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J. Biol. Chem., Vol. 277, Issue 21, 18365-18372, May 24, 2002
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From the Departments of The basic helix-loop-helix transcription factor
TAL1 (or SCL), originally identified from its involvement by a
chromosomal rearrangement in T-cell acute lymphoblastic leukemia, is
required for hematopoietic development. TAL1 also has a critical role
in embryonic vascular remodeling and is expressed in endothelial cells
postnatally, although little is known about its function or regulation
in this cell type. We report here that the important proangiogenic
stimulus hypoxia stimulates phosphorylation, ubiquitination, and
proteasomal breakdown of TAL1 in endothelial cells. Tryptic phosphopeptide mapping and chemical inhibitor studies showed that hypoxia induced the mitogen-activated protein kinase-mediated phosphorylation of a single serine residue, Ser122,
in the protein, and site-directed mutagenesis demonstrated that Ser122 phosphorylation was necessary for hypoxic
acceleration of TAL1 turnover in an immortalized murine endothelial
cell line. Finally, whereas TAL1 expression was detected in endothelial
cells from both large and small vessels, hypoxia-induced TAL1 turnover
was observed only in microvascular endothelial cells. Besides their implications for TAL1 function in angiogenic processes, these results demonstrate that a protein kinase(s) important for mitogenic signaling is also utilized in hypoxic endothelial cells to target a
transcription factor for destruction.
Phosphorylation by Mitogen-activated Protein Kinase Mediates the
Hypoxia-induced Turnover of the TAL1/SCL Transcription Factor in
Endothelial Cells*
,¶
**
Medicine and ¶ Cell
Biology and Vanderbilt-Ingram Cancer Center, Vanderbilt
University Medical Center, Nashville, Tennessee 37232, ** Veterans Affairs Tennessee Valley Health Care System,
Nashville, Tennessee 37232, and § Department of Dermatology,
Emory University School of Medicine, Atlanta, Georgia 30322
*
This work was supported in part by National Institutes of
Health Grant R01 HL49118 (to S. J. B.) and a Merit Review Award from
the Department of Veterans Affairs (to S. J. B.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Division of
Hematology-Oncology, Rm. 777, Preston Research Bldg., Vanderbilt
University Medical Center, Nashville, TN 37232. Tel.: 615-936-1809;
Fax: 615-936-3853; E-mail: stephen.brandt@mcmail.vanderbilt.edu.
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