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The BRCA2 transactivation domain does not interact with JNK
Author(s) -
May Gerhard H.W.,
Harris Fiona,
Gillespie David,
Black Donald M.
Publication year - 1999
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/(sici)1098-2264(199908)25:4<407::aid-gcc16>3.0.co;2-i
Subject(s) - transactivation , domain (mathematical analysis) , computer science , mathematics , biology , genetics , transcription factor , gene , mathematical analysis
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. © 1999 Wiley‐Liss, Inc.