MARTINA REINHOLD, Ph.D.
Instructor
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Department of Pathology – Mail Code 7750
The University of Texas Health Science Center
7703 Floyd Curl Drive
San Antonio, Texas 78229-3900 |
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| INFORMATION |
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| EDUCATION |
| 1997 |
PhD, Washington University, St. Louis |
| 1991 |
BS, University of Michigan, Ann Arbor |
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| POSTDOCTORAL TRAINING |
| 1997-99 |
Research Associate, HHMI, Washington University |
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DESCRIPTION OF RESEARCH
We have previously identified a cis-acting sequence in the
proximal promoter of the fibroblast growth factor receptor 3 (FGFR3) gene that
strongly activates transcription in chondrocytic cells. The transcriptional
activity of this sequence (FRE3) requires serum response factor and its cognate
recognition motif, serum response element. The FRE3 contains a single serum
response element and mutations thereof completely abolish the transcriptional
activity of the FRE3. Similarly, the transcriptional activity of the proximal
promoter of FGFR3 is suppressed by mutation of the serum response element. While
SRF is required for the activity of FRE3, there are other transcriptional
regulators that contribute to the activity of FRE3. Binding assays showed that
several protein nucleic acid complexes assemble on the FRE3 sequence. Mutation
of the sequence that neighbors the SRE disrupted a specific protein-DNA complex
that is distinct from SRF. In addition, this mutation diminished the
transcriptional activity of FRE3. This implies that a positive acting
transcriptional regulator may act in concert with SRF to regulate the FRE3. We
have identified a potential binding site for members of the T-box family of
transcription factors at the 5’-end of the SRE. Members of the T-box family have
been shown to play key roles in the regulation of embryonic development. Most
intriguing, a recent study suggests that the T-box containing transcription
factor Brachyury and FGFR3 are involved in an autoregulatory loop.
Presently, we are carrying out studies to test a potential role for T-box
proteins in the regulation of the FRE.
SELECTED PUBLICATIONS
1. Reinhold, M.I., Lindberg, F.P., Plas, D., Reynolds, S., Peters, M.G. &
Brown, E.J. In vivo expression of alternatively spliced forms of Integrin-associated
Protein (IAP). J. of Cell Science. 108, 3419-3425 (1995)
2. Lindberg, F.P., Gresham, H.D., Reinhold, M.I. & Brown, E.J. Integrin-associated
Protein immunoglobulin domain is necessary for efficient vitronectin bead
binding. The Journal of Cell Biology. 134, 1313-1322 (1996)
3. Reinhold, M.I., Lindberg, F.P., Kersh, G.J., Allen, P.M. & Brown, E.J.
Costimulation of T cell activation by Integrin-associated Protein (IAP/CD47) is
an adhesion-dependent, CD28-independent signaling pathway. Journal of
Experimental Medicine. 185, 1-11 (1997)
4. Reinhold, M.I., Green, J.M., Lindberg, F.P., Ticchioni, M., & Brown,
E.J. Cell spreading distinguishes the mechanism of augmentation of T cell
activation by Integrin-associated Protein/CD47 and CD28. International
Immunology. 11(5), 707-718 (1999)
5. Rebres, R.A., Green, J. M., Reinhold, M.I., Ticchioni, M., & Brown,
E.J. Membrane raft association of CD47 is necessary for actin polymerization and
protein kinase C theta translocation in its synergistic activation of T cells.
J. Biol. Chem. 276, 7672-80 (2001).
6. Tomita, M., Reinhold, M. I., Molkentin, J.D. and Naski, M. C.
Calcineurin and NFAT4 induce chondrogenesis. J. Biol. Chem. 277, 42214-42218
(2002).
ABSTRACTS
1. Reinhold, M.I., McEwen, D., Ornitz, D. and Naski, M.C. (2000).
Transcriptional Regulation of the FGF Receptor 3 gene. ASBMR Abstracts
Updated on 01/06/2003