Research Topics
| M VigSummaryAffiliation: Harvard University Country: USA Publications
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Publications
CRACM1 is a plasma membrane protein essential for store-operated Ca2+ entryM Vig
Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA
Science 312:1220-3. 2006..Although overexpression of CRACM1 did not affect CRAC currents, RNAi-mediated knockdown disrupted its activation. CRACM1 could be the CRAC channel itself, a subunit of it, or a component of the CRAC signaling machinery...
Defective mast cell effector functions in mice lacking the CRACM1 pore subunit of store-operated calcium release-activated calcium channelsMonika Vig
Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA
Nat Immunol 9:89-96. 2008..Thus, CRACM1 is crucial in mouse mast cell effector function, but mouse T cell calcium release-activated calcium channels are functional in the absence of CRACM1...
Calcium signaling in immune cellsMonika Vig
Laboratory of Allergy and Immunology, Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02115, USA
Nat Immunol 10:21-7. 2009..In this review, we highlight advances in the understanding of Ca2+ signaling in lymphocytes with special emphasis on SOC entry. We also discuss outstanding questions and probable future directions of the field...
CRACM1 multimers form the ion-selective pore of the CRAC channelMonika Vig
Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
Curr Biol 16:2073-9. 2006..Our data provide unequivocal evidence that CRACM1 multimers form the Ca(2+)-selective CRAC-channel pore...
The long and arduous road to CRACMonika Vig
Laboratory of Allergy and Immunology, Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA
Cell Calcium 42:157-62. 2007..The field is now actively engaged in deciphering the gating mechanism of CRAC channels. We summarize here the latest progress in this direction...
Amplification of CRAC current by STIM1 and CRACM1 (Orai1)Christine Peinelt
Center for Biomedical Research at The Queen s Medical Center and John A Burns School of Medicine at the University of Hawaii, Honolulu, HI 96813, USA
Nat Cell Biol 8:771-3. 2006..Overexpression of both proteins greatly potentiates I(CRAC), suggesting that STIM1 and CRACM1 mutually limit store-operated currents and that CRACM1 may be the long-sought CRAC channel...
Commitment of activated T cells to secondary responsiveness is enhanced by signals mediated by cAMP-dependent protein kinase A-IMonika Vig
National Institute of Immunology, New Delhi, India
Mol Pharmacol 62:1471-81. 2002..Together, our data suggest that PKA-I-mediated signals triggered by prolonging the half-life of cAMP induced during T-cell priming increase survival of activated T cells and enhance memory T cell commitment...
Essential role for STAT5 signaling in CD25+CD4+ regulatory T cell homeostasis and the maintenance of self-toleranceAndrey Antov
Center for Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
J Immunol 171:3435-41. 2003..Furthermore, transient activation of STAT5 is sufficient to increase CD25(+)CD4(+) T reg numbers in IL-2-deficient mice. Our study uncovers an essential role for STAT5 in maintaining CD25(+)CD4(+) T reg homeostasis and self-tolerance...
Inducible nitric oxide synthase in T cells regulates T cell death and immune memoryMonika Vig
National Institute of Immunology, New Delhi, India
J Clin Invest 113:1734-42. 2004....
