Cell Signaling Technology

Product Pathways - Protein Stability

HECTH9 (AX8D1) Mouse mAb #5695

Applications Reactivity Sensitivity MW (kDa) Isotype
W H M R Mk Endogenous 482 Mouse IgG1

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

Protocols

Specificity / Sensitivity

HECTH9 (AX8D1) Mouse mAb recognizes endogenous levels of total HECTH9 protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a recombinant protein specific to human HECTH9 protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using HECTH9 (AX8D1) Mouse mAb.

Background

The HECT domain-containing ubiquitin E3 ligase HECTH9 (also known as HUWE1, ARF-BP1, URE-B1, Mule, and LASU1) is critical for the ubiquitination and proteasomal degradation of many target proteins, and is involved in the regulation of a variety of cellular processes, including DNA replication and base excision repair, cellular proliferation, differentiation, and apoptosis. HECTH9 contains two Armadillo (ARM) repeat-like domains (ARLD1 and ARLD2), a ubiquitin-associated (UBA) domain, a WWE domain, a well-conserved BH3 domain, and a catalytic HECT domain that facilitates ubiquitination of target proteins. HECTH9 has been shown to polyubiquitinate p53 (1,2), Miz1 (3), N-Myc (4,5), Mcl-1 (6), Cdc 6 (7), and DNA polymerase beta (8) through K48-mediated linkage, thereby targeting these proteins for proteosomal degradation. The tumor suppressor protein ARF (known as p14 ARF in humans and p19 ARF in mice) binds to and inhibits the uibiquitin ligase activity toward p53, resulting in stabilization of p53 and induction of apoptosis (1). HECTH9 has also been shown to polyubiquitinate c-Myc through K63-linkage, which is required for recruitment of p300, activation of c-Myc target genes, and induction of cellular proliferation (9). HECTH9 is overexpressed in colon, lung, and breast cancer (1,9). In addition, defects in HECTH9 result in mental retardation syndromic X-linked Turner type (MRXST) and mental retardation X-linked type 17 (MRX17) syndromes (10).

  1. Chen, D. et al. (2005) Cell 121, 1071-83.
  2. Yoon, S.Y. et al. (2005) Biochem Biophys Res Commun 326, 7-17.
  3. Yang, Y. et al. (2010) Proc Natl Acad Sci U S A 107, 13444-9.
  4. Zhao, X. et al. (2008) Nat Cell Biol 10, 643-53.
  5. Zhao, X. et al. (2009) Dev Cell 17, 210-21.
  6. Zhong, Q. et al. (2005) Cell 121, 1085-95.
  7. Hall, J.R. et al. (2007) Mol Biol Cell 18, 3340-50.
  8. Parsons, J.L. et al. (2009) EMBO J 28, 3207-15.
  9. Adhikary, S. et al. (2005) Cell 123, 409-21.
  10. Froyen, G. et al. (2008) Am J Hum Genet 82, 432-43.

Application References

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

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