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. Author manuscript; available in PMC: 2014 Dec 1.
Published in final edited form as: Arthritis Rheum. 2013 Dec;65(12):3239–3247. doi: 10.1002/art.38137

Table 2.

Overlap of published genome-wide association study single nucleotide polymorphisms for autoimmune diseases with those for dermatomyositis*

Gene
Name
SNP Marker Original SNP/LD Chr: Position OR (CI) P FDR SNP
Disease
Source [ref]
PLCL1 rs7572733 rs6738825/0.979 2: 198929806 0.80 (0.72–0.88) 6.18E-06 0.00089 SLE [17]
PLCL1 rs1518364 rs6738825/0.958 2: 198809975 1.22 (1.11–1.35) 5.11E-05 0.0037 SLE [17]
PLCL1 rs938929 rs6738825/0.958 2: 198780860 1.22 (1.10–1.34) 0.00008322 0.0030 SLE [17]
BLK rs2736340 8: 11343973 1.25 (1.12–1.40) 0.0000653 0.0031 RA [14]
CCL21 rs2492358 rs951005/1.0 9: 34737828 0.77 (0.67–0.88) 0.0002093 0.0060 RA [14]
CCL21 rs951005 9: 34743681 0.77 (0.67–0.89) 0.000317 0.0076 RA [14]
*

Only SNPs with FDR < 0.05 are listed; SNP marker = directly genotyped single nucleotide polymorphism (SNP) by genome-wide association studies; Original SNP = original SNPs among 141 SNPs associated with autoimmune diseases, if not directly genotyped; LD = linkage disequilibrium in r2 with the directly genotyped SNP on Illumina arrays; Chr = chromosome; Position = base pair in hg19/build37 coordinate; OR = odds ratio; CI = 95% confidence interval; P = fixed effect P value in meta-analysis; FDR = false discovery rate; SLE = systemic lupus erythematosus; RA = rheumatoid arthritis.