Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV001806572 | SCV002050510 | uncertain significance | not provided | 2021-12-29 | criteria provided, single submitter | clinical testing | Not observed at significant frequency in large population cohorts (Lek et al., 2016); In silico analysis supports that this missense variant has a deleterious effect on protein structure/function; Has not been previously published as pathogenic or benign to our knowledge |
Fulgent Genetics, |
RCV002482332 | SCV002799629 | uncertain significance | Leber congenital amaurosis 10; Meckel syndrome, type 4; Senior-Loken syndrome 6; Joubert syndrome 5; Bardet-Biedl syndrome 14 | 2022-02-17 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV004980696 | SCV005554836 | uncertain significance | Inborn genetic diseases | 2024-11-20 | criteria provided, single submitter | clinical testing | The c.4736A>T (p.E1579V) alteration is located in exon 36 (coding exon 35) of the CEP290 gene. This alteration results from a A to T substitution at nucleotide position 4736, causing the glutamic acid (E) at amino acid position 1579 to be replaced by a valine (V). Based on insufficient or conflicting evidence, the clinical significance of this alteration remains unclear. |
Prevention |
RCV004733381 | SCV005356773 | uncertain significance | CEP290-related disorder | 2024-08-16 | no assertion criteria provided | clinical testing | The CEP290 c.4736A>T variant is predicted to result in the amino acid substitution p.Glu1579Val. To our knowledge, this variant has not been reported in the literature. This variant is reported in 0.0060% of alleles in individuals of European (Non-Finnish) descent in gnomAD. At this time, the clinical significance of this variant is uncertain due to the absence of conclusive functional and genetic evidence. |