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antibodies against pcaf  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc antibodies against pcaf
    Antibodies Against Pcaf, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+pcaf/pm41951013-207-0-49
    Average 86 stars, based on 1 article reviews
    antibodies against pcaf - by Bioz Stars, 2026-09
    86/100 stars

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    Related Articles

    other:

    Article Title: A Cancer-Specific Antigen Drives Histone Acetylation by Stabilizing the Acetyltransferases
    Article Snippet: Anti-MAGE-A10 (Cell Signaling Technology, 68978), anti-GCN5L2 (Cell Signaling Technology, 3305), anti-PCAF (Cell Signaling Technology, 3378), anti-Ubiquitin (Cell Signaling Technology, 20326), anti-Histone H3 (Abcam, ab1791), anti-Histone H3K9 (Abcam, ab4441), anti-Histone H3K14 (Abcam, ab52946), anti-HA tag (Abcam, ab9110), anti-SQSTM1/p62 (Abcam, ab56416), anti-LC3A/B (Abcam, ab62721), anti-CDT2/RAMP (Abcam, ab72264), anti-DDB1 (Abcam, ab109027), anti-LC3 (MBL, M152-3), anti-GCN5L2 (Sigma, SAB1403858), anti-CUL4A (Proteintech, 10693), anti-DDDDK-tag (ABclonal, AE063), anti-MYC-Tag (ABclonal, AE070), anti-His-tag (ABclonal, AE086), anti-c-Myc (ABclonal, A19032), anti-β-Tubulin (ABclonal, A12289), anti-GAPDH (ABclonal, AC002).

    Article Title: Dynamic regulation of mRNA acetylation at synapses by learning and memory
    Article Snippet: The following primary antibodies were used: anti-H3 (1:1000, Cell Signaling, 9715), anti-SYN1 (1:1000, Cell Signaling, 2312), anti-α-tubulin (1:10000, Cell Signaling, 3873), rabbit anti-NAT10 (1:1000, Abcam, ab194297), anti-Acetyl-Histone H3 (1:1000, Cell Signaling, 9649), anti-Arc (1:1000, Proteintech, 66550-1-Ig), anti-PSD95 (1:1000, Cell Signaling, 3450), anti-PCAF (1:1000, Cell Signaling, 3378), and rabbit anti-GAPDH (1:5000, Abways, ab0037).

    Article Title: Dynamic regulation of mRNA acetylation at synapses by spatial memory in mouse hippocampus
    Article Snippet: DOI: https://doi.org/10.7554/eLife.108995 20 of 32 3873), anti- NAT10 (1:1000, Abcam, ab194297), anti- Acetyl- Histone H3 (1:1000, Cell Signaling, 9649), anti- ARC (1:1000, Proteintech, 66550- 1- Ig), anti- PSD95 (1:1000, Cell Signaling, 3450), anti- PCAF (1:1000, Cell Signaling, 3378), and anti- GAPDH (1:5000, Abways, ab0037).

    Article Title: Hinokitiol preferentially suppresses metastatic lung adenocarcinoma via TMDD1-mediated ferroptosis induction and iron-sulfur cluster inhibition.
    Article Snippet: Dysregulated ISC metabolism has been implicated in cancer progression, but its role in LUAD pathogenesis and therapeutic targeting remains poorly understood.. Here, we demonstrate that ISC biogenesis is significantly upregulated in LUAD, driven by transcription factors KLF15 and ZNF384, which activate GLRX5, LYRM4, NFS1 and BOLA3 promoters.. IL-1β promotes PCAF mitochondrial translocation, releasing EP300 to amplify KLF15/ ZNF384-mediated transcriptional activation.

    Article Title: Dynamic regulation of mRNA acetylation at synapses by spatial memory in mouse hippocampus
    Article Snippet: The following primary antibodies were used: anti-Histone H3 (1:1000, Cell Signaling, 9715), anti-SYN1 (1:1000, Cell Signaling, 2312), anti-α-tubulin (1:10,000, Cell Signaling, 3873), anti-NAT10 (1:1000, Abcam, ab194297), anti-Acetyl-Histone H3 (1:1000, Cell Signaling, 9649), anti-ARC (1:1000, Proteintech, 66550-1-Ig), anti-PSD95 (1:1000, Cell Signaling, 3450), anti-PCAF (1:1000, Cell Signaling, 3378), and anti-GAPDH (1:5000, Abways, ab0037).

