The New England Journal of Medicine
e-mail icon  FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |    Advanced Search
Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe
 
Correspondence
PreviousPrevious
Volume 358:1965-1967 May 1, 2008 Number 18
NextNext

The HIF2A Gene in Familial Erythrocytosis

Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

 Sign up for free e-toc
 

This Article
-Full Text
- PDF
-PDA Full Text
-Purchase this article

Tools and Services
-Add to Personal Archive
-Add to Citation Manager
-Notify a Friend
-E-mail When Cited
-E-mail When Letters Appear

More Information
-Related Article
by Percy, M. J.
-PubMed Citation
To the Editor: Percy et al. (Jan. 10 issue)1 uncovered a mutation within the hypoxia-inducible factor 2{alpha} (HIF2A) gene as a cause of attenuated HIF-2{alpha} degradation and increased erythropoietin production in patients with familial erythrocytosis. This is an exciting observation, since studies on the relative contribution of HIF-1{alpha} and HIF-2{alpha} to hypoxia-driven gene expression are areas of intense investigation.2,3 A recent study of erythropoiesis in mice with tissue-specific deletion of Hif1a or Hif2a showed that hepatic erythropoietin production is preferentially regulated by Hif-2{alpha}.4 In contrast, renal erythropoietin appears to be regulated predominantly by Hif-1{alpha}.5 Do Percy . . . [Full Text of this Article]



HOME  |  SUBSCRIBE  |  SEARCH  |  CURRENT ISSUE  |  PAST ISSUES  |  COLLECTIONS  |  PRIVACY  |  TERMS OF USE  |  HELP  |  beta.nejm.org

Comments and questions? Please contact us.

The New England Journal of Medicine is owned, published, and copyrighted © 2009 Massachusetts Medical Society. All rights reserved.