Linked Life Data

7588410

Source:http://linkedlifedata.com/resource/pubmed/id/7588410

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1995-12-14
pubmed:abstractText
Excessive aldosterone secretion in some hypertensive patients may result from abnormal aldosterone synthase (AS) gene regulation in response to changes in dietary sodium intake. We have utilized NCI-H295 cells, which exhibit stable angiotensin-induced aldosterone secretion, for transient transfections with murine AS/human growth hormone reporter constructs. An angiotensin response element increasing AS gene transcription during angiotensin stimulation appears to reside within the initial 425 nt of the murine AS promoter. We also noted the possible presence of a negatively-acting cis element between nt -425 and -1500. These studies provide an initial step toward characterizing molecular mechanisms by which angiotensin regulates AS gene transcription.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0743-5800
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
455-62
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
Aldosterone synthase gene regulation by angiotensin.
pubmed:affiliation
Department of Internal Medicine, University of Texas Medical Branch, Galveston, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't