Cell Signaling Technology

Product Pathways - Chromatin Regulation / Epigenetics

CHD7 (D3F5) Rabbit mAb #6505

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP H M Endogenous 336 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human  M=Mouse
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

CHD7 (D3F5) Rabbit mAb recognizes endogenous levels of total CHD7 protein. This antibody also cross-reacts with proteins of unknown origin at 50-55 kDa.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a recombinant protein specific to the amino terminus of human CHD7 protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using CHD7 (D3F5) Rabbit mAb.

Background

CHD7 belongs to the chromodomain helicase DNA-binding (CHD) family of ATP-dependent chromatin remodeling proteins (1). The CHD family of proteins has been shown to play an important role in regulating gene expression by altering the chromatin structure at target genes (1,2). The nine members of the CHD family are characterized by the presence of two tandem chromodomains in the N-terminal region and an SNF2-like ATPase domain near the central region of the protein (2-4). The CHD proteins can be further divided into three subgroups based on the presence of additional conserved functional domains. CHD7 belongs to the third subgroup of CHD proteins together with CHD6, 8, and 9, which are distinguished by the presence of three conserved region (CR) domains, a switching-defective protein 3, adaptor 2, nuclear receptor co-repressor, transcription factor IIB (SANT) like domain, two brahma and kismet (BRK) domains, and a DNA binding domain (2). CHD7 regulates embryonic stem cell (ESC) specific gene expression together with ESC master regulators Oct-4, Sox2 and nanog, and is necessary for neural stem cell development and formation of the neural crest (5-7). Research studies have shown that CHD7 mutations are frequently found in patients with CHARGE syndrome (coloboma of the eye, heart defects, atresia of the choanae, retardation of growth/development, genital/urinary abnormalities, and ear abnormalities and deafness) (8).

  1. Hargreaves, D.C. and Crabtree, G.R. (2011) Cell Res 21, 396-420.
  2. Marfella, C.G. and Imbalzano, A.N. (2007) Mutat Res 618, 30-40.
  3. Delmas, V. et al. (1993) Proc Natl Acad Sci U S A 90, 2414-8.
  4. Woodage, T. et al. (1997) Proc Natl Acad Sci U S A 94, 11472-7.
  5. Schnetz, M.P. et al. (2010) PLoS Genet 6, e1001023.
  6. Engelen, E. et al. (2011) Nat Genet 43, 607-11.
  7. Bajpai, R. et al. (2010) Nature 463, 958-62.
  8. Vissers, L.E. et al. (2004) Nat Genet 36, 955-7.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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