The N-terminal region of BRCA2 has the capacity to activate transcription w
hen 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 i
nteracts with nor serves as a substrate for JNK, or any other kinase that c
an be detected in extracts from either fibroblasts or epithelial cells. Whi
le this clearly does not rule out a transcriptional role for BRCA2, our fin
dings indicate that BRCA2 is not regulated by the JNK pathway in a manner a
nalogous to JUN. Genes Chromosomes Cancer 25:407-409, 1999. (C) 1999 Wiley-
Liss, Inc.