Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

ACK (A-11) antibody


Antibody ID


Target Antigen

ACK (A-11) human, mouse, mouse, human

Proper Citation

(Santa Cruz Biotechnology Cat# sc-28336, RRID:AB_626629)


monoclonal antibody


validation status unknown check with seller; recommendations: WB, IP, IF, ELISA; ELISA; Western Blot; Immunofluorescence; Immunoprecipitation

Host Organism



Santa Cruz Biotechnology

Cat Num


Publications that use this research resource

Small molecule induced oligomerization, clustering and clathrin-independent endocytosis of the dopamine transporter.

  • Sorkina T
  • Elife
  • 2018 Apr 9

Literature context:


Clathrin-independent endocytosis (CIE) mediates internalization of many transmembrane proteins but the mechanisms of cargo recruitment during CIE are poorly understood. We found that the cell-permeable furopyrimidine AIM-100 promotes dramatic oligomerization, clustering and CIE of human and mouse dopamine transporters (DAT), but not of their close homologues, norepinephrine and serotonin transporters. All effects of AIM-100 on DAT and the occupancy of substrate binding sites in the transporter were mutually exclusive, suggesting that AIM-100 may act by binding to DAT. Surprisingly, AIM-100-induced DAT endocytosis was independent of dynamin, cholesterol-rich microdomains and actin cytoskeleton, implying that a novel endocytic mechanism is involved. AIM-100 stimulated trafficking of internalized DAT was also unusual: DAT accumulated in early endosomes without significant recycling or degradation. We propose that AIM-100 augments DAT oligomerization through an allosteric mechanism associated with the DAT conformational state, and that oligomerization-triggered clustering leads to a coat-independent endocytosis and subsequent endosomal retention of DAT.

Funding information:
  • National Institutes of Health - DA014204()
  • NIAID NIH HHS - U01 AI101981(United States)

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()