Total submissions: 10
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000667892 | SCV000792404 | likely pathogenic | Usher syndrome type 2A; Retinitis pigmentosa 39 | 2017-06-23 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001067077 | SCV001232110 | pathogenic | not provided | 2023-11-28 | criteria provided, single submitter | clinical testing | This sequence change replaces glycine, which is neutral and non-polar, with arginine, which is basic and polar, at codon 1723 of the USH2A protein (p.Gly1723Arg). This variant also falls at the last nucleotide of exon 25, which is part of the consensus splice site for this exon. The frequency data for this variant in the population databases is considered unreliable, as metrics indicate poor data quality at this position in the gnomAD database. This missense change has been observed in individuals with USH2A-related conditions (PMID: 24944099, 25404053, 26667666). ClinVar contains an entry for this variant (Variation ID: 552599). An algorithm developed to predict the effect of missense changes on protein structure and function (PolyPhen-2) suggests that this variant is likely to be disruptive. Variants that disrupt the consensus splice site are a relatively common cause of aberrant splicing (PMID: 17576681, 9536098). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. For these reasons, this variant has been classified as Pathogenic. |
Blueprint Genetics | RCV001075428 | SCV001241051 | pathogenic | Retinal dystrophy | 2018-08-26 | criteria provided, single submitter | clinical testing | |
Gene |
RCV001067077 | SCV002756935 | likely pathogenic | not provided | 2022-11-15 | criteria provided, single submitter | clinical testing | Located at the last nucleotide position of the exon 25, which is part of the splice donor site, and predicted to result in aberrant splicing; although in the absence of functional evidence, the actual effect of this sequence change is unknown; In silico analysis supports that this missense variant has a deleterious effect on protein structure/function; This variant is associated with the following publications: (PMID: 31589614, 25404053, 24944099, 26667666, 36362125) |
Fulgent Genetics, |
RCV000667892 | SCV002810442 | likely pathogenic | Usher syndrome type 2A; Retinitis pigmentosa 39 | 2021-07-16 | criteria provided, single submitter | clinical testing | |
Prevention |
RCV004533468 | SCV004117507 | pathogenic | USH2A-related disorder | 2023-12-12 | criteria provided, single submitter | clinical testing | The USH2A c.5167G>C variant is predicted to result in the amino acid substitution p.Gly1723Arg. This variant has been reported in the heterozygous state along with other USH2A loss-of-function variants in multiple individuals with Usher syndrome or retinitis pigmentosa (Table S1, Baux et al. 2014. PubMed ID: 24944099, Table 3, Aparisi et al. 2014. PubMed ID: 25404053; Table 1, Ge et al. 2015. PubMed ID: 26667666). This variant is reported in 0.014% of alleles in individuals of Latino descent in gnomAD. An in vitro experimental study suggests this variant weakens the canonical splice donor site leading to the skipping of exon 25 and/or 26 (Table 2, Reurink et al. 2022. PubMed ID: 36362125). This variant is interpreted as pathogenic. |
Genome- |
RCV003451666 | SCV004181837 | likely pathogenic | Retinitis pigmentosa 39 | 2023-11-04 | criteria provided, single submitter | clinical testing | |
Genome- |
RCV001276250 | SCV004181838 | likely pathogenic | Usher syndrome type 2A | 2023-11-04 | criteria provided, single submitter | clinical testing | |
Baylor Genetics | RCV003451666 | SCV004208257 | pathogenic | Retinitis pigmentosa 39 | 2024-03-16 | criteria provided, single submitter | clinical testing | |
Natera, |
RCV001276250 | SCV001462258 | pathogenic | Usher syndrome type 2A | 2020-09-16 | no assertion criteria provided | clinical testing |