using chemical probes to target SAGA/ATAC-dependent histone acetylation (GSK4027, CPTH2, garcinol), SAGA-dependent H2A/H2B de-ubiquitination (USP22si-02), or WDR5-mediated H3K4me3 methylation (OICR-9529, WM856, WDR5-IN-4, and WDR5-IN-6). d, Average normalized cell viability from CellTiter-Glo assays conducted seven days after starting treatment of H3K27M mutant cells (teal curves) or non-transformed, H3 wildtype, control cells (black curves) with increasing doses of the KAT2A/2B bromodomain-targeting acetyltransferase inhibitor, GSK4027. e, Immunoblots confirming that treatment of BT245 cells with GSK4027 reduced H3K9ac in a dose-dependent manner, but not total H3 or SGF29 protein abundance. f-h, Dose response curves showing inhibition of H3K27M mutant DMG cell viability, but no effect on control H3 wild-type cells (black curves) following seven days of treatment with the DUB inhibitor, USP22i-S02 ( f, yellow curves), the WDR5 WIN site inhibitor, WDR5-IN-4 ( g, blue curves), or the WDR5 WBM site inhibitor, WDR5-IN-6 ( h, blue curves). i-j Average number of live SU-DIPGXIIIP*+ZsG/luc cells ( i ), and average BT245 ( j ) cell viability (CellTiter-Glo) following treatment with combinations of GSK4027 and USP22si-02 to simultaneously target both SAGA/ATAC-dependent histone acetyltransferase activity and SAGA-dependent H2A/H2B de-ubiquitination. k-l, BLISS synergy plots showing a combined effect of GSK4027 and WDR5-IN-6 treatment in reducing SU-DIPGXIIIP*+ZsG/luc growth ( k, **p<1.74×10 -3 ), and a combined effect of GSK4027 and WDR5-IN-4 treatment in reducing BT245 cell growth ( l , ****p<2.5×10 -10 ).

Article Snippet: The following compounds were used in this study: SGF29-IN-1 (cat# HY-158009, MedChemExpress), GSK4027 (cat# SML2018, Sigma Aldrich), CPTH2 (cat# J65939LB0, ThermoFisher), garcinol (cat# 14076, Active Motif), USP22si-02 (cat# SML3875, Sigma Aldrich), WDR5-IN-4 (WIN site inhibitor, cat# HY-111753, MedChemExpress), WDR5-IN-6 (WBM site inhibitor, cat# T77495, TargetMol), OICR9429 (cat# T6916, TargetMol), WM586 (WDR5/Myc inhibitor, cat# HY-153728, MedChemExpress), YM-53601 (cat# HY-100313A, MedChemExpress), NB-598 (cat# HY-16343, MedChemExpress), terbinafine (cat# T3677, TCI Chemicals), Atorvastatin (cat# SML3030, Sigma Aldrich), and Pitavastatin (cat# AMBH2D6EF677, Ambeed)

Techniques: Transduction, Knockdown, Control, shRNA, Expressing, Plasmid Preparation, Activity Assay, Inhibition, Ubiquitin Proteomics, Methylation, Mutagenesis, Transformation Assay, Western Blot, Quantitative Proteomics