    Western Blot:

    Article Title: The SAGA acetyltransferase module is required for the maintenance of MAF and MYC oncogenic gene expression programs in multiple myeloma
    Article Snippet: Protein samples were resolved by SDS-PAGE on 4%–12% Nu-Page gels (Life Technologies) and transferred to PVDF membranes. .. The following antibodies were used: anti-ADA2B (1:1000 [Abcam discontinued] or 1:500 [Santa Cruz Biotechnology sc-130479,]), anti-GCN5L2 (1:1000; Cell Signaling Technology 3305), anti-PCAF (1:1000; Cell Signaling Technology 3378), anti-ADA1 (1:2000; Proteintech 20337-1-AP), anti-USP22 (1:2000; Abcam ab235923), anti-MYC (1:1000; Cell Signaling Technology 9402), anti-MAF (1:1000; Abcam ab243901), anti-E2F1 (1:1000; Santa Cruz Biotechnology sc-251), anti-DP1 (1:1000; Santa Cruz Biotechnology sc-53642), anti-IRF4 (1:500; Santa Cruz Biotechnology sc-48338), anti-TAF8 (1:100; Abcam ab204894), anti-H3K9ac (1:1000; Abcam ab32129), anti-H3 (1:20,000; Abcam ab1791), anti-GAPDH (1:10,000; Millipore Sigma MAB374), anti-β-Tubulin (1:1000; Cell Signaling Technology 2146), anti-HA (1:1000; Cell Signaling Technology 3724), apoptosis Western blot cocktail (1:250; Abcam ab136812), and secondary horseradish peroxidase (HRP)-conjugated antibodies (1:8000; Cytiva mouse IgG [NA931] or rabbit IgG [NA934]). .. Amersham ECL Prime Western blotting detection reagent (GE Healthcare) was used for chemiluminescent protein detection.

    Control:

    Article Title: PCAF promotes R-loop resolution via histone acetylation.
    Article Snippet: .. Primary antibodies used in this study were Anti-S9.6 (Kerafest, #ENH001); Anti-ssDNA (Millipore, #MAB3034); AntiNucleolin (Abcam, #ab50279); Anti-PCAF (Cell Signaling, #3378); Anti-H4K8ac (Millipore, #07-328); Anti-MRE11 (Novus Biologicals, #NB100-142); Anti-EXO1 (Genetex, #GTX109891); Anti-FANCM (Cell Signaling, #57697); AntiBLM (Abcam, #ab2179); Anti-GFP (Abcam, #ab290); AntimCherry (Abcam, #ab167453); Anti-Flag (Sigma-Aldrich, #F1804; Millipore, #F7425), Anti- β-actin (Sigma-Aldrich, #A5441); Anti-mouse IgG isotype control (Santa-Cruz, #sc2025). .. Secondary antibodies used were anti-mouse HRP (Cell Signaling, #7076), anti-rabbit HRP (Cell Signaling, #7074), Alexa Fluor 488 goat anti-mouse IgG (Invitrogen, #A11029), Alexa Fluor 594 goat anti-mouse IgG (Invitrogen, # # # W S e t 1 i s i i r t H R S a T d k B o a s t m q d S w N a fl c I C 2 C i h b b s w L ( s t G i T ( H ( w t D ow nloaded from https://academ ic.oup.com /nar/advance-article/doi/10.1093/nar/gkae558/7699953 by guest on 06 July 2024 A11032), Alexa Fluor 488 goat anti-rabbit IgG (Invitrogen, A11034), Alexa Fluor 594 goat anti-rabbit IgG (Invitrogen, A11037). estern blotting amples were subjected to electrophoresis on an 8–16% gradint SDS-PAGE gel for 90 min (120 V) and were subsequently ransferred onto a nitrocellulose membrane (Cytiva) for 2 h at 00V.

