Linked Life Data

9278856

Source:http://linkedlifedata.com/resource/pubmed/id/9278856

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1997-10-10
pubmed:abstractText
In murine species, the GH receptor (mGHR) gene encodes a full-length membrane-anchored mGHR and a truncated soluble receptor ectodomain (the GH-binding protein; mGHBP). The mGHR and mGHBP mRNAs are generated by alternative pre-mRNA splicing. Similar GHR/GHBP pairs are generated in other species by proteolysis of the GHR. The regulation of GHBP expression and the biological role of GHBP are not clear. In order to begin to dissect the factors responsible for regulating expression of mGHR and mGHBP, we have cloned a mouse GH receptor/binding protein (mGHR/BP) minigene consisting of two mGHR cDNA fragments and an mGHR/BP genomic sequence, such that the mGHR and mGHBP can be derived from the minigene by mimicking native alternative pre-mRNA splicing. To study the possible role of selection of polyadenylation relative to the expression of mGHR and mGHBP, we deleted the two tandem poly A addition signals and the flanking AT-rich region within the exon (exon 8A) that encodes the carboxy terminus of mGHBP. In addition, two other mutated forms of the minigene, one containing a mutated alternative splice acceptor site (SAS) near exon 8A and the other possessing a deletion of the intron between exons 7 and 8A (intron 7/8A), were generated. Expression of the mGHR/BP minigene and its mutated forms in transfected mouse L cells revealed that removal of the polyadenylation signals diminished but did not abolish either mGHR or mGHBP production. However, mutation of the SAS yielded normal mGHR and an mGHBP which may be a result of the translation of an mRNA possessing an open reading frame in intron 7/8A. Additionally, removal of intron 7/8A abolished mGHR expression but resulted in mGHBP production. The results suggest that selection of alternative polyadenylation sites of the mGHR/BP gene does not play a major role in the regulation of expression of mGHR and mGHBP in vitro. These results also suggest that mutation of the SAS near exon 8A does not abolish the ability of mGHR/BP gene to produce an mGHBP that retains the ability to bind GH, although the new mGHBP may be different from the natural mGHBP at its carboxy terminus.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0952-5041
pubmed:author
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-13
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Deletion of the mouse GH-binding protein (mGHBP) mRNA polyadenylation and splicing sites does not abolish production of mGHBP.
pubmed:affiliation
Edison Biotechnology Institute, Molecular and Cellular Biology Program, Athens, Ohio, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't