Trial Size Available
Carrier-Free Available

| Document Name | |
|---|---|
| Datasheet | Download Here |
| Material Safety Data Sheet | Download Here |
| Applications | Tested Dilutions | Protocol | Note |
|---|---|---|---|
| Flow Cytometry (Flow) | 1-2ug/million cells | Flow Cytometry Protocol | |
| Immunohistochemistry (IHC) | 1-2ug/ml | IHC Protocol | 30 min at RT. Staining of formalin-fixed tissues requires heating tissue sections in 10mM Tris with 1mM EDTA, pH 9.0, for 45 min at 95°C followed by cooling at RT for 20 minutes |
Component of the NuA4 histone acetyltransferase (HAT) complex which is involved in transcriptional activation of select genes principally by acetylation of nucleosomal histones H4 and H2A. This modification may both alter nucleosome – DNA interactions and promote interaction of the modified histones with other proteins which positively regulate transcription. This complex may be required for the activation of transcriptional programs associated with oncogene and proto-oncogene mediated growth induction, tumor suppressor mediated growth arrest and replicative senescence, apoptosis, and DNA repair. The NuA4 complex ATPase and helicase activities seem to be, at least in part, contributed by the association of RUVBL1 and RUVBL2 with EP400. NuA4 may also play a direct role in DNA repair when directly recruited to sites of DNA damage. As part of the SIN3B complex represses transcription and counteracts the histone acetyltransferase activity of EP300 through the recognition H3K27ac marks by PHF12 and the activity of the histone deacetylase HDAC2 (PubMed:12391155, PubMed:14966270, PubMed:37137925). SIN3B complex is recruited downstream of the constitutively active genes transcriptional start sites through interaction with histones and mitigates histone acetylation and RNA polymerase II progression within transcribed regions contributing to the regulation of transcription (PubMed:21041482). Required for homologous recombination repair (HRR) and resistance to mitomycin C (MMC). Involved in the localization of PALB2, BRCA2 and RAD51, but not BRCA1, to DNA-damage foci.
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