Bimal Ray
Professor
PhD, Calcutta University
Research emphasis: Research in my laboratory focuses on the
elucidation of the molecular mechanisms associated with inflammation-induced
diseases that include atherosclerosis, amyloidosis, rheumatoid and osteoarthritis.
Inflammatory disease is a consequence of a host response to infection and
other environmental insults. The inflammatory response is exquisitely complex
as it was evolved to defend the host organism from myriads of external insults;
but by virtue of its complexity it often becomes uncontrollable and thus switching
a beneficial event to a harmful effect. Control of inflammatory diseases obviously
requires extensive knowledge of the underlying molecular events. We have been
interested in gaining a new insight into this process and therefore, studies
on inflammation have been one of the major foci of research in our laboratory.
This process which is triggered by pro-inflammatory cytokine-induced signal
transduction regulates transcription of many genes via changes in the activity
of a number of transcription factors. Our laboratory has been interested in
studying these molecular events associated with inflammation. Activation of
transcription factors by mechanisms involving signal transducing protein kinases
and proteolytic processing of transcription factors via proteosome action
are some of the critical molecular events we have been investigating. Our
studies have revealed the identity of a novel transcription factor called
SAF, serum amyloid A activating factor. We have extensively studied the structural
features of this protein, which belongs to a family of at least four members.
Long term goal of our research is to develop a molecular approach to control
inflammatory disease by using siRNA technology, developing specific inhibitor
molecules to control the activity of transcription factors which has gone
awry during different inflammatory conditions.
Teaching: Molecular Biology
Selected publications:
Ray, A., Shakya, A., Kumar, D. and Ray, B.K. (2004) Overexpression of SAF-1 inhibits cell proliferation by the induction of cyclin-dependent protein kinase inhibitor p21 expression. J. Immunol. 172: 5006-5015.
Ray, A., Kumar, D., Shakya, A., Brown, C.R. Cook, J.L. and Ray, B.K. (2004) SAF-1 transgenic mice are prone to develop severe form of inflammation-induced arthritis. J. Immunol. 173: 4684-4691.
Ray, A., Kumar, D., Ray, P., and Ray, B.K. (2004) Transcriptional activity of SAF-1 is regulated by distinct functional modules. J. Biol. Chem. 279: 54637-54646.
Ray, B.K., Shakya, A., Turk, J.R., Apte, S.S., and Ray, A. (2004) Induction of the MMP-14 Gene in Macrophages of the Atherosclerotic Plaque: Role of SAF-1 in the Induction Process. Circulation Res. 95: 1082-1090.
Ray, A., Ray, P., Guthrie, N., Shakya, A., Kumar, D. and Ray, B.K. (2003) Protein kinase A signaling pathway regulates transcriptional activity of SAF-1 by unmasking its DNA-binding domains. J. Biol. Chem. 278: 22586-22595
Ray, A., Kuroki, K., Cook, J.L., Bal, B.S., Kenter, K., Aust, G., and Ray, B.K. (2003) Induction of matrix metalloproteinases-1 gene expression is regulated by inflammation-responsive transcription factor SAF-1 in osteoarthritis. Arthritis & Rheumatism 48: 134-145
Ray, A., Yu, G.-Y and Ray, B.K. (2002) Cytokine responsive induction of SAF-1 activity is mediated by a MAP kinase signaling pathway - Mol. Cell. Biol. 22: 1027-1035.
Ray, B.K., Murphy, R., Ray, P., and Ray, A. (2002) SAF-2, a splice variant of SAF-1 acts as a negative regulator of transcription - J. Biol. Chem. 277: 46822-46830