Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Genetic Services Laboratory, |
RCV000145741 | SCV000192865 | pathogenic | Rubinstein-Taybi syndrome due to CREBBP mutations | 2013-02-08 | criteria provided, single submitter | clinical testing | |
Wessex Regional Genetics Laboratory, |
RCV000145741 | SCV000999450 | pathogenic | Rubinstein-Taybi syndrome due to CREBBP mutations | 2019-11-05 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001390957 | SCV001592864 | pathogenic | Rubinstein-Taybi syndrome | 2020-07-25 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Donor and acceptor splice site variants typically lead to a loss of protein function (PMID: 16199547), and loss-of-function variants in CREBBP are known to be pathogenic (PMID: 17052327, 18792986). This variant has been observed in individual(s) with Rubinstein-Taybi syndrome (PMID: 25388907, 16359492). In at least one individual the variant was observed to be de novo. This variant is also known as IVS22+1G>A. ClinVar contains an entry for this variant (Variation ID: 158361). This variant is not present in population databases (ExAC no frequency). This sequence change affects a donor splice site in intron 21 of the CREBBP gene. It is expected to disrupt RNA splicing and likely results in an absent or disrupted protein product. |
Gene |
RCV004589638 | SCV005078835 | pathogenic | not provided | 2023-12-05 | criteria provided, single submitter | clinical testing | Canonical splice site variant expected to result in aberrant splicing, although in the absence of functional evidence the actual effect of this sequence change is unknown; Not observed at significant frequency in large population cohorts (gnomAD); Also known as IVS22+1 G>A; This variant is associated with the following publications: (PMID: 25525159, 16359492, 32827181) |