    Article Title: PCAF promotes R-loop resolution via histone acetylation
    Article Snippet: .. Primary antibodies used in this study were Anti-S9.6 (Kerafest, #ENH001); Anti-ssDNA (Millipore, #MAB3034); Anti-Nucleolin (Abcam, #ab50279); Anti-PCAF (Cell Signaling, #3378); Anti-H4K8ac (Millipore, #07-328); Anti-MRE11 (Novus Biologicals, #NB100-142); Anti-EXO1 (Genetex, #GTX109891); Anti-FANCM (Cell Signaling, #57697); Anti-BLM (Abcam, #ab2179); Anti-GFP (Abcam, #ab290); Anti-mCherry (Abcam, #ab167453); Anti-Flag (Sigma-Aldrich, #F1804; Millipore, #F7425), Anti-β-actin (Sigma-Aldrich, #A5441); Anti-mouse IgG isotype control (Santa-Cruz, #sc-2025). .. Secondary antibodies used were anti-mouse HRP (Cell Signaling, #7076), anti-rabbit HRP (Cell Signaling, #7074), Alexa Fluor 488 goat anti-mouse IgG (Invitrogen, #A11029), Alexa Fluor 594 goat anti-mouse IgG (Invitrogen, #A11032), Alexa Fluor 488 goat anti-rabbit IgG (Invitrogen, #A11034), Alexa Fluor 594 goat anti-rabbit IgG (Invitrogen, #A11037).



