Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Department of Biochemistry, |
RCV001352913 | SCV001547518 | uncertain significance | X-linked progressive cerebellar ataxia | 2021-03-25 | criteria provided, single submitter | research | Using whole-exome sequencing and Sanger sequencing we identified the variant NM_021949.3(ATP2B3):c.2086C>T (p.Arg696Cys) in a male patient with intellectual disability and spasticity. The variant was absent in his father and heterozygous in his mother. It was reported once in the gnomAD v2.1.1 database; heterozygous in an African\African American female. Nevertheless, NM_021949.3(ATP2B3):c.2086C>T (p.Arg696Cys) had an allelic variant, NM_021949.3 (ATP2B3):c.2086C>A (p.Arg696Ser) reported in four females and one male from gnomAD v2.1.1 Latino/Admixed American population (its gnomAD v2.1.1 global frequency was 0.00002). The variant NM_021949.3(ATP2B3):c.2086C>T (p.Arg696Cys) alters a highly conserved amino acid located in the ATPase domain of the ATP2B3 protein. It was predicted by multiple in silico tools including Sift, Polyphen 2, MutationTaster, LRT, and Provean. |
Ambry Genetics | RCV002547572 | SCV003685743 | uncertain significance | Inborn genetic diseases | 2022-05-04 | criteria provided, single submitter | clinical testing | The c.2086C>T (p.R696C) alteration is located in exon 12 (coding exon 12) of the ATP2B3 gene. This alteration results from a C to T substitution at nucleotide position 2086, causing the arginine (R) at amino acid position 696 to be replaced by a cysteine (C). Based on insufficient or conflicting evidence, the clinical significance of this alteration remains unclear. |