Gene | Chr | SBP | EGVped | EGVsnp | EGVseq |
---|
LEPR
|
1
| 7 | 4 | 6 | 4 |
LRP8
|
1
| 6 | 0 | 8 | 5 |
NEXN
|
1
| 1 | 1 | 2 | 1 |
BTD
|
3
| 16 | 16 | 22 | 20 |
DNASE1L3
|
3
| 100 | 95 | 100 | 99 |
MAP4
|
3
| 100 | 95 | 100 | 99 |
SUMF1
|
3
| 33 | 14 | 34 | 39 |
MTRR
|
5
| 3 | 0 | 3 | 4 |
RHOD
|
11
| 2 | 0 | 1 | 1 |
TCIRG1
|
11
| 2 | 1 | 1 | 1 |
CYP1A2
|
15
| 0 | 0 | 1 | 0 |
C1QBP
|
17
| 0 | 1 | 0 | 1 |
KRT23
|
17
| 0 | 1 | 0 | 1 |
RAI1
|
17
| 0 | 1 | 0 | 1 |
SAT2
|
17
| 0 | 0 | 1 | 1 |
COL5A3
|
19
| 0 | 1 | 1 | 0 |
- For each gene contributing to simulated SBP, the table lists the number of replicates (out of 100) in which at least one significant association was found. Variants in 24 additional genes have small effects on SBP but were never detected and were omitted from the table. Due to extended linkage disequilibrium, more than one gene may be tagged by a single variant; in particular, the associations in DNASE1L3 are likely due to strong LD with major causative gene MAP4.