Linked Life Data

16554418

Source:http://linkedlifedata.com/resource/pubmed/id/16554418

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-7-7
pubmed:abstractText
Tissue hypoxia not only occurs under pathological conditions but is also an important microenvironmental factor that is critical for normal embryonic development. Hypoxia-inducible factors HIF-1 and HIF-2 are oxygen-sensitive basic helix-loop-helix transcription factors, which regulate biological processes that facilitate both oxygen delivery and cellular adaptation to oxygen deprivation. HIFs consist of an oxygen-sensitive alpha-subunit, HIF-alpha, and a constitutively expressed beta-subunit, HIF-beta, and regulate the expression of genes that are involved in energy metabolism, angiogenesis, erythropoiesis and iron metabolism, cell proliferation, apoptosis, and other biological processes. Under conditions of normal Po(2), HIF-alpha is hydroxylated and targeted for rapid proteasomal degradation by the von Hippel-Lindau (VHL) E3-ubiquitin ligase. When cells experience hypoxia, HIF-alpha is stabilized and either dimerizes with HIF-beta in the nucleus to form transcriptionally active HIF, executing the canonical hypoxia response, or it physically interacts with unrelated proteins, thereby enabling convergence of HIF oxygen sensing with other signaling pathways. In the normal, fully developed kidney, HIF-1alpha is expressed in most cell types, whereas HIF-2alpha is mainly found in renal interstitial fibroblast-like cells and endothelial cells. This review summarizes some of the most recent advances in the HIF field and discusses their relevance to renal development, normal kidney function and disease.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1931-857X
pubmed:author
pubmed:issnType
Print
pubmed:volume
291
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
F271-81
pubmed:dateRevised
2011-4-28
pubmed:meshHeading
pubmed-meshheading:16554418-Animals, pubmed-meshheading:16554418-Anoxia, pubmed-meshheading:16554418-Apoptosis, pubmed-meshheading:16554418-Aryl Hydrocarbon Receptor Nuclear Translocator, pubmed-meshheading:16554418-Basic Helix-Loop-Helix Transcription Factors, pubmed-meshheading:16554418-Disease Models, Animal, pubmed-meshheading:16554418-Erythropoiesis, pubmed-meshheading:16554418-Gene Expression Regulation, pubmed-meshheading:16554418-Gene Expression Regulation, Developmental, pubmed-meshheading:16554418-Gene Expression Regulation, Neoplastic, pubmed-meshheading:16554418-Humans, pubmed-meshheading:16554418-Hypoxia-Inducible Factor 1, alpha Subunit, pubmed-meshheading:16554418-Kidney, pubmed-meshheading:16554418-Kidney Neoplasms, pubmed-meshheading:16554418-Mice, pubmed-meshheading:16554418-Signal Transduction
pubmed:year
2006
pubmed:articleTitle
Hypoxia-inducible factors in the kidney.
pubmed:affiliation
Renal Electrolyte and Hypertension Division, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-6144, USA. vhaase@mail.med.upenn.edu
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural