Nucleic Acids Research, Vol 26, Issue 18 4100-4107, Copyright © 1998 by Oxford University Press
MD Smith, SJ Dawson, LM Boxer and DS Latchman
The ability of the POU family transcription factor Brn-3a to stimulate
neurite outgrowth and the expression of the genes encoding neuronal
proteins such as the neurofilaments and SNAP-25 has previously been shown
to be dependent upon the C-terminal POU domain which can mediate both DNA
binding and transcriptional activation. We show here, however, that the
ability of Brn-3a to activate Bcl-2 expression and protect neuronal cells
from apoptosis (programmed cell death) requires a distinct N-terminal
activation domain. Bcl-2 gene activation and protection from apoptosis are
thus produced only by the long form of Brn-3a which contains this domain
and not by a naturally occurring short form lacking this domain or by the
isolated POU domain, although all these forms of Brn-3a can stimulate
neurite outgrowth. Hence Brn-3a is a multi-functional transcription factor
with different regions of the factor mediating its different effects and
two distinct forms with different properties being generated by alternative
splicing.
ARTICLES
The N-terminal domain unique to the long form of the Brn-3a transcription factor is essential to protect neuronal cells from apoptosis and for the activation of Bbcl-2 gene expression
Department of Molecular Pathology, Windeyer Institute of Medical Sciences, University College London,Cleveland Street, London W1P 6DB, UK and Department of Medicine, Stanford University Medical Center, Stanford, CA 94305-5112, USA.
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