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    A Molecular docking simulated the binding affinities of <t>PCAF</t> for acetyl-CoA and lactyl-CoA. B Co-IP was performed to confirm the interaction between H3K18la and PCAF in PANC1 and KPC cells. PCAF and H3K18la were detected on the same gel. C, D Western blot analysis demonstrates the level of H3K18la in PDAC cells with or without the treatment of PCAF inhibitors (bromosporine or Embelin). <t>Histone</t> <t>H3</t> and H3K18la blots are from parallel-processed separate gels (size conflict) with samples from the same experiment. E Western blot analysis demonstrates the level of H3K18la in PDAC cells following the knockdown of Pcaf . Histone H3, PCAF, β-actin and H3K18la blots are from parallel-processed separate gels with samples from the same experiment. F Western blots of in vitro histone acetylation or lactylation assay, the samples as indicated. Blots are from parallel-processed separate gels with samples from the same experiment. G , H Relative Cxcl1 RNA and protein levels with the vehicle or bromosporine treatment were analyzed by qRT-PCR and ELISA ( n = 3 independent experiments), respectively. I Relative Cxcl1 RNA levels after Pcaf knockdown were analyzed by qRT-PCR ( n = 3 independent experiments). J A schematic diagram showing the orthotopic tumor construction in C57BL/6 J mice ( n = 5 mice per group in one experiment, 2 × 10 6 KPC-luc cells per mouse) with or without bromosporine treatment. K , L Image and weights of the orthotopic tumors in the experimental groups from ( J ) at the end of the experiments ( n = 5 mice per group). M Lactylation levels of H3K18 and PanK in orthotopic tumors with or without bromosporine treatment were detected by western blot ( n = 4 biologically independent samples per group). Histone H3, H3K18la, and PanKla blots are from parallel-processed separate gels (size conflict) with samples from the same experiment. N Serum CXCL1 levels in mice with or without bromosporine treatment were measured by ELISA ( n = 5 mice per group). O – R Tumor-infiltrating neutrophils, CD8 + T cells, GZMB + CD8 + T cells, and PD-1 + CD8 + T cells isolated from the orthotopic tumors were analyzed using flow cytometry. Representative graphs of flow cytometry (left panel) and statistical analysis of the cell ratio (right panel) ( n = 5 mice per group). S The migratory abilities of neutrophils co-incubated with the culture medium supernatant from shNTC/ Pcaf PDAC cells treated with recombinant CXCL1 were analyzed by counting the penetrated cell numbers ( n = 3 biologically independent samples). T Representative IHC images stained by CXCL1 or H3K18la antibody (scale bar = 100 μm, left panel), correlation analysis of H-scores of CXCL1 and H3K18la in PDAC samples ( n = 21 patients, right panel). Data represent mean ± SEM. Statistical analysis was conducted using the two-tailed unpaired Student’s t test ( G – I , L , and N – S ) and two-tailed Pearson’s correlation analysis ( T ). Unless otherwise indicated, all western blots had three independent experimental repetitions with consistent results. Source data are provided as a Source Data file.
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    A Molecular docking simulated the binding affinities of <t>PCAF</t> for acetyl-CoA and lactyl-CoA. B Co-IP was performed to confirm the interaction between H3K18la and PCAF in PANC1 and KPC cells. PCAF and H3K18la were detected on the same gel. C, D Western blot analysis demonstrates the level of H3K18la in PDAC cells with or without the treatment of PCAF inhibitors (bromosporine or Embelin). <t>Histone</t> <t>H3</t> and H3K18la blots are from parallel-processed separate gels (size conflict) with samples from the same experiment. E Western blot analysis demonstrates the level of H3K18la in PDAC cells following the knockdown of Pcaf . Histone H3, PCAF, β-actin and H3K18la blots are from parallel-processed separate gels with samples from the same experiment. F Western blots of in vitro histone acetylation or lactylation assay, the samples as indicated. Blots are from parallel-processed separate gels with samples from the same experiment. G , H Relative Cxcl1 RNA and protein levels with the vehicle or bromosporine treatment were analyzed by qRT-PCR and ELISA ( n = 3 independent experiments), respectively. I Relative Cxcl1 RNA levels after Pcaf knockdown were analyzed by qRT-PCR ( n = 3 independent experiments). J A schematic diagram showing the orthotopic tumor construction in C57BL/6 J mice ( n = 5 mice per group in one experiment, 2 × 10 6 KPC-luc cells per mouse) with or without bromosporine treatment. K , L Image and weights of the orthotopic tumors in the experimental groups from ( J ) at the end of the experiments ( n = 5 mice per group). M Lactylation levels of H3K18 and PanK in orthotopic tumors with or without bromosporine treatment were detected by western blot ( n = 4 biologically independent samples per group). Histone H3, H3K18la, and PanKla blots are from parallel-processed separate gels (size conflict) with samples from the same experiment. N Serum CXCL1 levels in mice with or without bromosporine treatment were measured by ELISA ( n = 5 mice per group). O – R Tumor-infiltrating neutrophils, CD8 + T cells, GZMB + CD8 + T cells, and PD-1 + CD8 + T cells isolated from the orthotopic tumors were analyzed using flow cytometry. Representative graphs of flow cytometry (left panel) and statistical analysis of the cell ratio (right panel) ( n = 5 mice per group). S The migratory abilities of neutrophils co-incubated with the culture medium supernatant from shNTC/ Pcaf PDAC cells treated with recombinant CXCL1 were analyzed by counting the penetrated cell numbers ( n = 3 biologically independent samples). T Representative IHC images stained by CXCL1 or H3K18la antibody (scale bar = 100 μm, left panel), correlation analysis of H-scores of CXCL1 and H3K18la in PDAC samples ( n = 21 patients, right panel). Data represent mean ± SEM. Statistical analysis was conducted using the two-tailed unpaired Student’s t test ( G – I , L , and N – S ) and two-tailed Pearson’s correlation analysis ( T ). Unless otherwise indicated, all western blots had three independent experimental repetitions with consistent results. Source data are provided as a Source Data file.
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    A Molecular docking simulated the binding affinities of <t>PCAF</t> for acetyl-CoA and lactyl-CoA. B Co-IP was performed to confirm the interaction between H3K18la and PCAF in PANC1 and KPC cells. PCAF and H3K18la were detected on the same gel. C, D Western blot analysis demonstrates the level of H3K18la in PDAC cells with or without the treatment of PCAF inhibitors (bromosporine or Embelin). <t>Histone</t> <t>H3</t> and H3K18la blots are from parallel-processed separate gels (size conflict) with samples from the same experiment. E Western blot analysis demonstrates the level of H3K18la in PDAC cells following the knockdown of Pcaf . Histone H3, PCAF, β-actin and H3K18la blots are from parallel-processed separate gels with samples from the same experiment. F Western blots of in vitro histone acetylation or lactylation assay, the samples as indicated. Blots are from parallel-processed separate gels with samples from the same experiment. G , H Relative Cxcl1 RNA and protein levels with the vehicle or bromosporine treatment were analyzed by qRT-PCR and ELISA ( n = 3 independent experiments), respectively. I Relative Cxcl1 RNA levels after Pcaf knockdown were analyzed by qRT-PCR ( n = 3 independent experiments). J A schematic diagram showing the orthotopic tumor construction in C57BL/6 J mice ( n = 5 mice per group in one experiment, 2 × 10 6 KPC-luc cells per mouse) with or without bromosporine treatment. K , L Image and weights of the orthotopic tumors in the experimental groups from ( J ) at the end of the experiments ( n = 5 mice per group). M Lactylation levels of H3K18 and PanK in orthotopic tumors with or without bromosporine treatment were detected by western blot ( n = 4 biologically independent samples per group). Histone H3, H3K18la, and PanKla blots are from parallel-processed separate gels (size conflict) with samples from the same experiment. N Serum CXCL1 levels in mice with or without bromosporine treatment were measured by ELISA ( n = 5 mice per group). O – R Tumor-infiltrating neutrophils, CD8 + T cells, GZMB + CD8 + T cells, and PD-1 + CD8 + T cells isolated from the orthotopic tumors were analyzed using flow cytometry. Representative graphs of flow cytometry (left panel) and statistical analysis of the cell ratio (right panel) ( n = 5 mice per group). S The migratory abilities of neutrophils co-incubated with the culture medium supernatant from shNTC/ Pcaf PDAC cells treated with recombinant CXCL1 were analyzed by counting the penetrated cell numbers ( n = 3 biologically independent samples). T Representative IHC images stained by CXCL1 or H3K18la antibody (scale bar = 100 μm, left panel), correlation analysis of H-scores of CXCL1 and H3K18la in PDAC samples ( n = 21 patients, right panel). Data represent mean ± SEM. Statistical analysis was conducted using the two-tailed unpaired Student’s t test ( G – I , L , and N – S ) and two-tailed Pearson’s correlation analysis ( T ). Unless otherwise indicated, all western blots had three independent experimental repetitions with consistent results. Source data are provided as a Source Data file.
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    Image Search Results


