HDAC6 Polyclonal Antibody

Rabbit

synthetic peptide corresponding to amino acids 1-16 of human HDAC-6

For immunochemical detection of HDAC6

Histone deacetylase (HDAC) and histone acetyltransferase (HAT) are enzymes that regulate transcription by selectively deacetylating or acetylating the ε-amino groups of lysines located near the amino termini of core histone proteins.1 Eleven members of the HDAC family have been identified in the past several years.2,3 These HDAC family members are divided into two classes, I and II. HDAC6 is a Class II HDAC that can shuttle between the nucleus and cytoplasm, suggesting potential extranuclear functions by regulating the acetylation status of non-histone substrates. By modifying chromatin structure and other non-histone proteins, HDACs play important roles in controlling complex biological events, including cell development, differentiation, programmed cell death, angiogenesis, and inflammation.4,5 Considering these major roles, it is conceivable that dysregulation of HDACs and subsequent imbalance of acetylation and deacetylation may be involved in the pathogenesis of various diseases, including cancer and inflammatory diseases.4

IgG

WB, IP, and ChIP

(+) Human HDAC6 (+) Mouse HDAC6

Histone Deacetylase 6

≥ 1 year

1.Cress, W.D., and Seto, E.J. Histone deacetylases, transcriptional control, and cancer. Journal of Cellular Physiology 184, 1-16 (2000).
2.Meinke, P.T., and Liberator, P. Histone deacetylase: A target for antiproliferative and antiprotozoal agents. Current Medicinal Chemistry 8(2), 211-235 (2001).
3.Nakayama, T., and Takami, Y. Participation of histones and histone-modifying enzymes in cell functions through alterations in chromatin structure. Journal of Biochemistry 129, 491-499 (2001).
4.Lin, H.Y.,Chen, C.S.,Lin, S.P., et al. Targeting histone deacetylase in cancer therapy. Medicinal Research Reviews 26(4), 397-413 (2006).
5.Huang, L. Targeting histone deacetylases for the treatment of cancer and inflammatory diseases. Journal of Cellular Physiology 39.1, 611-616 (2006).