Total submissions: 8
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Blueprint Genetics | RCV001074399 | SCV001239979 | pathogenic | Retinal dystrophy | 2019-08-07 | criteria provided, single submitter | clinical testing | |
Ocular Genomics Institute, |
RCV001376314 | SCV001573416 | pathogenic | Retinitis pigmentosa 39 | 2021-04-08 | criteria provided, single submitter | research | The USH2A c.11389+3A>T variant was identified in an individual with retinitis pigmentosa with a presumed recessive inheritance pattern. Through a review of available evidence we were able to apply the following criteria: PM2, PP3, PP1, PVS1. Based on this evidence we have classified this variant as Pathogenic. |
Labcorp Genetics |
RCV001386131 | SCV001586256 | pathogenic | not provided | 2022-07-19 | criteria provided, single submitter | clinical testing | This sequence change falls in intron 58 of the USH2A gene. It does not directly change the encoded amino acid sequence of the USH2A protein. It affects a nucleotide within the consensus splice site. This variant is present in population databases (rs753886165, gnomAD 0.006%). This variant has been observed in individual(s) with Usher syndrome (PMID: 28714225; Invitae). In at least one individual the data is consistent with being in trans (on the opposite chromosome) from a pathogenic variant. ClinVar contains an entry for this variant (Variation ID: 427867). 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. |
Gene |
RCV001386131 | SCV002027980 | pathogenic | not provided | 2025-02-06 | criteria provided, single submitter | clinical testing | RNA studies demonstrate a damaging effect resulting in protein truncation and the skipping of exon 58 (PMID: 28714225); Not observed at a significant frequency in large population cohorts (gnomAD); In silico analysis supports a deleterious effect on splicing; This variant is associated with the following publications: (PMID: 31045651, 31047384, 32093671, 33608557, 36110214, 34519870, 34906470, 32467589, 28714225, 35052368, 34148116, 35870892, 36819107, Li2022[paper], 38790200) |
Genome- |
RCV001376314 | SCV004173939 | likely pathogenic | Retinitis pigmentosa 39 | 2023-04-11 | criteria provided, single submitter | clinical testing | |
Baylor Genetics | RCV001376314 | SCV004208271 | pathogenic | Retinitis pigmentosa 39 | 2023-11-16 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV005018824 | SCV005645310 | pathogenic | Usher syndrome type 2A; Retinitis pigmentosa 39 | 2024-02-10 | criteria provided, single submitter | clinical testing | |
Rui Chen Lab, |
RCV000515699 | SCV000579424 | pathogenic | Usher syndrome type 2A | 2017-05-09 | no assertion criteria provided | research |