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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-5-30
pubmed:abstractText
Chromosomal rearrangements of the HMGA2 locus belong to the most common aberrations in human benign tumors. HMGA2 rearrangements often result in chimeric genes expressing transcripts consisting of the first three exons of HMGA2 followed by ectopic sequences derived from intron 3 of that gene. RT-PCR-based expression studies of 4 of these HMGA2 transcripts revealed a co-expression with the "wild-type" HMGA2a in tumor samples as well as in normal tissues. Northern blot hybridizations of the lipoma cell line Li-14 revealed the expression of five additional HMGA2 transcripts consisting of exons 1 to 3 but not exons 4 to 5 besides the full-length HMGA2a transcript. In silico analyses have been performed showing a high homology to well-established consensus sequences for the 3' splice acceptor site, the branch site, and poly(A) signal. Thus, it is quite obvious that the HMGA2 transcripts described herein are alternative, not aberrant, splice-products of the HMGA2 gene. It is hypothesized that HMGA2-dependent tumorigenesis is caused by a disturbed equilibrium in the co-expression of the HMGA2 splice variants leading to aberrant cell proliferation and/or malignant transformation of cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0006-3002
pubmed:author
pubmed:issnType
Print
pubmed:day
25
pubmed:volume
1729
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
24-31
pubmed:dateRevised
2005-11-2
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Extensive expression studies revealed a complex alternative splicing pattern of the HMGA2 gene.
pubmed:affiliation
ZytoVision GmbH, Fischkai 1, D-27572 Bremerhaven, Germany.
pubmed:publicationType
Journal Article