Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000760427 | SCV000890310 | pathogenic | not provided | 2019-01-11 | criteria provided, single submitter | clinical testing | The Q82X variant in the LMX1B gene has been reported previously, using alternate nomenclature as Gln59Ter, in multiple affected individuals from a large family with nail patella syndrome (Vollrath et al., 1998). This variant is predicted to cause loss of normal protein function either through protein truncation or nonsense-mediated mRNA decay. The Q82X variant is not observed in large population cohorts (Lek et al., 2016). We interpret Q82X as a pathogenic variant. |
Labcorp Genetics |
RCV000760427 | SCV001588938 | pathogenic | not provided | 2023-11-04 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Gln82*) in the LMX1B gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in LMX1B are known to be pathogenic (PMID: 9590287, 15498463). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with nail-patella syndrome (PMID: 9618165). It has also been observed to segregate with disease in related individuals. This variant is also known as p.Gln59Ter. ClinVar contains an entry for this variant (Variation ID: 7005). For these reasons, this variant has been classified as Pathogenic. |
OMIM | RCV000007420 | SCV000027620 | pathogenic | Nail-patella syndrome | 1998-07-01 | no assertion criteria provided | literature only |