| Literature DB >> 10398438 |
G H May1, F Harris, D Gillespie, D M Black.
Abstract
The N-terminal region of BRCA2 has the capacity to activate transcription when fused to a heterologous DNA binding domain and includes a segment with amino acid similarity to the JNK-docking site in the cellular JUN protein. However, unlike JUN, we have determined that this region of BRCA2 neither interacts with nor serves as a substrate for JNK, or any other kinase that can be detected in extracts from either fibroblasts or epithelial cells. While this clearly does not rule out a transcriptional role for BRCA2, our findings indicate that BRCA2 is not regulated by the JNK pathway in a manner analogous to JUN. Genes Chromosomes Cancer 25:407-409, 1999. Copyright 1999 Wiley-Liss, Inc.Entities:
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Year: 1999 PMID: 10398438 DOI: 10.1002/(sici)1098-2264(199908)25:4<407::aid-gcc16>3.0.co;2-i
Source DB: PubMed Journal: Genes Chromosomes Cancer ISSN: 1045-2257 Impact factor: 5.006