    A Molecular docking simulated the binding affinities of PCAF for acetyl-CoA and lactyl-CoA. B Co-IP was performed to confirm the interaction between H3K18la and PCAF in PANC1 and KPC cells. PCAF and H3K18la were detected on the same gel. C, D Western blot analysis demonstrates the level of H3K18la in PDAC cells with or without the treatment of PCAF inhibitors (bromosporine or Embelin). Histone H3 and H3K18la blots are from parallel-processed separate gels (size conflict) with samples from the same experiment. E Western blot analysis demonstrates the level of H3K18la in PDAC cells following the knockdown of Pcaf . Histone H3, PCAF, β-actin and H3K18la blots are from parallel-processed separate gels with samples from the same experiment. F Western blots of in vitro histone acetylation or lactylation assay, the samples as indicated. Blots are from parallel-processed separate gels with samples from the same experiment. G , H Relative Cxcl1 RNA and protein levels with the vehicle or bromosporine treatment were analyzed by qRT-PCR and ELISA ( n = 3 independent experiments), respectively. I Relative Cxcl1 RNA levels after Pcaf knockdown were analyzed by qRT-PCR ( n = 3 independent experiments). J A schematic diagram showing the orthotopic tumor construction in C57BL/6 J mice ( n = 5 mice per group in one experiment, 2 × 10 6 KPC-luc cells per mouse) with or without bromosporine treatment. K , L Image and weights of the orthotopic tumors in the experimental groups from ( J ) at the end of the experiments ( n = 5 mice per group). M Lactylation levels of H3K18 and PanK in orthotopic tumors with or without bromosporine treatment were detected by western blot ( n = 4 biologically independent samples per group). Histone H3, H3K18la, and PanKla blots are from parallel-processed separate gels (size conflict) with samples from the same experiment. N Serum CXCL1 levels in mice with or without bromosporine treatment were measured by ELISA ( n = 5 mice per group). O – R Tumor-infiltrating neutrophils, CD8 + T cells, GZMB + CD8 + T cells, and PD-1 + CD8 + T cells isolated from the orthotopic tumors were analyzed using flow cytometry. Representative graphs of flow cytometry (left panel) and statistical analysis of the cell ratio (right panel) ( n = 5 mice per group). S The migratory abilities of neutrophils co-incubated with the culture medium supernatant from shNTC/ Pcaf PDAC cells treated with recombinant CXCL1 were analyzed by counting the penetrated cell numbers ( n = 3 biologically independent samples). T Representative IHC images stained by CXCL1 or H3K18la antibody (scale bar = 100 μm, left panel), correlation analysis of H-scores of CXCL1 and H3K18la in PDAC samples ( n = 21 patients, right panel). Data represent mean ± SEM. Statistical analysis was conducted using the two-tailed unpaired Student’s t test ( G – I , L , and N – S ) and two-tailed Pearson’s correlation analysis ( T ). Unless otherwise indicated, all western blots had three independent experimental repetitions with consistent results. Source data are provided as a Source Data file.

