Kimberly, Faculty Advisor, Dr. Robert

Rea, Brian

Su, Faculty Advisor, Dr. Kaihong

Digital Commons @ Illinois Wesleyan University

Illinois Wesleyan UniversityDigital Commons @ IWUJohn Wesley Powell Student ResearchConference 2008, 19th Annual JWP ConferenceApr 12th, 9:00 AM - 10:00 AMFunctional Analysis of the Human FCGRTPromoter PolymorphismsBrian ReaIllinois Wesleyan UniversityDr. Robert Kimberly, Faculty AdvisorIllinois Wesleyan UniversityDr. Kaihong Su, Faculty AdvisorUniversity of Alabama at BirminghamFollow this and additional works at: http://digitalcommons.iwu.edu/jwprcThis Event is brought to you for free and open access by The Ames Library, the Andrew W. Mellon Center for Curricular and FacultyDevelopment, the Office of the Provost and the Office of the President. It has been accepted for inclusion in Digital Commons @ IWU bythe faculty at Illinois Wesleyan University. For more information, please contact digitalcommons@iwu.edu.©Copyright is owned by the author of this document.Brian Rea; Dr. Robert Kimberly, Faculty Advisor; and Dr. Kaihong Su, Faculty Advisor, "Functional Analysis of theHuman FCGRT Promoter Polymorphisms" (April 12, 2008). John Wesley Powell Student Research Conference. Paper 20.http://digitalcommons.iwu.edu/jwprc/2008/posters/20THE JOHN WESLEY POWELL STUDENT RESEARCH CONFERENCE - APRIL 2008 Poster Presentation P41 FUNCTIONAL ANALYSIS OF THE HUMAN FCGRT PROMOTER POL YMORPmSMS Brian Rea and Dr. Robert Kimbedy* and Dr. Kaihong Su* Biology Department, Illinois Wesleyan University University of Alabama at Birmingham Recent studies have indicated that the neonatal Fc Receptor may play a role in autoimmune diseases such as Systemic Lupus Erythematosus (SLE). The neonatal Fc receptor (FCGRT, also called FcRn) mediates transmission of immunoglobulin G (IgG) from mother to fetus perinatally and also plays a central role in the protection of serum IgG from catabolism. The expression levels of FCGRT directly correlate with serum IgG concentrations. FCGRT deficient mice were protected against SLE because serum IgG level is not at the concentration necessary to produce autoantibodies leading to the disease. Therefore, understanding the transcriptional regulation of the human FCGRT gene and how genetic polymorphisms in the promoter affect the receptor expression will help identify alleles that contribute to autoimmune diseases. In this study, we sequenced 20 individuals and identified a 37 base pair deletion in the promoter region. Promoter reporter analyses in both monocytic U937 cells and epithelial MDA468 cells demonstrated that the proximal 1 kb promoter of human FCGRT confers the greatest promoter activity and the 1 kb promoter with the 37 nucleotide deletion leads to decreased promoter activity. Our data suggests that the transcriptional control of the human FCGRT gene may reside within 1 kb proximal promoter and the deletion polymorphism decreases the promoter activity. These results provide insights for the regulation of the endogenous FCGRT receptor expression and predict that individuals with the deletion polymorphism express lower levels of FCGRT. Lower levels of FCGRT may indicate that the deletion polymorphism acts as a protection against autoimmune disease. 

Functional Analysis of the Human FCGRT Promoter Polymorphisms

http://digitalcommons.iwu.edu/cgi/viewcontent.cgi?article=2055&context=jwprc

Functional Analysis of the Human FCGRT Promoter Polymorphisms

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