Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Human Developmental Genetics Laboratory, |
RCV002293409 | SCV002538944 | pathogenic | Axenfeld-Rieger syndrome type 1 | 2022-06-23 | criteria provided, single submitter | research | |
Ambry Genetics | RCV003242963 | SCV003952579 | likely pathogenic | Inborn genetic diseases | 2023-04-11 | criteria provided, single submitter | clinical testing | The c.185G>A (p.R62H) alteration is located in exon 4 (coding exon 2) of the PITX2 gene. This alteration results from a G to A substitution at nucleotide position 185, causing the arginine (R) at amino acid position 62 to be replaced by a histidine (H). This variant was not reported in population-based cohorts in the Genome Aggregation Database (gnomAD). This alteration was reported in multiple individuals or families with clinical features of PITX2-related Axenfeld-Rieger syndrome (Xia, 2004; Reis, 2012; Ma, 2020). This amino acid position is highly conserved in available vertebrate species. The p.R62H amino acid is located in the homeodomain. Molecular modeling predicted this alteration would have minor or no impact on the structure of PITX2 (Seifi, 2018). This alteration is predicted to be deleterious by in silico analysis. Based on the available evidence, this alteration is classified as likely pathogenic. |
OMIM | RCV000008562 | SCV000028770 | pathogenic | Ring dermoid of cornea | 2004-12-01 | no assertion criteria provided | literature only | |
Eye Genetics Research Group, |
RCV001200039 | SCV001370531 | pathogenic | Anterior segment dysgenesis | 2020-03-31 | no assertion criteria provided | clinical testing |