Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001383446 | SCV001582594 | pathogenic | not provided | 2023-12-28 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Gly233Valfs*22) in the BCS1L gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in BCS1L are known to be pathogenic (PMID: 12215968, 17314340, 19162478, 19508421, 22277166, 25895478). This variant is present in population databases (rs775388576, gnomAD 0.009%). This variant has not been reported in the literature in individuals affected with BCS1L-related conditions. ClinVar contains an entry for this variant (Variation ID: 1028218). For these reasons, this variant has been classified as Pathogenic. |
Fulgent Genetics, |
RCV002486327 | SCV002791032 | likely pathogenic | Pili torti-deafness syndrome; GRACILE syndrome; Mitochondrial complex III deficiency nuclear type 1 | 2021-08-16 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV002546308 | SCV003552515 | pathogenic | Inborn genetic diseases | 2022-07-28 | criteria provided, single submitter | clinical testing | The c.696delT (p.G233Vfs*22) alteration, located in exon 6 (coding exon 4) of the BCS1L gene, consists of a deletion of one nucleotide at position 696, causing a translational frameshift with a predicted alternate stop codon after 22 amino acids. This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. Based on the available evidence, this alteration is classified as pathogenic. |
Baylor Genetics | RCV003473864 | SCV004210824 | pathogenic | Pili torti-deafness syndrome | 2024-03-24 | criteria provided, single submitter | clinical testing |