    Journal: Nature Communications

    Article Title: Histone lactylation increases CXCL1 expression for neutrophil infiltration and immune escape in pancreatic cancer

    doi: 10.1038/s41467-026-69311-5

    Figure Lengend Snippet: A Molecular docking simulated the binding affinities of PCAF for acetyl-CoA and lactyl-CoA. B Co-IP was performed to confirm the interaction between H3K18la and PCAF in PANC1 and KPC cells. PCAF and H3K18la were detected on the same gel. C, D Western blot analysis demonstrates the level of H3K18la in PDAC cells with or without the treatment of PCAF inhibitors (bromosporine or Embelin). Histone H3 and H3K18la blots are from parallel-processed separate gels (size conflict) with samples from the same experiment. E Western blot analysis demonstrates the level of H3K18la in PDAC cells following the knockdown of Pcaf . Histone H3, PCAF, β-actin and H3K18la blots are from parallel-processed separate gels with samples from the same experiment. F Western blots of in vitro histone acetylation or lactylation assay, the samples as indicated. Blots are from parallel-processed separate gels with samples from the same experiment. G , H Relative Cxcl1 RNA and protein levels with the vehicle or bromosporine treatment were analyzed by qRT-PCR and ELISA ( n = 3 independent experiments), respectively. I Relative Cxcl1 RNA levels after Pcaf knockdown were analyzed by qRT-PCR ( n = 3 independent experiments). J A schematic diagram showing the orthotopic tumor construction in C57BL/6 J mice ( n = 5 mice per group in one experiment, 2 × 10 6 KPC-luc cells per mouse) with or without bromosporine treatment. K , L Image and weights of the orthotopic tumors in the experimental groups from ( J ) at the end of the experiments ( n = 5 mice per group). M Lactylation levels of H3K18 and PanK in orthotopic tumors with or without bromosporine treatment were detected by western blot ( n = 4 biologically independent samples per group). Histone H3, H3K18la, and PanKla blots are from parallel-processed separate gels (size conflict) with samples from the same experiment. N Serum CXCL1 levels in mice with or without bromosporine treatment were measured by ELISA ( n = 5 mice per group). O – R Tumor-infiltrating neutrophils, CD8 + T cells, GZMB + CD8 + T cells, and PD-1 + CD8 + T cells isolated from the orthotopic tumors were analyzed using flow cytometry. Representative graphs of flow cytometry (left panel) and statistical analysis of the cell ratio (right panel) ( n = 5 mice per group). S The migratory abilities of neutrophils co-incubated with the culture medium supernatant from shNTC/ Pcaf PDAC cells treated with recombinant CXCL1 were analyzed by counting the penetrated cell numbers ( n = 3 biologically independent samples). T Representative IHC images stained by CXCL1 or H3K18la antibody (scale bar = 100 μm, left panel), correlation analysis of H-scores of CXCL1 and H3K18la in PDAC samples ( n = 21 patients, right panel). Data represent mean ± SEM. Statistical analysis was conducted using the two-tailed unpaired Student’s t test ( G – I , L , and N – S ) and two-tailed Pearson’s correlation analysis ( T ). Unless otherwise indicated, all western blots had three independent experimental repetitions with consistent results. Source data are provided as a Source Data file.

