1. Catalog
  2. Nodes
  3. g(DBSNP:rs104893877)

g(DBSNP:rs104893877)

Orthologies: 0 | Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Entity

Name
rs104893877
Namespace
DBSNP
Namespace Version
None
Pattern
rs[0-9]+

Appears in Networks 1

TAU and Interaction Partners v1.2.5

TAU Interactions Section of NESTOR

In-Edges 2

complex(GO:"Lewy body") positiveCorrelation g(DBSNP:rs104893877) View Subject | View Object

Recent studies of an individual with Parkinson’s disease (IX-47) of the Contursi kindred with the rare A53T alpha-synuclein mutation revealed widespread -syn and tau inclusions (15). Post-mortem examination of another affected member (IX-51) of this kindred also demonstrated abundant -syn and tau inclusions(figs. S1 and S2). Thus, a pathogenic mutation in alpha-synuclein that is known to increase the propensity of alpha-synuclein to fibrillize (8, 9) also promotes formation of tau inclusions in humans. PubMed:12714745

Appears in Networks:
Annotations
Disease Ontology (DO)
Parkinson's disease

complex(GO:"neurofibrillary tangle") positiveCorrelation g(DBSNP:rs104893877) View Subject | View Object

Recent studies of an individual with Parkinson’s disease (IX-47) of the Contursi kindred with the rare A53T alpha-synuclein mutation revealed widespread -syn and tau inclusions (15). Post-mortem examination of another affected member (IX-51) of this kindred also demonstrated abundant -syn and tau inclusions(figs. S1 and S2). Thus, a pathogenic mutation in alpha-synuclein that is known to increase the propensity of alpha-synuclein to fibrillize (8, 9) also promotes formation of tau inclusions in humans. PubMed:12714745

Appears in Networks:
Annotations
Disease Ontology (DO)
Parkinson's disease

Out-Edges 2

g(DBSNP:rs104893877) positiveCorrelation complex(GO:"neurofibrillary tangle") View Subject | View Object

Recent studies of an individual with Parkinson’s disease (IX-47) of the Contursi kindred with the rare A53T alpha-synuclein mutation revealed widespread -syn and tau inclusions (15). Post-mortem examination of another affected member (IX-51) of this kindred also demonstrated abundant -syn and tau inclusions(figs. S1 and S2). Thus, a pathogenic mutation in alpha-synuclein that is known to increase the propensity of alpha-synuclein to fibrillize (8, 9) also promotes formation of tau inclusions in humans. PubMed:12714745

Appears in Networks:
Annotations
Disease Ontology (DO)
Parkinson's disease

g(DBSNP:rs104893877) positiveCorrelation complex(GO:"Lewy body") View Subject | View Object

Recent studies of an individual with Parkinson’s disease (IX-47) of the Contursi kindred with the rare A53T alpha-synuclein mutation revealed widespread -syn and tau inclusions (15). Post-mortem examination of another affected member (IX-51) of this kindred also demonstrated abundant -syn and tau inclusions(figs. S1 and S2). Thus, a pathogenic mutation in alpha-synuclein that is known to increase the propensity of alpha-synuclein to fibrillize (8, 9) also promotes formation of tau inclusions in humans. PubMed:12714745

Appears in Networks:
Annotations
Disease Ontology (DO)
Parkinson's disease

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.