Linked Life Data

10488155

Source:http://linkedlifedata.com/resource/pubmed/id/10488155

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
39
pubmed:dateCreated
1999-11-4
pubmed:abstractText
The human fibroblast growth factor receptor-1 primary transcript is alternatively processed to produce receptor forms that vary in their affinity for fibroblast growth factor. The inclusion of a single exon (alpha) in normal brain glial cells produces a low affinity form of the receptor. Recognition of the alpha-exon is dysregulated during neoplastic transformation of glial cells to produce a high affinity receptor form. In this study, we have identified a second intronic repressor of RNA splicing located approximately 250 nucleotides upstream of the alpha-exon. Deletion or mutation of this sequence resulted in a significant increase in exon recognition in glioblastoma cells. This intronic repressor was found to share significant sequence homology with an intronic repressor element located downstream of the alpha-exon. The two repressor elements are functionally redundant in that they are capable of inhibiting alpha-exon recognition when positioned upstream or downstream of the exon. Finally, the elements were found to mediate enhanced exclusion of an unrelated exon, but only the repressors were placed flanking the exon. However, under these conditions, the cell-specific exon exclusion was no longer maintained. These results suggest that although the alpha-exon inclusion is actively repressed in glioblastomas, the absence of trans-activators appears to be key to the production of the high affinity form of fibroblast growth factor receptor-1 in glioblastomas.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
24
pubmed:volume
274
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
28035-41
pubmed:dateRevised
2010-5-26
pubmed:meshHeading
pubmed-meshheading:10488155-Alternative Splicing, pubmed-meshheading:10488155-Animals, pubmed-meshheading:10488155-Base Sequence, pubmed-meshheading:10488155-DNA Primers, pubmed-meshheading:10488155-Exons, pubmed-meshheading:10488155-Fibroblast Growth Factors, pubmed-meshheading:10488155-Glioblastoma, pubmed-meshheading:10488155-Humans, pubmed-meshheading:10488155-Introns, pubmed-meshheading:10488155-Molecular Sequence Data, pubmed-meshheading:10488155-Rats, pubmed-meshheading:10488155-Receptor, Fibroblast Growth Factor, Type 1, pubmed-meshheading:10488155-Receptor Protein-Tyrosine Kinases, pubmed-meshheading:10488155-Receptors, Fibroblast Growth Factor, pubmed-meshheading:10488155-Recombinant Proteins, pubmed-meshheading:10488155-Repressor Proteins, pubmed-meshheading:10488155-Sequence Deletion, pubmed-meshheading:10488155-Transcription, Genetic, pubmed-meshheading:10488155-Transfection, pubmed-meshheading:10488155-Tumor Cells, Cultured
pubmed:year
1999
pubmed:articleTitle
Redundant intronic repressors function to inhibit fibroblast growth factor receptor-1 alpha-exon recognition in glioblastoma cells.
pubmed:affiliation
Section of Endocrine Neoplasia and Hormonal Disorders, Department of Medical Specialties, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't