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Mono-Methyl-Histone H3 (Lys4) (D1A9) XP Rabbit mAb antibody


Antibody ID


Target Antigen

Mono-Methyl-Histone H3 (Lys4) (D1A9) XP Rabbit mAb h, m, r, mk, human, mouse, non-human primate, rat

Proper Citation

(Cell Signaling Technology Cat# 5326, RRID:AB_10695148)


monoclonal antibody


Applications: W, IF-IC, F, ChIP, ChIP-seq. Consolidation on 11/2018: AB_10694535, AB_10695148, AB_2616017.

Host Organism



Cell Signaling Technology

Cat Num


Publications that use this research resource

Inhibition of Methyltransferase Setd7 Allows the In Vitro Expansion of Myogenic Stem Cells with Improved Therapeutic Potential.

  • Judson RN
  • Cell Stem Cell
  • 2018 Feb 1

Literature context:


The development of cell therapy for repairing damaged or diseased skeletal muscle has been hindered by the inability to significantly expand immature, transplantable myogenic stem cells (MuSCs) in culture. To overcome this limitation, a deeper understanding of the mechanisms regulating the transition between activated, proliferating MuSCs and differentiation-primed, poorly engrafting progenitors is needed. Here, we show that methyltransferase Setd7 facilitates such transition by regulating the nuclear accumulation of β-catenin in proliferating MuSCs. Genetic or pharmacological inhibition of Setd7 promotes in vitro expansion of MuSCs and increases the yield of primary myogenic cell cultures. Upon transplantation, both mouse and human MuSCs expanded with a Setd7 small-molecule inhibitor are better able to repopulate the satellite cell niche, and treated mouse MuSCs show enhanced therapeutic potential in preclinical models of muscular dystrophy. Thus, Setd7 inhibition may help bypass a key obstacle in the translation of cell therapy for muscle disease.

Funding information:
  • BLRD VA - I01 BX002324()
  • NCI NIH HHS - R01 CA073808(United States)
  • NIA NIH HHS - P01 AG036695()
  • NIAMS NIH HHS - R21 AR071039()
  • RRD VA - I01 RX001222()

ACK1/TNK2 Regulates Histone H4 Tyr88-phosphorylation and AR Gene Expression in Castration-Resistant Prostate Cancer.

  • Mahajan K
  • Cancer Cell
  • 2017 Jun 12

Literature context:


The androgen receptor (AR) is critical for the progression of prostate cancer to a castration-resistant (CRPC) state. AR antagonists are ineffective due to their inability to repress the expression of AR or its splice variant, AR-V7. Here, we report that the tyrosine kinase ACK1 (TNK2) phosphorylates histone H4 at tyrosine 88 upstream of the AR transcription start site. The WDR5/MLL2 complex reads the H4-Y88-phosphorylation marks and deposits the transcriptionally activating H3K4-trimethyl marks promoting AR transcription. Reversal of the pY88-H4 epigenetic marks by the ACK1 inhibitor (R)-9bMS-sensitized naive and enzalutamide-resistant prostate cancer cells and reduced AR and AR-V7 levels to mitigate CRPC tumor growth. Thus, a feedforward ACK1/pY88-H4/WDR5/MLL2/AR epigenetic circuit drives CRPC and is necessary for maintenance of the malignant state.

Funding information:
  • NCI NIH HHS - P30 CA076292()
  • NCI NIH HHS - R01 CA135328()