Abstract

The Genetic Epidemiology and Biostatistics Core combines the expertise in genetic analysis of Wake Forest University School of Medicine and the University of Alabama at Birmingham. The Core will continue to guide the experimental design for collection of clinical and genetic data. The Core will continue to offer expertise in data management, statistical and genetic data analysis. The goals of the Genetic Epidemiology and Biostatistics Core are to (1) provide appropriate experimental designs tailored to address specific genetic and epidemiologic hypotheses, (2) facilitate efficient data collection procedures for preparation of data analysis, (3) refine regions of susceptibility using linkage disequilibrium and association methods, and (4) utilize and, in some cases, develop novel methods for analysis of SLE phenotypes. The long-term goals of the Genetic Epidemiology and Biostatistics Core are to utilize genetic and epidemiologic data collected on SLE patients and their family members in order to identify genetic and epidemiologic risk factors that contribute to the susceptibility for SLE. A detailed plan to assure that the Core is successful in meeting its objectives is described.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
Type
Research Program Projects (P01)
Project #
5P01AR049084-10
Application #
8378135
Study Section
Special Emphasis Panel (ZAR1-MLB-G)
Project Start
Project End
2014-03-31
Budget Start
2012-04-01
Budget End
2013-03-31
Support Year
10
Fiscal Year
2012
Total Cost
$162,832
Indirect Cost
$26,261

  Institution

Name
University of Alabama Birmingham
Department
Type
DUNS #
063690705
City
Birmingham
State
AL
Country
United States
Zip Code
35294

  Publications

Patel, Zubin; Lu, Xiaoming; Miller, Daniel et al. (2018) A plausibly causal functional lupus-associated risk variant in the STAT1-STAT4 locus. Hum Mol Genet :
Langefeld, Carl D; Ainsworth, Hannah C; Cunninghame Graham, Deborah S et al. (2017) Transancestral mapping and genetic load in systemic lupus erythematosus. Nat Commun 8:16021
Deng, Yun; Zhao, Jian; Sakurai, Daisuke et al. (2016) Decreased SMG7 expression associates with lupus-risk variants and elevated antinuclear antibody production. Ann Rheum Dis 75:2007-2013
Alarcón-Riquelme, Marta E; Ziegler, Julie T; Molineros, Julio et al. (2016) Genome-Wide Association Study in an Amerindian Ancestry Population Reveals Novel Systemic Lupus Erythematosus Risk Loci and the Role of European Admixture. Arthritis Rheumatol 68:932-43
Lessard, Christopher J; Sajuthi, Satria; Zhao, Jian et al. (2016) Identification of a Systemic Lupus Erythematosus Risk Locus Spanning ATG16L2, FCHSD2, and P2RY2 in Koreans. Arthritis Rheumatol 68:1197-1209
Lu, Rufei; Munroe, Melissa E; Guthridge, Joel M et al. (2016) Dysregulation of innate and adaptive serum mediators precedes systemic lupus erythematosus classification and improves prognostic accuracy of autoantibodies. J Autoimmun 74:182-193
Zhao, Jian; Giles, Brendan M; Taylor, Rhonda L et al. (2016) Preferential association of a functional variant in complement receptor 2 with antibodies to double-stranded DNA. Ann Rheum Dis 75:242-52
Liu, Ke; Kurien, Biji T; Zimmerman, Sarah L et al. (2016) X Chromosome Dose and Sex Bias in Autoimmune Diseases: Increased Prevalence of 47,XXX in Systemic Lupus Erythematosus and Sjögren's Syndrome. Arthritis Rheumatol 68:1290-1300
Taylor, Rhonda L; Cruickshank, Mark N; Karimi, Mahdad et al. (2016) Focused transcription from the human CR2/CD21 core promoter is regulated by synergistic activity of TATA and Initiator elements in mature B cells. Cell Mol Immunol 13:119-31
Lu, Xiaoming; Zoller, Erin E; Weirauch, Matthew T et al. (2015) Lupus Risk Variant Increases pSTAT1 Binding and Decreases ETS1 Expression. Am J Hum Genet 96:731-9

Showing the most recent 10 out of 215 publications