HDAC2 is a member of the deacetylase family that forms transcriptional repressor complexes. Studies have reported that HDAC2 negatively regulates synaptic plasticity, learning and memory functions. In colorectal carcinogenesis, loss of APC is known to induce HDAC2 expression. Rabbit Anti-HDAC2 recognizes bovine, human, canine, chicken, rat, and mouse HDAC2.
Immunogen
Synthetic peptide directed towards the C terminal region of human HDAC2
Application
Rabbit Anti-HDAC2 antibody can be used for western blot (0.2-2.0μg/ml) and IHC (4-8μg/ml) applications.
Biochem/physiol Actions
Histone deacetylase 2 (HDAC2), or transcriptional regulator homolog RPD3 L1, is highly homologous to the yeast transcription factor RPD3 (reduced potassium dependency 3) gene. As in yeast, human HDA2 is likely to be involved in regulating chromatin structure during transcription. It has been implicated to associate with YY1, a mammalian zinc-finger transcription factor, which negatively regulates transcription by tethering RPD3 to DNA as a cofactor. This process is highly concerved from yeast to human.
Sequence
Synthetic peptide located within the following region: EEFSDSEDEGEGGRRNVADHKKGAKKARIEEDKKETEDKKTDVKEEDKSK
Physical form
Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Inappropriate transcriptional repression involving histone deacetylases (HDACs) is a prominent cause for the development of leukemia. We now identify faulty expression of a specific mediator of transcriptional repression in a solid tumor. Loss of the adenomatosis polyposis coli (APC) tumor
Chromatin modifications, especially histone-tail acetylation, have been implicated in memory formation. Increased histone-tail acetylation induced by inhibitors of histone deacetylases (HDACis) facilitates learning and memory in wild-type mice as well as in mouse models of neurodegeneration. Harnessing the therapeutic potential
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