| pubmed-article:17404621 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17404621 | lifeskim:mentions | umls-concept:C0014822 | lld:lifeskim |
| pubmed-article:17404621 | lifeskim:mentions | umls-concept:C0205054 | lld:lifeskim |
| pubmed-article:17404621 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:17404621 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
| pubmed-article:17404621 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:17404621 | pubmed:dateCreated | 2007-4-3 | lld:pubmed |
| pubmed-article:17404621 | pubmed:abstractText | Erythropoiesis is critically dependent on erythropoietin (EPO), a glycoprotein hormone that is regulated by hypoxia-inducible factor (HIF). Hepatocytes are the primary source of extrarenal EPO in the adult and express HIF-1 and HIF-2, whose roles in the hypoxic induction of EPO remain controversial. In order to define the role of HIF-1 and HIF-2 in the regulation of hepatic EPO expression, we have generated mice with conditional inactivation of Hif-1alpha and/or Hif-2alpha (Epas1) in hepatocytes. We have previously shown that inactivation of the von Hippel-Lindau tumor suppressor pVHL, which targets both HIFs for proteasomal degradation, results in increased hepatic Epo production and polycythemia independent of Hif-1alpha. Here we show that conditional inactivation of Hif-2alpha in pVHL-deficient mice suppressed hepatic Epo and the development of polycythemia. Furthermore, we found that physiological Epo expression in infant livers required Hif-2alpha but not Hif-1alpha and that the hypoxic induction of liver Epo in anemic adults was Hif-2alpha dependent. Since other Hif target genes such phosphoglycerate kinase 1 (Pgk) were Hif-1alpha dependent, we provide genetic evidence that HIF-1 and HIF-2 have distinct roles in the regulation of hypoxia-inducible genes and that EPO is preferentially regulated by HIF-2 in the liver. | lld:pubmed |
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| pubmed-article:17404621 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17404621 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17404621 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:17404621 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17404621 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:17404621 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:17404621 | pubmed:author | pubmed-author:SimonM... | lld:pubmed |
| pubmed-article:17404621 | pubmed:author | pubmed-author:JohnsonRandal... | lld:pubmed |
| pubmed-article:17404621 | pubmed:author | pubmed-author:LiuQingduQ | lld:pubmed |
| pubmed-article:17404621 | pubmed:author | pubmed-author:RankinErinn... | lld:pubmed |
| pubmed-article:17404621 | pubmed:author | pubmed-author:BijuMangatt... | lld:pubmed |
| pubmed-article:17404621 | pubmed:author | pubmed-author:KeithBrianB | lld:pubmed |
| pubmed-article:17404621 | pubmed:author | pubmed-author:HaaseVolker... | lld:pubmed |
| pubmed-article:17404621 | pubmed:author | pubmed-author:UngerTravis... | lld:pubmed |
| pubmed-article:17404621 | pubmed:author | pubmed-author:RhaJenniferJ | lld:pubmed |
| pubmed-article:17404621 | pubmed:issnType | Print | lld:pubmed |
