Millipore Sigma Vibrant Logo
 

+hat++assay


101 Results 고급 검색  
검색결과 보기
제품 정보 (1)
문서 정보 (100)
웹 페이지 (0)

결과내 검색 검색을 미세조정하려면 아래의 필터를 이용하십시오

찾으시는 것을 발견할 수 없으십니까?
고객 서비스에 연락하십시오

 
문서 검색을 위한 도움이 필요하신가요?
  • CoA나 CoQ, MSDS 검색을 위해 문서 검색기를 이용해 보세요.
  • 사용자 가이드 또는 매뉴얼을 원하시면 고객 서비스팀에 연락주시기 바랍니다.

  • The transforming acidic coiled coil proteins interact with nuclear histone acetyltransferases. 14767476

    Dysregulation of the human transforming acidic coiled coil (TACC) genes is thought to be important in the development of multiple myeloma, breast and gastric cancer. However, even though these proteins have been implicated in the control of cell growth and differentiation, the mechanism by which they function still remains to be clarified. Using the yeast two-hybrid assay, we have now identified the histone acetyltransferase (HAT) hGCN5L2 as a TACC2-binding protein. GST pull-down analysis subsequently confirmed that all human TACC family members can bind in vitro to hGCN5L2. The authenticity of these interactions was validated by coimmunoprecipitation assays within the human embryonic kidney cell line HEK293, which identified the TACC2s isoform as a component consistently bound to several different members of HAT family. This raises the possibility that aberrant expression of one or more TACC proteins may affect gene regulation through their interaction with components of chromatin remodeling complexes, thus contributing to tumorigenesis.
    문서 타입:
    Reference
    카탈로그 번호:
    07-228
    제품명:
    Anti-TACC2 Antibody

  • BTG3 tumor suppressor gene promoter demethylation, histone modification and cell cycle arrest by genistein in renal cancer. 19221000

    BTG3/ANA/APRO4 has been reported to be a tumor suppressor gene in some malignancies. It constitutes important negative regulatory mechanism for Src-mediated signaling, a negative regulator of the cell cycle and inhibits transcription factor E2F1. We report that BTG3 is downregulated in renal cancer and that the mechanism of inactivation is through promoter hypermethylation. Quantitative real-time polymerase chain reaction (PCR) showed that BTG3 was downregulated in cancer tissues and cells. Genistein and 5-aza-2'-deoxycytidine (5Aza-C) induced BTG3 messenger RNA (mRNA) expression in A498, ACHN and HEK-293 renal cell carcinoma (RCC) cell lines. Bisulfite-modified PCR and DNA sequencing results showed complete methylation of BTG3 promoter in tumor samples and cancer cell lines. Genistein and 5Aza-C treatment significantly decreased promoter methylation, reactivating BTG3 expression. Chromatin immunoprecipitation assay revealed that genistein and 5Aza-C increased levels of acetylated histones 3, 4, 2H3K4, 3H3K4 and RNA polymerase II at the BTG3 promoter indicative of active histone modifications. Enzymatic assays showed genistein and 5Aza-C decreased DNA Methyltransferase, methyl-CpG-binding domain 2 activity and increased HAT activity. Cell cycle and 3-(4,5-dimethylthiazole-2-yl)-2,5-biphenyl tetrazolium bromide cell proliferation assays showed that genistein has antiproliferative effect on cancer cell growth through induction of cell cycle arrest. This is the first report to show that BTG3 is epigenetically silenced in RCC and can be reactivated by genistein-induced promoter demethylation and active histone modification. Genistein had similar effects to that of 5Aza-C, which is a potent demethylating agent with high toxicity and instability. Genistein being a natural, non-toxic, dietary isoflavone is effective in retarding the growth of RCC cells, making it a promising candidate for epigenetic therapy in renal carcinoma.
    문서 타입:
    Reference
    카탈로그 번호:
    Multiple
    제품명:
    Multiple