Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000219594 | SCV000278996 | pathogenic | not provided | 2015-01-12 | criteria provided, single submitter | clinical testing | The c.132_135dupGTGT mutation in the LPIN2 gene causes a frameshift starting with codon Serine 46, changes this amino acid to a Valine residue and creates a premature Stop codon at position 22 of the new reading frame, denoted p.Ser46ValfsX22. This mutation is predicted to cause loss of normal protein function through protein truncation or nonsense-mediated mRNA decay. Although this mutation has not been previously reported to our knowledge, its presence is consistent with a diagnosis of Majeed syndrome. |
Labcorp Genetics |
RCV001854731 | SCV002163357 | pathogenic | Majeed syndrome | 2022-05-25 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 234327). This variant has not been reported in the literature in individuals affected with LPIN2-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Ser46Valfs*22) in the LPIN2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in LPIN2 are known to be pathogenic (PMID: 15994876, 23087183). |