Total submissions: 8
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
UCLA Clinical Genomics Center, |
RCV000200261 | SCV000255381 | pathogenic | Muscular dystrophy-dystroglycanopathy (congenital with brain and eye anomalies), type A14; Muscular dystrophy-dystroglycanopathy (congenital with intellectual disability), type B14; Autosomal recessive limb-girdle muscular dystrophy type 2T | 2014-01-28 | criteria provided, single submitter | clinical testing | |
Genetic Services Laboratory, |
RCV000503216 | SCV000595011 | likely pathogenic | Muscular dystrophy-dystroglycanopathy | 2017-05-23 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV000623944 | SCV000742877 | pathogenic | Inborn genetic diseases | 2017-08-07 | criteria provided, single submitter | clinical testing | |
Rady Children's Institute for Genomic Medicine, |
RCV000503216 | SCV001445862 | pathogenic | Muscular dystrophy-dystroglycanopathy | 2019-05-29 | criteria provided, single submitter | clinical testing | This variant has been previously reported as a homozygous change in 6 patients with hypotonia, muscle weakness, cataracts, and elevated serum creatine kinase (PMID: 23768512, 29054425). Functional studies have shown reduced alpha-dystroglycan glycosylation in muscle and fibroblasts of individuals with this variant (PMID: 23768512). It is present in the heterozygous state in the gnomAD population database at a frequency of 0.0036% (9/250,734) and thus is presumed to be rare. The c.553C>T (p.Arg185Cys) variant affects a highly conserved amino acid and is predicted by multiple in silico tools to have a deleterious effect on protein function. Based on the available evidence, the c.553C>T (p.Arg185Cys) variant is classified as Pathogenic. |
Revvity Omics, |
RCV001781385 | SCV002018486 | likely pathogenic | not provided | 2022-09-27 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000200261 | SCV002296015 | likely pathogenic | Muscular dystrophy-dystroglycanopathy (congenital with brain and eye anomalies), type A14; Muscular dystrophy-dystroglycanopathy (congenital with intellectual disability), type B14; Autosomal recessive limb-girdle muscular dystrophy type 2T | 2022-08-16 | criteria provided, single submitter | clinical testing | In summary, the currently available evidence indicates that the variant is pathogenic, but additional data are needed to prove that conclusively. Therefore, this variant has been classified as Likely Pathogenic. This sequence change replaces arginine, which is basic and polar, with cysteine, which is neutral and slightly polar, at codon 185 of the GMPPB protein (p.Arg185Cys). This variant is present in population databases (rs397509425, gnomAD 0.01%). This missense change has been observed in individuals with clinical features of GMPPB-related conditions (PMID: 23768512, 25326637, 30684953, 32403337, 32404165). ClinVar contains an entry for this variant (Variation ID: 60543). Algorithms developed to predict the effect of missense changes on protein structure and function are either unavailable or do not agree on the potential impact of this missense change (SIFT: "Deleterious"; PolyPhen-2: "Probably Damaging"; Align-GVGD: "Class C0"). Experimental studies are conflicting or provide insufficient evidence to determine the effect of this variant on GMPPB function (PMID: 23768512). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may create or strengthen a splice site. |
OMIM | RCV000054436 | SCV000082913 | pathogenic | Muscular dystrophy-dystroglycanopathy (congenital with intellectual disability), type B14 | 2013-07-11 | no assertion criteria provided | literature only | |
OMIM | RCV000054437 | SCV000082914 | pathogenic | Autosomal recessive limb-girdle muscular dystrophy type 2T | 2013-07-11 | no assertion criteria provided | literature only |