Source: UNIVERSITY OF MISSOURI submitted to NRP
COMPLEXITY OF INFLAMMATORY RESPONSE BY ALTERNATIVE SPLICING OF SAF GENE
Sponsoring Institution
Cooperating Schools of Veterinary Medicine
Project Status
COMPLETE
Funding Source
STATE
Reporting Frequency
Annual
Accession No.
0213298
Grant No.
(N/A)
Cumulative Award Amt.
(N/A)
Proposal No.
(N/A)
Multistate No.
(N/A)
Project Start Date
Jan 1, 2008
Project End Date
Dec 31, 2009
Grant Year
(N/A)
Program Code
[(N/A)]- (N/A)
Recipient Organization
UNIVERSITY OF MISSOURI
(N/A)
COLUMBIA,MO 65211
Performing Department
Veterinary Pathobiology
Non Technical Summary
Inflammatory diseases are the result of abnormal host response. The mechanism by which inflammation is induced is beginning to unravel. This project aims at understanding a crucial event in the process of inflammation. Once we understand the molecular mechanism underlying the crucial event in inflammation, a new therapeutic regimen can be developed that could be more robust and effective to control several inflammatory diseases.
Animal Health Component
(N/A)
Research Effort Categories
Basic
100%
Applied
(N/A)
Developmental
(N/A)
Classification

Knowledge Area (KA)Subject of Investigation (SOI)Field of Science (FOS)Percent
3053840106050%
3053840109050%
Knowledge Area
305 - Animal Physiological Processes;

Subject Of Investigation
3840 - Laboratory animals;

Field Of Science
1090 - Immunology; 1060 - Biology (whole systems);
Goals / Objectives
The goal of this project is to determine the molecular mechanism of alternative splicing that is responsible for differential accumulation of two SAF isoforms called SAF-2 and SAF-3 that play crucial roles in the induction of risk factor genes associated with inflammation. It is anticipated that understanding how these splicing events are linked to the production of SAF-2 and SAF-3, we would be able to develop a new therapeutic approach to control inflammatory diseases such as arthritis and atherosclerosis.
Project Methods
We have three specific aims to test our hypothesis and the experimental approach to accomplish these specific aims involves identification of specific splicing factors that interact with the involved RNA elements in the precursor SAF mRNA. Using mobility shift assay, Western immunoblot and MALDI-TOF analysis we plan to identity these proteins. Furthermore, we plan to investigate how these proteins may be activated by specific kinases. Using several purified kinases, antibodies against these kinases and specific inhibitors, we plan to characterize the activation mechanism of involved splicing factors.

Progress 01/01/08 to 12/31/09

Outputs
OUTPUTS: The goal of this project is to determine the molecular mechanism of alternative splicing that is responsible for differential accumulation of two SAF isoforms called SAF-2 and SAF-3 that play crucial roles in the induction of risk factor genes associated with inflammation. PARTICIPANTS: Not relevant to this project. TARGET AUDIENCES: Not relevant to this project. PROJECT MODIFICATIONS: Not relevant to this project.

Impacts
Using mobility shift assay, Western immunoblot and MALDI-TOF analysis we plan to identity proteins that interact with the involved RNA elements in the precursor SAF mRNA.

Publications

  • No publications reported this period