Cell Signaling Technology

Product Pathways - Protein Stability

USP9X Antibody #5751

Applications Reactivity Sensitivity MW (kDa) Source
W H M R Mk Dg Endogenous 270 Rabbit

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

Protocols

Specificity / Sensitivity

USP9X Antibody recognizes endogenous levels of total USP9X protein. This antibody may also cross-react with USP9Y.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Phe2137 of human USP9X protein. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using USP9X Antibody.

Background

Protein ubiquitination and deubiquitination is a reversible process catalyzed by ubiquitinating enzymes (UBEs) and deubiquitinating enzymes (DUBs) (1,2). DUBs are categorized into five subfamiles-USP, UCH, OTU, MJD, and JAMM. USP9X/hFAM is an X-linked member of the ubiquitin-specific protease (USP) subfamily of DUBs and possesses a well-conserved catalytic domain with cysteine peptidase activity, which allows for cleavage of ubiquitin and polyubiquitin conjugates. USP9X is the mammalian homolog of the Drosophila fat-facets (faf) gene, which is essential for normal eye development and viability of the early fly embryo (3,4). While USP9X expression is also critical for normal mammalian development (5-7), many of its substrates are only beginning to be elucidated. There is mounting evidence that USP9X functions in the formation of cell-cell contacts during the polarization of epithelial cells, in part through deubiquitination-dependent stabilization of molecules involved in maintaining the integrity of both adherens and tight junctions. Indeed, USP9X has been found to associate with AF-6, the β-catenin-E-cadherin complex, and EFA6 (8-11). Studies have also demonstrated that USP9X is an integral component of the TGF-β/BMP signaling cascade and regulates TGF-β responsiveness by opposing TRIM33-mediated monoubiquitination of SMAD4 (12). Recently, USP9X was shown to be overexpressed in a variety of human cancers, which was linked to enhanced cell survival and chemoresistance through its ability to deubiquitinate and stabilize the Mcl-1 oncoprotein. This evidence supports USP9X as a therapeutic target in the context of human malignancies such as follicular lymphomas and diffuse large B-cell lymphomas (13).

  1. Nijman, S.M. et al. (2005) Cell 123, 773-86.
  2. Nalepa, G. et al. (2006) Nat Rev Drug Discov 5, 596-613.
  3. Huang, Y. et al. (1995) Science 270, 1828-31.
  4. Huang, Y. and Fischer-Vize, J.A. (1996) Development 122, 3207-16.
  5. Pantaleon, M. et al. (2001) Mech Dev 109, 151-60.
  6. Noma, T. et al. (2002) Mech Dev 119 Suppl 1, S91-5.
  7. Xu, J. et al. (2005) J Neurosci Res 80, 47-55.
  8. Taya, S. et al. (1998) J Cell Biol 142, 1053-62.
  9. Taya, S. et al. (1999) Genes Cells 4, 757-67.
  10. Murray, R.Z. et al. (2004) Mol Biol Cell 15, 1591-9.
  11. Théard, D. et al. (2010) EMBO J 29, 1499-509.
  12. Dupont, S. et al. (2009) Cell 136, 123-35.
  13. Schwickart, M. et al. (2010) Nature 463, 103-7.

Application References

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