Area:
Molecular Biology, Pathology
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High-probability grants
According to our matching algorithm, Bimal K. Ray is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1992 |
Ray, Bimal K |
R15Activity Code Description: Supports small-scale research projects at educational institutions that provide baccalaureate or advanced degrees for a significant number of the Nation’s research scientists but that have not been major recipients of NIH support. The goals of the program are to (1) support meritorious research, (2) expose students to research, and (3) strengthen the research environment of the institution. Awards provide limited Direct Costs, plus applicable F&A costs, for periods not to exceed 36 months. This activity code uses multi-year funding authority; however, OER approval is NOT needed prior to an IC using this activity code. |
Regulation of Serum Amyloid a Protein Synthesis @ University of Missouri-Columbia
DESCRIPTION: (Adapted from the investigator's abstract). The goal of the proposed research is to elucidate the molecular mechanism of induction of serum amyloid A (SAA) protein synthesis in liver. SAA protein is an acute phase protein and is the precursor of amyloid protein A (AA), the main protein constituent of amyloid fibrils deposited in tissues in the disease associated with chronic inflammation e.g., rheumatoid arthritis, juvenile chronic arthritis. During periods of inflammation SAA protein synthesis in liver increases dramatically which has been found to be due to increased transcription of this gene. The objective is therefore to identify the regulatory elements of the SAA gene and the molecular events involved in this inducible biosynthetic process. To achieve these objectives investigators intend to specifically pursue the following sequences: (1) identification of DNA-binding domains that are required for the transcriptional activation; (2) determining the sequence of the regulatory regions; (3) characterization of these regions using a reporter chloramphenicol acetyl transferase (CAT) gene. Specific DNA binding domain, where transcription factor(s) bind to influence transcription of the gene, will be determined by DNA- protein gel retardation assay using fragments of the SAA genomic DNA. Identity and sequence of the binding domain will be determined by methylation interference assay. This regulatory structural element (s) will be characterized by ligating these sequences to an easily identifiable chloramphenicol acetyl transferase gene, whose transient expression in a transfected primary culture of hepatocytes will be followed in presence and in absence of SAA inducer (interleukin-1, interleukin-6). The potential importance of this project is to gain insight into cellular control mechanism of SAA gene induction. These studies will enable the formation of the basis for future work regarding the regulation of SAA biosynthesis in patients with disease which predisposes to amyloidosis.
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1 |
1996 — 2005 |
Ray, Bimal K |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. R56Activity Code Description: To provide limited interim research support based on the merit of a pending R01 application while applicant gathers additional data to revise a new or competing renewal application. This grant will underwrite highly meritorious applications that if given the opportunity to revise their application could meet IC recommended standards and would be missed opportunities if not funded. Interim funded ends when the applicant succeeds in obtaining an R01 or other competing award built on the R56 grant. These awards are not renewable. |
Mechanism of Serum Amyloid a Protein Synthesis @ University of Missouri-Columbia |
1 |
2002 — 2004 |
Ray, Bimal K |
R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
Mechanism of Mmp Gene Induction in Osteoarthritis @ University of Missouri-Columbia
DESCRIPTION (provided by applicant): The goal proposed research is to elucidate the induction mechanism of matrix metalloproteinases (MMP) in chondrocyte cells of the osteoarthritis-affected joint tissue. Osteoarthritis (OA) is manifested by the degradation of cartilage leading to a total loss of the cushion between the bones of the joints causing stiffness, swelling and limitation of joint mobility. In normal cartilage, expression of each MMP is tightly regulated. During OA condition, however, MMPs are overexpressed resulting in the degradation of Collagen and other joint tissue-associated proteins necessary for maintaining normal environment of the cartilage. We hypothesize that a set of transcription factors, responsible for the increased expression of MMPs, is present at a higher active level in the chondrocyte cells of OA-cartilage. Consistent with this hypothesis, preliminary studies indicated that chondrocyte cells of the OA joint tissue contain a significantly higher level of several transcription factors, of which one is identified as SAF-1, an inflammation-responsive transcription factor. Over-expression of SAF-1 enhances MMP-1 expression in cultured chondrocyte cells. SAF-1 also interacts with the promoters of MMP-9 and -14 genes indicating its possible role in regulating expression of these MMP genes in OA condition. Identification of the involved transcription factors will provide a molecular basis for regulating their activity for future therapeutic efforts against OA. This research thus focuses on defining the role of SAF-1 in regulating expression of MMP-1, -9 and -14 genes. Another goal of this proposal is to identify other transcription factors involved in this process. Although pathology of OA most likely starts with biomechanical stress on the cartilage, cytokines appear at later stages of the disease. Therefore, an OA-like condition will be created by combining both biomechanical stress and cytokines and mechanisms of MMP gene induction will be studied in response to these signals. Towards this goal, the following specific aims are planned: 1) Characterize the role of SAF-1 in MMP-1 gene induction in chondrocytes of OA-cartilage. Define other responsive elements and factors involved in increasing MMP-1 expression in OA condition. 2) Investigate the role of SAF-1 in the induction of MMP-9 gene expression in OA-cartilage. Identify other regulatory elements and factors involved in this process. 3) Assess the role of SAF-1 in the induction of MMP-1 4 gene and identify other regulatory elements and factors involved in increasing MMP-1 4 expression in chondrocytes under OA-like condition. Completion of the above experimental objectives will form the basis for future investigation on: a) transmembrane signaling pathways in OA chondrocytes that enhance transcriptional activity, and b) evaluation of inhibitors of involved signaling pathway as potential therapeutic agents to control abnormal MMP expression.
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1 |