Product Pathways - Chromatin Regulation / Epigenetics
SATB1 (P472) Antibody #3643
|3643S||100 µl (10 western blots)||---||In Stock||---|
|3643||carrier free and custom formulation / quantity||email request|
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|W||1:1000||Human, Mouse, Rat||Endogenous||100||Rabbit|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation
Species predicted to react based on 100% sequence homology: Monkey, Bovine, Pig, Horse.
Specificity / Sensitivity
SATB1 (P472) Antibody detects endogenous levels of total SATB1 protein.
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to the human SATB1 protein. Antibodies are purified by protein A and peptide affinity chromatography.
Special AT-rich binding protein 1 (SATB1) functions as both a global chromatin organizer and a gene-specific transcription factor (1). SATB1 cooperates with promyelocytic leukemia protein (PML) to regulate global chromatin architecture by organizing chromatin into distinct loops via periodic anchoring of matrix attachment regions (MARs) in DNA to the nuclear matrix (1-3). In addition, SATB1 recruits multiple chromatin-remodeling proteins that contribute to specific gene activation and repression, including the chromatin remodeling enzymes ACF and ISWI, the histone deacetylase HDAC1, and the histone acetyltransferases PCAF and p300/CBP (4-6). Phosphorylation of SATB1 on Ser185 by protein kinase C regulates its interaction with HDAC1 and PCAF. While unphosphorylated SATB1 binds to PCAF, phosphorylated SATB1 preferentially binds to HDAC1 (6). Acetylation of SATB1 on Lys136 by PCAF impairs its DNA binding activity, thereby removing SATB1 from gene promoters (6). SATB1 is expressed predominantly in thymocytes and is involved in gene regulation during T cell activation (1). SATB1 is also expressed in metastatic breast cancer cells and is a potential prognostic marker and therapeutic target for metastatic breast cancer (7). In a mouse model system, RNAi-mediated knockdown of SATB1 reversed tumorigenesis by inhibiting tumor growth and metastasis, while ectopic expression of SATB1 in non-metastatic breast cancer cells produced invasive tumors.
- Galande, S. et al. (2007) Curr Opin Genet Dev 17, 408-14.
- Cai, S. et al. (2006) Nat Genet 38, 1278-88.
- Kumar, P.P. et al. (2007) Nat Cell Biol 9, 45-56.
- Yasui, D. et al. (2002) Nature 419, 641-5.
- Kumar, P.P. et al. (2005) Mol Cell Biol 25, 1620-33.
- Pavan Kumar, P. et al. (2006) Mol Cell 22, 231-43.
- Han, H.J. et al. (2008) Nature 452, 187-93.
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