Linked Life Data

2166044

Source:http://linkedlifedata.com/resource/pubmed/id/2166044

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
23
pubmed:dateCreated
1990-9-13
pubmed:abstractText
The 98-base pair enhancer/promoter sequence is critical for cell type-specific transcription of the human neurotropic viral promoter, JCVE, in glial cells. Transcriptionally active extracts were prepared from glial cells and used to identify cis- and trans-acting regulatory elements that are involved in the glial-specific activation of the JCVE promoter. Results indicate that multiple regulatory sequences within the 98-base pair repeat specifically bind to nuclear proteins present in glial cells and positively regulate viral early RNA synthesis. The central region of the repeat, designated domain-B, interacts with a 45-kDa nuclear protein present in brain cells. This brain-specific protein was purified by conventional and DNA affinity chromatography. Complementation of the highly purified protein with HeLa extract significantly increased JCVE promoter activity. Thus, association of the novel glial-origin transcription factor with its target sequence increases transcription of the JCVE promoter in a non-glial context.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
265
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
13899-905
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
A nuclear protein derived from brain cells stimulates transcription of the human neurotropic virus promoter, JCVE, in vitro.
pubmed:affiliation
Department of Biochemistry and Molecular Biology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't