Welcome! Click here to login or here to register.
 |
|||||||||||||||||||
|
|||||||||||||||||||
 |
|||||||||||||||||||
"Allelic knockout of novel splice variants of human recombination repair gene RAD51B in t(12;14) uterine leiomyomas." |
Schoenmakers EF, Huysmans C, Van de Ven WJ |
Published Feb. 1, 1999 in Cancer Res volume 59 .
Pubmed ID: 9892177
Abstract:
| Recently, the high mobility group protein gene HMGIC was identified as the chromosome 12q15 target gene in a variety of benign solid tumors. Here, we report that the recombinational repair gene RAD51B on chromosome 14q23-24 is the preferential translocation partner of HMGIC in uterine leiomyomas. The pathogenetically critical sequences seem to reside in the last coding exon of a novel RAD51B isoform, which encode a domain containing a putative transmembrane anchor and are expressed in the uterus but not in a wide variety of other tissues tested. By fluorescence in situ hybridization, rapid amplification of 3' cDNA ends, and reverse transcription-PCR analysis, we demonstrated consistent chromosomal rearrangements within RAD51B and expression of fusion transcripts, structurally resulting in an allelic knockout of the uterine isoform of RAD51B and confirming a pleiotropic function of this gene. |
This publication refers to following REPAIRtoire entries:
| Proteins |
Last modification of this entry: Oct. 6, 2010
Add your own comment!
There is no comment yet.
|
|
|
|