Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
OMIM | RCV000001105 | SCV000021255 | pathogenic | Focal segmental glomerulosclerosis 5 | 2010-01-01 | no assertion criteria provided | literature only | |
Prevention |
RCV003934790 | SCV004749537 | pathogenic | INF2-related disorder | 2024-06-06 | no assertion criteria provided | clinical testing | The INF2 c.556T>C variant is predicted to result in the amino acid substitution p.Ser186Pro. This variant has been reported to be pathogenic for autosomal dominant focal segmental glomerulosclerosis (FSGS); and this variant has been shown to likely increase INF2 interaction with profilin 2 and the F-actin capping protein, resulting in aberrant regulation of actin dynamics (Brown et al. 2010. PubMed ID: 20023659; Rollason et al. 2016. PubMed ID: 26764407). This variant has not been reported in a large population database, indicating this variant is rare. This variant is interpreted as pathogenic. |