Cell Signaling Technology

Product Pathways - Chromatin Regulation / Epigenetics

SNF5 (D9C2) Rabbit mAb #8745

Applications Reactivity Sensitivity MW (kDa) Isotype
W H M R Mk (Hm) (C) (X) (B) Endogenous 44 Rabbit IgG

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  R=Rat  Hm=Hamster  Mk=Monkey  C=Chicken  X=Xenopus  B=Bovine
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

SNF5 (D9C2) Rabbit mAb recognizes endogenous levels of total SNF5 protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gln244 of human SNF5 protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using SNF5 (D9C2) Rabbit mAb.

Background

ATP-dependent chromatin remodeling complexes play an essential role in the regulation of nuclear processes such as transcription and DNA replication and repair (1,2). The SWI/SNF chromatin remodeling complex consists of more than 10 subunits and contains a single molecule of either BRM or BRG1 as the ATPase catalytic subunit. The activity of the ATPase subunit disrupts histone-DNA contacts and changes the accessibility of crucial regulatory elements to the chromatin. The additional core and accessory subunits play a scaffolding role to maintain stability and provide surfaces for interaction with various transcription factors and chromatin (2-5). The interactions between SWI/SNF subunits and transcription factors, such as nuclear receptors, p53, Rb, BRCA1, and MyoD, facilitate recruitment of the complex to target genes for regulation of gene activation, cell growth, cell cycle, and differentiation processes (1,6-9).

SNF5, one of the core subunits of the SWI/SNF complex, is necessary for efficient nucleosome remodeling by BRG1 in vitro (10). SNF5 is an essential part of the esBAF (mouse embryonic stem cell specific SWI/SNF complex) and is necessary for early embryogenesis and hepatocyte differentiation (11,12). In addition, SNF5 is considered to be a tumor suppressor protein; inactivating mutations have been indentified in a large number of malignant rhabdoid tumors (13,14).

  1. Ho, L. and Crabtree, G.R. (2010) Nature 463, 474-84.
  2. Becker, P.B. and Hörz, W. (2002) Annu Rev Biochem 71, 247-73.
  3. Eberharter, A. and Becker, P.B. (2004) J Cell Sci 117, 3707-11.
  4. Bowman, G.D. (2010) Curr Opin Struct Biol 20, 73-81.
  5. Gangaraju, V.K. and Bartholomew, B. (2007) Mutat Res 618, 3-17.
  6. Lessard, J.A. and Crabtree, G.R. (2010) Annu Rev Cell Dev Biol 26, 503-32.
  7. Morettini, S. et al. (2008) Front Biosci 13, 5522-32.
  8. Wolf, I.M. et al. (2008) J Cell Biochem 104, 1580-6.
  9. Simone, C. (2006) J Cell Physiol 207, 309-14.
  10. Phelan, M.L. et al. (1999) Mol Cell 3, 247-53.
  11. Klochendler-Yeivin, A. et al. (2000) EMBO Rep 1, 500-6.
  12. Gresh, L. et al. (2005) EMBO J 24, 3313-24.
  13. Versteege, I. et al. (1998) Nature 394, 203-6.
  14. Biegel, J.A. et al. (1999) Cancer Res 59, 74-9.

Application References

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

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