Loss of JAK2 regulation via a heterodimeric VHL-SOCS1 E3 ubiquitin ligase underlies Chuvash polycythemia-Reference-Cited by-同舟云学术

Loss of JAK2 regulation via a heterodimeric VHL-SOCS1 E3 ubiquitin ligase underlies Chuvash polycythemia

Published:2011-06-19 Issue:7 Volume:17 Page:845-853
ISSN:1078-8956
Container-title:Nature Medicine
language:en
Short-container-title:Nat Med

Author:

Russell Ryan C,Sufan Roxana I,Zhou Bing,Heir Pardeep,Bunda Severa,Sybingco Stephanie S,Greer Samantha N,Roche Olga,Heathcote Samuel A,Chow Vinca W K,Boba Lukasz M,Richmond Terri D,Hickey Michele M,Barber Dwayne L,Cheresh David A,Simon M Celeste,Irwin Meredith S,Kim William Y,Ohh Michael

Publisher

Springer Science and Business Media LLC

Subject

General Biochemistry, Genetics and Molecular Biology,General Medicine

Link

http://www.nature.com/articles/nm.2370.pdf

Reference59 articles.

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3. Maxwell, P.H. et al. The von Hippel-Lindau gene product is necessary for oxygen dependent proteolysis of hypoxia-inducible factor α subunits. Nature 399, 271–275 (1999).

4. Ohh, M. et al. Ubiquitination of hypoxia-inducible factor requires direct binding to the β-domain of the von Hippel-Lindau protein. Nat. Cell Biol. 2, 423–427 (2000).

5. Roberts, A.M. & Ohh, M. Beyond the hypoxia-inducible factor-centric tumour suppressor model of von Hippel-Lindau. Curr. Opin. Oncol. 20, 83–89 (2008).

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