Table S1: GWAS significant SNPs selected for analysis of regulatory function

S. No / Ref SNP ID / Gene / Locus / Location / P-Value / Risk Allele / References
1 / rs6795735 / ADAMTS9-AS2 / 3p14.1 / Intergenic / 7.40E-11 / C / Zegginiet al.[1]
2 / rs11717195 / ADCY5 / 3q21.1 / Intron / 6.50E-14 / T / Morris et al.[2]
3 / rs2028299 / AP3S2 / 15q26.1 / UTR 3 / 1.90E-11 / C / Kooneret al. [3]
4 / rs1552224 / ARAP1 (CENTD2) / 11q13.4 / Intron / 1.80E-10 / A / Voightet al. [4]
5 / rs243021 / BCL11A / 2p16.1 / Intergenic / 3.00E-15 / A / Morris et al.[2], Voightet al. [4]
6 / rs7172432 / C2CD4A/B / 15q22.2 / Intergenic / 7.48E-08 / G / Voightet al. [4]
7 / rs1048886 / C6orf57 / 6q13 / Mis-sense Mutation / 3E-08 / G / Voightet al. [4]
8 / rs12779790 / CDC123 / 10p13 / Intergenic / 1.00E-10 / G / Zegginiet al.[1]
9 / rs7756992 / CDKAL1 / 6p22.3 / Intron / 7.00E-35 / G / Cho et al. [5]
10 / rs10811661 / CDKN2A/B / 9p21.3 / Intergenic / 3.70E-27 / T / Zegginiet al.[1], Saxenaet al. [6]
11 / rs13292136 / CHCHD9 / 9q21.31 / Intergenic / 2.8E-08 / C / Voightet al. [4]
12 / rs17168486 / DGKB / 7p21.2 / Intergenic / 5.90E-11 / T / Morris et al.[2]
13 / rs9936385 / FTO / 16q12.2 / Intron / 2.60E-23 / C / Voightet al. [4]
14 / rs6467136 / GCC1-PAX4 / 7q32.1 / Intergenic / 4.96E-11 / G / Morris et al.[2]
15 / rs7041847 / GLIS3 / 9p24.2 / Intron / 1.99E-14 / A / Morris et al.[2]
16 / rs3923113 / GRB14 / 2q24.3 / Intergenic / 1.60E-09 / A / Morris et al.[2], Kooneret al. [3]
17 / rs1111875 / HHEX/IDE / 10q23.33 / Intergenic / 2.00E-19 / C / Morris et al.[2]
18 / rs7178572 / HMG20A / 15q24.3 / Intron / 7.10E-11 / G / Kooneret al. [3], Saxenaet al. [6]
19 / rs2261181 / HMGA2 / 12q14.3 / Intergenic / 1.20E-09 / T / Morris et al.[2]
20 / rs12427353 / HNF1A (TCF1) / 12q24.31 / Intron / 6.5E-08 / G / Morris et al.[2]
21 / rs4812829 / HNF4A / 20q13.12 / Intergenic / 2.60E-10 / A / Kooneret al. [3]
22 / rs4402960 / IGF2BP2 / 3q27.2 / Intron / 8.90E-16 / T / Kooneret al. [3], Saxenaet al. [6]
23 / rs7578326 / IRS1 / 2q36.3 / Intergenic / 5.00E-20 / A / Zegginiet al.[1], Voightet al. [4]
24 / rs849135 / JAZF1 / 7p15.1 / Intron / 3.10E-17 / G / Zegginiet al.[1]
25 / rs5215 / KCNJ11 / 11p15.1 / Mis-sense Mutation / 5.00E-11 / C / Zegginiet al.[1]
26 / rs163182 / KCNQ1 / 11p15.4 / Intron / 2.00E-17 / G / Morris et al.[2]
27 / rs972283 / KLF14 / 7q32.3 / Intergenic / 2.00E-10 / G / Voightet al. [4]
28 / rs10830963 / MTNR1B / 11q14.3 / Intron / 5.30E-13 / G / Morris et al.[2]
29 / rs10923931 / NOTCH2 / 1p12 / Intron / 4E-08 / T / Zegginiet al.[1]
30 / rs1801282 / PPARG / 3p25.2 / Intron / 1.10E-12 / C / Saxenaet al. [6]
31 / rs8042680 / PRC1 / 15q26.1 / Intron / 2.00E-10 / A / Voightet al. [4]
32 / rs2075423 / PROX1 / 1q32.3 / Intergenic / 8.10E-09 / G / Morris et al.[2]
33 / rs831571 / PSMD6 / 3p14.1 / Intergenic / 8.41E-11 / C / Morris et al.[2]
34 / rs17584499 / PTPRD / 9p24.1 / Intron / 9.00E-10 / T / Morris et al.[2]
35 / rs9552911 / SGCG / 13q12.12 / Intron / 1.82E-08 / G / Saxenaet al. [7]
36 / rs3802177 / SLC30A8 / 8q24.11 / UTR 3 / 1.30E-21 / G / Voightet al. [4], Saxenaet al. [6]
37 / rs1359790 / SPRY2 / 13q31.1 / Intergenic / 1.4E-08 / G / Morris et al.[2]
38 / rs391300 / SRR / 17p13.3 / Intron / 3E-09 / T / Morris et al.[2]
39 / rs16861329 / ST6GAL1 / 3q27.3 / Intron / 3.4E-08 / T / Kooneret al. [3]
40 / rs7903146 / TCF7L2 / 10q25.2 / Intron / 2.20E-51 / T / Zegginiet al.[1], Saxenaet al. [7]
41 / rs10203174 / THADA / 2p21 / Intron / 9.50E-12 / C / Zegginiet al.[1]
42 / rs896854 / TP53INP1 / 8q22.1 / Intron / 1E-09 / T / Voightet al. [4]
43 / rs7961581 / TSPAN8/ LGR5 / 12q21.1 / Intergenic / 1.10E-09 / C / Zegginiet al.[1]
44 / rs7612463 / UBE2E2 / 3p24.3 / Intron / 2.27E-09 / C / Morris et al.[2]
45 / rs1802295 / VPS26A / 10q22.1 / UTR 3 / 4.1E-08 / T / Kooneret al. [3]
46 / rs10010131 / WFS1 / 4p16.1 / Intron / 2.00E-15 / G / Rees et al. [8]
47 / rs17797882 / WWOX / 16q23.2 / Intergenic / 9.5E-07 / T / Cho et al. [5]
48 / rs6878122 / ZBED3 / 5q13.3 / Intergenic / 5.00E-11 / G / Voightet al. [4]
49 / rs9470794 / ZFAND3 / 6p21.2 / Intron / 2.06E-10 / C / Zegginiet al.[1]

