Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ambry Genetics | RCV002400446 | SCV002673126 | pathogenic | Maturity onset diabetes mellitus in young | 2017-12-13 | criteria provided, single submitter | clinical testing | The p.E256* pathogenic mutation (also known as c.766G>T), located in coding exon 7 of the GCK gene, results from a G to T substitution at nucleotide position 766. This changes the amino acid from a glutamic acid to a stop codon within coding exon 7. This mutation was identified in one maturity-onset diabetes of the young (MODY) family; however, specific clinical information was not provided (Osbak KK et al. Hum. Mutat., 2009 Nov;30:1512-26). This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. As such, this alteration is interpreted as a disease-causing mutation. |
Labcorp Genetics |
RCV003099711 | SCV003439896 | pathogenic | not provided | 2022-07-14 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. This premature translational stop signal has been observed in individual(s) with Maturity onset diabetes of the young (PMID: 19790256). This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Glu256*) in the GCK gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in GCK are known to be pathogenic (PMID: 7553875, 9867845, 14578306, 24323243, 25015100). |