Loss of JAK2 regulation via a heterodimeric VHL-SOCS1 E3 ubiquitin ligase underlies Chuvash polycythemia
Open Access
- 19 June 2011
- journal article
- research article
- Published by Springer Science and Business Media LLC in Nature Medicine
- Vol. 17 (7), 845-853
- https://doi.org/10.1038/nm.2370
Abstract
No abstract availableThis publication has 60 references indexed in Scilit:
- A Gain-of-Function Mutation in theHIF2AGene in Familial ErythrocytosisThe New England Journal of Medicine, 2008
- von Hippel–Lindau mutation in mice recapitulates Chuvash polycythemia via hypoxia-inducible factor-2α signaling and splenic erythropoiesisJCI Insight, 2007
- A novel erythrocytosis-associated PHD2 mutation suggests the location of a HIF binding grooveBlood, 2007
- Failure to prolyl hydroxylate hypoxia-inducible factor α phenocopies VHL inactivation in vivoThe EMBO Journal, 2006
- A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia veraNature, 2005
- Inhibition of HIF2α Is Sufficient to Suppress pVHL-Defective Tumor GrowthPLoS Biology, 2003
- Overproduction of Polypeptides Corresponding to the Amino Terminus of the F-Box Proteins Cdc4p and Met30p Inhibits Ubiquitin Ligase Activities of Their SCF ComplexesEukaryotic Cell, 2003
- Disruption of oxygen homeostasis underlies congenital Chuvash polycythemiaNature Genetics, 2002
- Structural basis for the recognition of hydroxyproline in HIF-1α by pVHLNature, 2002
- MUF1, A Novel Elongin BC-interacting Leucine-rich Repeat Protein That Can Assemble with Cul5 and Rbx1 to Reconstitute a Ubiquitin LigaseOnline Journal of Public Health Informatics, 2001