Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Provincial Medical Genetics Program of British Columbia, |
RCV000010037 | SCV002320825 | likely pathogenic | Rubinstein-Taybi syndrome due to CREBBP mutations | 2022-01-01 | criteria provided, single submitter | clinical testing | |
Rady Children's Institute for Genomic Medicine, |
RCV005249986 | SCV005900533 | likely pathogenic | CREBBP-related disorder | 2024-02-19 | criteria provided, single submitter | clinical testing | The CREBBP gene is constrained against variation (Z-score= 4.76 and pLI = 1). The c.4133G>C (p.Arg1378Pro) variant affects a highly conserved amino acid and is predicted by multiple in silico tools to have a deleterious effect on protein function. Multiple splice prediction tools also suggest that this variant is likely to interfere with normal splicing. This variant has been previously reported as a heterozygous change in patients with autosomal dominant Rubinstein-Taybi syndrome (PMID: 11331617, 25388907). Functional studies indicate this variant leads to reduced histone acetyltransferase activity (PMID: 11331617). The c.4133G>C (p.Arg1378Pro) variant is absent from the gnomAD v4 population database and thus is presumed to be rare. Analysis of the parental samples was negative for the variant, indicating this variant likely occurred as a de novo event. Based on the available evidence, c.4133G>C (p.Arg1378Pro) is classified as Likely Pathogenic. |
OMIM | RCV000010037 | SCV000030258 | pathogenic | Rubinstein-Taybi syndrome due to CREBBP mutations | 2001-05-01 | no assertion criteria provided | literature only |