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CRM1-mediated nuclear export and regulated activity of the Receptor Tyrosine Kinase antagonist YAN require specific interactions with MAE
Tina L. Tootle1,2,
Philina S. Lee2, and
1 Whitehead Institute, Massachusetts Institute of Technology, Cambridge, MA
02142, USA 2 Department of Biology, Massachusetts Institute of Technology, Cambridge, MA
Author for correspondence (e-mail:
Accepted for publication 27 November 2002.
ETS family transcription factors serve as downstream effectorsof signal
transduction pathways, mediating cellular proliferation,differentiation and,
when misregulated, tumorigenesis. The transcriptionalrepressor YAN prevents
inappropriate responses to Receptor TyrosineKinase signaling by outcompeting
POINTED for access to targetgene promoters. We demonstrate that the molecular
mechanismunderlying downregulation of YAN involves CRM1-mediated nuclear
exportand define a novel role in this context for MAE, a co-factorpreviously
implicated in facilitating MAPK phosphorylation ofYAN. In addition to
promoting YAN downregulation, MAE also participatesin an inhibitory feedback
loop that attenuates POINTED-P2 activation.Thus, we propose that MAE plays
multiple independent roles infine-tuning the levels of POINTED and YAN
activity in accordancewith changing RTK signaling conditions.
Using Drosophila to Decipher How Mutations Associated With Human Branchio-Oto-Renal Syndrome and Optical Defects Compromise the Protein Tyrosine Phosphatase and Transcriptional Functions of Eyes Absent.
M. Mutsuddi, B. Chaffee, J. Cassidy, S. J. Silver, T. L. Tootle, and I. Rebay (2005)
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