Linked Life Data

8009830

Source:http://linkedlifedata.com/resource/pubmed/id/8009830

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1994-7-15
pubmed:abstractText
The PstI-N genomic fragment of Autographa californica nuclear polyhedrosis virus (AcNPV) encodes an immediate-early protein, IE2, that functions as a promiscuous transactivator of other early viral promoters and heterologous promoters both in vivo and in vitro. IE2 contains several sequence motifs that are common to transcriptional activators. We have employed site-directed mutagenesis coupled with transient-expression assays to identify the amino acid sequences of IE2 that are essential for transactivation. Sequential deletion of amino-terminal sequences of IE2 gradually decreased the activity of the protein. Carboxy-terminal truncations of IE2 resulted in a dramatic loss of transactivation activities. Analysis of IE2 internal-deletion mutants demonstrated that the acidic amino acid-rich region between amino acids 198 and 206 possessed significant transactivation potential for all target promoters tested. In addition, squelching phenomena exhibited by wild-type IE2 and IE2 deletions containing the acidic amino acid-rich region indirectly demonstrated that this region may be involved in interactions with factors of the basic transcription machinery.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0042-6822
pubmed:author
pubmed:issnType
Print
pubmed:volume
202
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
164-72
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Functional dissection of the ie2 gene product of the baculovirus Autographa californica nuclear polyhedrosis virus.
pubmed:affiliation
Department of Biochemistry, Texas A&M University, College Station 77843-2475.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.