rs74315405
Orientation | plus |
Stabilized | plus |
Geno | Mag | Summary |
---|---|---|
(C;T) | 9 | Gerstmann–Straussler–Scheinker syndrome |
(T;T) | 0 | common in clinvar |
Make rs74315405(C;C) |
Reference | GRCh38 38.1/141 |
Chromosome | 20 |
Position | 4699813 |
Gene | PRNP |
is a | snp |
is | mentioned by |
dbSNP | rs74315405 |
dbSNP (classic) | rs74315405 |
ClinGen | rs74315405 |
ebi | rs74315405 |
HLI | rs74315405 |
Exac | rs74315405 |
Gnomad | rs74315405 |
Varsome | rs74315405 |
LitVar | rs74315405 |
Map | rs74315405 |
PheGenI | rs74315405 |
Biobank | rs74315405 |
1000 genomes | rs74315405 |
hgdp | rs74315405 |
ensembl | rs74315405 |
geneview | rs74315405 |
scholar | rs74315405 |
rs74315405 | |
pharmgkb | rs74315405 |
gwascentral | rs74315405 |
openSNP | rs74315405 |
23andMe | rs74315405 |
SNPshot | rs74315405 |
SNPdbe | rs74315405 |
MSV3d | rs74315405 |
GWAS Ctlg | rs74315405 |
Max Magnitude | 9 |
c.593T>C (p.Phe198Ser)
23andMe calls this i5004356
ClinVar | |
---|---|
Risk | rs74315405(C;C) |
Alt | rs74315405(C;C) |
Reference | Rs74315405(T;T) |
Significance | Pathogenic |
Disease | Gerstmann-Straussler-Scheinker syndrome Genetic prion diseases |
Variation | info |
Gene | PRNP |
CLNDBN | Gerstmann-Straussler-Scheinker syndrome Genetic prion diseases |
Reversed | 0 |
HGVS | NC_000020.10:g.4680459T>C |
CLNSRC | OMIM Allelic Variant UniProtKB (protein) |
CLNACC | RCV000014340.24, RCV000020252.1, |
[PMID 1357663] Prion protein preamyloid and amyloid deposits in Gerstmann-Straussler-Scheinker disease, Indiana kindred.
[PMID 1363809] Linkage of the Indiana kindred of Gerstmann-Straussler-Scheinker disease to the prion protein gene.
[PMID 1363810] Mutant prion proteins in Gerstmann-Straussler-Scheinker disease with neurofibrillary tangles.
[PMID 2812321] Gerstmann-Straussler-Scheinker disease. I. Extending the clinical spectrum.
[PMID 7954833] Amyloid fibrils in Gerstmann-Straussler-Scheinker disease (Indiana and Swedish kindreds) express only PrP peptides encoded by the mutant allele.
[PMID 12372829] Disease-associated F198S mutation increases the propensity of the recombinant prion protein for conformational conversion to scrapie-like form.