Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
MGZ Medical Genetics Center | RCV002290370 | SCV002580475 | likely pathogenic | Intellectual disability-facial dysmorphism syndrome due to SETD5 haploinsufficiency | 2021-07-15 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV003101674 | SCV003011717 | pathogenic | not provided | 2022-03-27 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. This variant has not been reported in the literature in individuals affected with SETD5-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Ser668*) in the SETD5 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in SETD5 are known to be pathogenic (PMID: 24680889). |
Laboratoire de Génétique Moléculaire, |
RCV002290370 | SCV003836671 | pathogenic | Intellectual disability-facial dysmorphism syndrome due to SETD5 haploinsufficiency | 2019-10-07 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV003365729 | SCV004070106 | pathogenic | Inborn genetic diseases | 2023-07-17 | criteria provided, single submitter | clinical testing | The c.2003C>G (p.S668*) alteration, located in exon 15 (coding exon 13) of the SETD5 gene, consists of a C to G substitution at nucleotide position 2003. This changes the amino acid from a serine (S) to a stop codon at amino acid position 668. This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. This variant was not reported in population-based cohorts in the Genome Aggregation Database (gnomAD). This variant has been reported as de novo in an individual with features consistent with SETD5-related neurodevelopmental disorder (Arteche-López, 2021). Based on the available evidence, this alteration is classified as pathogenic. |