Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001390100 | SCV001591721 | pathogenic | Charcot-Marie-Tooth disease type 2 | 2023-05-01 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Experimental studies have shown that this premature translational stop signal affects LMNA function (PMID: 20160190). Algorithms developed to predict the effect of variants on protein structure and function are not available or were not evaluated for this variant. ClinVar contains an entry for this variant (Variation ID: 66803). This variant is also known as c.1307_1308insGCAC, p.Ser437HisfsX1. This premature translational stop signal has been observed in individual(s) with autosomal dominant dilated cardiomyopathy (PMID: 30012837). This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Ser437Hisfs*2) in the LMNA gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in LMNA are known to be pathogenic (PMID: 18585512, 18926329). |
Clinical Genetics Laboratory, |
RCV000057266 | SCV005199062 | pathogenic | not provided | 2022-11-15 | criteria provided, single submitter | clinical testing | |
Epithelial Biology; Institute of Medical Biology, |
RCV000057266 | SCV000088379 | not provided | not provided | no assertion provided | not provided | ||
Blueprint Genetics | RCV000157296 | SCV000207028 | pathogenic | Cardiomyopathy | 2014-10-27 | no assertion criteria provided | clinical testing | |
University of Washington Center for Mendelian Genomics, |
RCV001257938 | SCV001434748 | uncertain significance | Primary dilated cardiomyopathy | no assertion criteria provided | research |