Total submissions: 9
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000666120 | SCV000790363 | pathogenic | Autosomal recessive nonsyndromic hearing loss 2; Usher syndrome type 1 | 2017-03-16 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV000763282 | SCV000893926 | pathogenic | Autosomal dominant nonsyndromic hearing loss 11; Autosomal recessive nonsyndromic hearing loss 2; Usher syndrome type 1 | 2018-10-31 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001038543 | SCV001202018 | pathogenic | not provided | 2024-01-16 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg1373*) in the MYO7A gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in MYO7A are known to be pathogenic (PMID: 8900236, 25404053). This variant is present in population databases (rs766641715, gnomAD 0.009%). This premature translational stop signal has been observed in individual(s) with Usher syndrome (PMID: 16470552, 21436283). ClinVar contains an entry for this variant (Variation ID: 551138). For these reasons, this variant has been classified as Pathogenic. |
Institute of Medical Genetics and Applied Genomics, |
RCV001038543 | SCV001447894 | pathogenic | not provided | 2020-10-23 | criteria provided, single submitter | clinical testing | |
Gene |
RCV001038543 | SCV001802076 | pathogenic | not provided | 2022-07-18 | criteria provided, single submitter | clinical testing | Nonsense variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss-of-function is a known mechanism of disease; Published functional studies demonstrate defects in electrophysiology, morphology, and pluripotency in p.(R1373*) cell lines that were resolved to levels close to controls by genetic correction of p.(R1373*) (Tang et al., 2016); This variant is associated with the following publications: (PMID: 21436283, 31589614, 33576163, 27013738, 16470552) |
Revvity Omics, |
RCV001038543 | SCV002017706 | pathogenic | not provided | 2021-03-16 | criteria provided, single submitter | clinical testing | |
SN ONGC Dept of Genetics and Molecular biology Vision Research Foundation | RCV003389476 | SCV003927127 | pathogenic | Usher syndrome | 2022-12-31 | criteria provided, single submitter | research | |
Neuberg Centre For Genomic Medicine, |
RCV004764795 | SCV005374824 | uncertain significance | Usher syndrome type 1 | criteria provided, single submitter | clinical testing | The observed stop gained c.4117C>T(p.Arg1373Ter) variant in MYO7A gene has been reported previously in compound heterozygous state in multiple individuals affected with Usher syndrome (Roux AF, et al., 2011; Jaijo T, et al., 2006; HURPADE, S., et al.). The c.4117C>T variant has been reported with allele frequency of 0.001% in gnomAD Exomes. This variant has been reported to the ClinVar database as Pathogenic (multiple submissions). Computational evidence (MutationTaster - Disease causing) predicts damaging effect on protein structure and function for this variant. The nucleotide change c.4117C>T in MYO7A is predicted as conserved by GERP++ and PhyloP across 100 vertebrates. This sequence change creates a premature translational stop signal (p.Arg1373Ter) in the MYO7A gene. This variant is predicted to cause loss of normal protein function through protein truncation. Loss of function variants in MYO7A gene have been previously reported to be disease causing (Weston MD, et al., 1996). For these reasons, this variant has been classified as Pathogenic. The same variant in MYO7A gene has been identified in heterozygous state in sibling [SURAJ SHIVAJI GADEKAR, id: 30607400181]. This variant is absent in paternal cousin [Mrs. SHITAL RAM GIRAM, id: 30607400182]. | |
Natera, |
RCV001835074 | SCV002088436 | pathogenic | Usher syndrome type 1B | 2020-11-13 | no assertion criteria provided | clinical testing |