*SNPs selected for this study were selected fromZegginiet al. [1], Morris et al.[2], Kooneret al.[3], Voightet al.[4],Cho et al. [5], Saxenaet al.[6], Saxenaet al.[7], and Rees et al.[8].

References for Supplementary Table 1

1.Zeggini E, Scott LJ, Saxena R et al. Meta-analysis of genome-wide association data and large-scale replication identifies additional susceptibility loci for type 2 diabetes. Nature genetics 2008; 40: 638-645 DOI: 10.1038/ng.120

2.Morris AP, Voight BF, Teslovich TM et al. Large-scale association analysis provides insights into the genetic architecture and pathophysiology of type 2 diabetes. Nature genetics 2012; 44: 981-990 DOI: 10.1038/ng.2383

3.Kooner JS, Saleheen D, Sim X et al. Genome-wide association study in individuals of South Asian ancestry identifies six new type 2 diabetes susceptibility loci. Nature genetics 2011; 43: 984-989 DOI: 10.1038/ng.921

4.Voight BF, Scott LJ, Steinthorsdottir V et al. Twelve type 2 diabetes susceptibility loci identified through large-scale association analysis. Nature genetics 2010; 42: 579-589 DOI: 10.1038/ng.609

5.Cho YS, Chen CH, Hu C et al. Meta-analysis of genome-wide association studies identifies eight new loci for type 2 diabetes in east Asians. Nature genetics 2012; 44: 67-72 DOI: 10.1038/ng.1019

6.Saxena R, Voight BF, Lyssenko V et al. Genome-wide association analysis identifies loci for type 2 diabetes and triglyceride levels. Science 2007; 316: 1331-1336 DOI: 10.1126/science.1142358

7.Saxena R, Saleheen D, Been LF et al. Genome-Wide Association Study Identifies a Novel Locus Contributing to Type 2 Diabetes Susceptibility in Sikhs of Punjabi Origin From India. Diabetes 2013: DOI: 10.2337/db12-1077

8.Rees SD, Hydrie MZ, Shera AS et al. Replication of 13 genome-wide association (GWA)-validated risk variants for type 2 diabetes in Pakistani populations. Diabetologia 2011; 54: 1368-1374 DOI: 10.1007/s00125-011-2063-2