    Article Snippet: The primary antibodies used here included anti-LDHA antibody (Proteintech, #19987-1-AP, 1:3000), anti-LDHB antibody (Proteintech, #14824-1-AP, 1:5000), anti-H3 antibody (Proteintech, #17168-1-Ap, 1:3000), anti-PCAF antibody (Cell Signaling Technology, #3378S, 1:1000), anti-P300 antibody (Proteintech, #20695-1-AP, 1:500), anti-GCN5 antibody (Proteintech, #66575-1-Ig, 1:3000), anti-beta Actin antibody (PTMBIO, #PTM-5028, 1:1000), anti-human CXCL1 Polyclonal antibody (Proteintech, #12335-1-AP), anti-mouse CXCL1 Polyclonal antibody (Proteintech, #30322-1-AP), anti-L-Lactyl Lysine antibody (PTMBIO, #PTM-1401RM, 1:1000), anti-L-Lactyl-Histone H3K18 antibody (PTMBIO, #PTM-1406RM, 1:1000), anti-L-Lactyl-Histone H3K9 antibody (PTMBIO, #PTM-1419RM, 1:1000), anti-L-Lactyl-Histone H3K14 antibody (PTMBIO, #PTM-1414RM, 1:1000), anti-H4 antibody (PTMBIO, #PTM-1009, 1:1000), anti-L-Lactyl-Histone H4K12 antibody (PTMBIO, #PTM-1411RM, 1:1000), anti-L-Lactyl-Histone H4K8 antibody (PTMBIO, #PTM-1415RM, 1:1000), anti-Acetyl-Histone H3 (Lys18) antibody (PTMBIO, #PTM-114RM, 1:1000), anti-Acetyllysine antibody (PTMBIO, #PTM-101, 1:1000), and anti-Acetyl-Histone H4 (Lys8) antibody (PTMBIO, #PTM-190, 1:1000).

    Techniques: Binding Assay, Co-Immunoprecipitation Assay, Western Blot, Knockdown, In Vitro, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Isolation, Flow Cytometry, Incubation, Recombinant, Staining, Two Tailed Test

    A A schematic diagram showing the subcutaneous tumor model ( n = 6 mice per group in one experiment, 6 × 10 6 PANC02 cells per mouse) treated with bromosporine and anti-PD-1 antibody. B. The tumor volume growth curves of subcutaneous tumors from ( A ). C , D Image and weights of the subcutaneous tumors at the end point of experiments ( n = 6 mice per group). E The statistical analysis of the cell ratio of tumor-infiltrating neutrophils and CD8 + T cells isolated from subcutaneous tumors ( n = 3 mice per group). F Western blot analysis demonstrates H3K18la levels in the subcutaneous tumors ( n = 3 biologically independent samples per group) from ( A ). Histone H3 and H3K18la blots are from parallel-processed separate gels (size conflict) with samples from the same experiment. G Relative serum CXCL1 levels in mice treated with or without bromosporine/anti-PD-1 antibody were measured by ELISA ( n = 6 mice per group). H A schematic diagram showing the combinational treatment schedule for the orthotopic KPC-luc tumor model ( n = 21 mice per group in one experiment, 2 × 10 6 KPC-luc cells per mouse). I , J Image and weights of the orthotopic tumors at the end point of experiments ( n = 6 mice per group). K – N Tumor-infiltrating neutrophils, CD8 + T cells, GZMB + CD8 + T cells, and PD-1 + CD8 + T cells were analyzed using flow cytometry. Representative graphs of flow cytometry (left panel) and statistical analysis of the cell ratio (right panel) ( n = 6 mice per group). O Western blot analysis showing the H3K18la levels in the orthotopic tumors ( n = 3 biologically independent samples per group) from ( H ). Histone H3 and H3K18la blots are from parallel-processed separate gels (size conflict) with samples from the same experiment. P Representative luminescence images and Quantification of radiance intensity of the mouse model in ( H ). Q Survival probability of mice with orthotopically transplanted PDAC ( n = 15 mice per group). R A working model displaying the signaling pathway through which the aerobic glycolysis-mediated Lactate-PCAF-H3K18la-CXCL1 axis modulates the tumor microenvironment in pancreatic cancer, and the scientific basis for the development of a novel therapeutic strategy for PDAC. Data represent mean ± SEM. Statistical analysis was conducted using the two-tailed unpaired Student’s t test ( B , D , E , G , J – N , P ) and the log-rank test ( Q ). Source data are provided as a Source Data file.

