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A bridge from
Science to
Patient Care
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Mercedes Rincon, Ph.D. |
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Contact Information
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Mercedes Rincón Ph.D.
Director, Transgenic/Knockout Mouse Facility
Associate Professor, Department of Medicine Immunobiology Program
Room D307, Given
University of Vermont, College of Medicine
Burlington, VT. 05405
Voice: (802) 656-0937
Fax: (802) 656-3854
Email:Mercedes.Rincon@uvm.edu
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Training and Professional Experience
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- Ph.D. (1990) Immunology; Hospital de la Princesa/Univ. Autonoma de Madrid
- Postdoctoral Fellow (1991-1993) Immunobiology; Yale University School of Medicine, New Haven CT.
- Postdoctoral Associate (1993-1995) Immunobiology; Yale University School of Medicine, New Haven CT.
- Postdoctoral Associate Research Scientist (1995-1996) Immunobiology; Yale University School of Medicine, New Haven CT.
- Assistant Professor (1998-2002), Dept. of Medicine/Immunobiology Program; University of Vermont, Burlington, VT
- Associate Professor (2002-Present), Dept. of Medicine/Immunobiology Program; University of Vermont, Burlington, VT
- Director, University of Vermont Transgenic Mouse Facility
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Research Interests
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The main focus of the group is the molecular mechanisms (signaling pathways and gene regulation) that control the:
- Development of T cells in the thymus
- Activation and differentiation of CD4+ Th1 and Th2 cells
- Activation, differentiation and death of CD8+ Th2 cells
- generation of memory CD4+ T cells
Signaling pathways include p38 MAP kinase, JNK and JAK pathways. Transcription factors include NFAT, NF-kB, AP-1, C/EBP and STAT.
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Selected Publications
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- Activation of the p38 mitogen-activated protein kinase pathway arrests cell cycle progression and differentiation of immature thymocytes in vivo.
- Regulation of c-Jun NH(2)-terminal kinase (Jnk) gene expression during T cell activation
- Inhibition of NF-kappaB activity and enhancement of apoptosis by the neuropeptide calcitonin gene-related peptide
- Activation of p38 MAP kinase in T cells facilitates the immune response to the influenza virus
- Inhibition of Th1 differentiation by IL-6 is mediated by SOCS1
- MAP-kinase signaling pathways in T cells
- Autocrine production of interleukin 6 causes multidrug resistance in breast cancer cells
- c-Jun NH(2)-terminal kinase (JNK)1 and JNK2 have distinct roles in CD8(+) T cell activation
- Induction of NFATc2 expression by interleukin 6 promotes T helper type 2 differentiation
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