    Journal: Nature Communications

    Article Title: Histone lactylation increases CXCL1 expression for neutrophil infiltration and immune escape in pancreatic cancer

    doi: 10.1038/s41467-026-69311-5

    Figure Lengend Snippet: A A schematic diagram showing the subcutaneous tumor model ( n = 6 mice per group in one experiment, 6 × 10 6 PANC02 cells per mouse) treated with bromosporine and anti-PD-1 antibody. B. The tumor volume growth curves of subcutaneous tumors from ( A ). C , D Image and weights of the subcutaneous tumors at the end point of experiments ( n = 6 mice per group). E The statistical analysis of the cell ratio of tumor-infiltrating neutrophils and CD8 + T cells isolated from subcutaneous tumors ( n = 3 mice per group). F Western blot analysis demonstrates H3K18la levels in the subcutaneous tumors ( n = 3 biologically independent samples per group) from ( A ). Histone H3 and H3K18la blots are from parallel-processed separate gels (size conflict) with samples from the same experiment. G Relative serum CXCL1 levels in mice treated with or without bromosporine/anti-PD-1 antibody were measured by ELISA ( n = 6 mice per group). H A schematic diagram showing the combinational treatment schedule for the orthotopic KPC-luc tumor model ( n = 21 mice per group in one experiment, 2 × 10 6 KPC-luc cells per mouse). I , J Image and weights of the orthotopic tumors at the end point of experiments ( n = 6 mice per group). K – N Tumor-infiltrating neutrophils, CD8 + T cells, GZMB + CD8 + T cells, and PD-1 + CD8 + T cells were analyzed using flow cytometry. Representative graphs of flow cytometry (left panel) and statistical analysis of the cell ratio (right panel) ( n = 6 mice per group). O Western blot analysis showing the H3K18la levels in the orthotopic tumors ( n = 3 biologically independent samples per group) from ( H ). Histone H3 and H3K18la blots are from parallel-processed separate gels (size conflict) with samples from the same experiment. P Representative luminescence images and Quantification of radiance intensity of the mouse model in ( H ). Q Survival probability of mice with orthotopically transplanted PDAC ( n = 15 mice per group). R A working model displaying the signaling pathway through which the aerobic glycolysis-mediated Lactate-PCAF-H3K18la-CXCL1 axis modulates the tumor microenvironment in pancreatic cancer, and the scientific basis for the development of a novel therapeutic strategy for PDAC. Data represent mean ± SEM. Statistical analysis was conducted using the two-tailed unpaired Student’s t test ( B , D , E , G , J – N , P ) and the log-rank test ( Q ). Source data are provided as a Source Data file.

    Article Snippet: The primary antibodies used here included anti-LDHA antibody (Proteintech, #19987-1-AP, 1:3000), anti-LDHB antibody (Proteintech, #14824-1-AP, 1:5000), anti-H3 antibody (Proteintech, #17168-1-Ap, 1:3000), anti-PCAF antibody (Cell Signaling Technology, #3378S, 1:1000), anti-P300 antibody (Proteintech, #20695-1-AP, 1:500), anti-GCN5 antibody (Proteintech, #66575-1-Ig, 1:3000), anti-beta Actin antibody (PTMBIO, #PTM-5028, 1:1000), anti-human CXCL1 Polyclonal antibody (Proteintech, #12335-1-AP), anti-mouse CXCL1 Polyclonal antibody (Proteintech, #30322-1-AP), anti-L-Lactyl Lysine antibody (PTMBIO, #PTM-1401RM, 1:1000), anti-L-Lactyl-Histone H3K18 antibody (PTMBIO, #PTM-1406RM, 1:1000), anti-L-Lactyl-Histone H3K9 antibody (PTMBIO, #PTM-1419RM, 1:1000), anti-L-Lactyl-Histone H3K14 antibody (PTMBIO, #PTM-1414RM, 1:1000), anti-H4 antibody (PTMBIO, #PTM-1009, 1:1000), anti-L-Lactyl-Histone H4K12 antibody (PTMBIO, #PTM-1411RM, 1:1000), anti-L-Lactyl-Histone H4K8 antibody (PTMBIO, #PTM-1415RM, 1:1000), anti-Acetyl-Histone H3 (Lys18) antibody (PTMBIO, #PTM-114RM, 1:1000), anti-Acetyllysine antibody (PTMBIO, #PTM-101, 1:1000), and anti-Acetyl-Histone H4 (Lys8) antibody (PTMBIO, #PTM-190, 1:1000).

    Techniques: Isolation, Western Blot, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Two Tailed Test