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p(HGNC:SNCA, var("?"))

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Entity

Name
SNCA
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 7

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New insights into the role of microRNAs and long noncoding RNAs in most common neurodegenerative diseases v1.0.0

mTOR-Related Brain Dysfunctions in Neuropsychiatric Disorders v1.0.0

In-Edges 7

p(HGNC:SNCA) hasVariant p(HGNC:SNCA, var("?")) View Subject | View Object

Appears in Networks:

path(MESH:"Parkinsonian Disorders") association p(HGNC:SNCA, var("?")) View Subject | View Object

It is important to note that while mutations in the nonglycosylated 14 kDa form of alphaSYN have been linked to the pathogenesis of PD (see below), to date, they have not been linked with Parkin-associated AR-JP. PubMed:14556719

Appears in Networks:

path(HP:Neurodegeneration) association p(HGNC:SNCA, var("?")) View Subject | View Object

Early studies demonstrated that overexpression of a specific human HSP70 (HSPA1L) in a Drosophila disease model suppressed neurodegeneration associated with expression of polyQ-containing forms of both ataxin 3 or androgen receptor, and α -synuclein (Warrick et al., 1999; Chan et al., 2000, 2002; Auluck et al., 2002). PubMed:27491084

Appears in Networks:

bp(GO:"chaperone-mediated autophagy") association p(HGNC:SNCA, var("?")) View Subject | View Object

Cuervo et al. have revealed a distinct interaction of wild-type and mutant α-synuclein proteins with CMA [64] PubMed:29758300

Appears in Networks:

bp(GO:autophagy) increases deg(p(HGNC:SNCA, var("?"))) View Subject | View Object

That neurodegenerative disease-causing proteins are frequently degraded by autophagy was demonstrated by a series of in vitro studies which showed that pharmacological induction or inhibition of macroautophagy alters the rate of turnover of a number of disease-related proteins including polyglutamine-expanded proteins, polyalanine-expanded proteins, as well as wild type and mutant forms of α-synuclein [25,26] PubMed:18930136

Appears in Networks:

p(HGNC:SNCA, var("?")) decreases tloc(p(HGNC:SNCA, var("?")), fromLoc(GO:cytoplasm), toLoc(GO:"lysosomal lumen")) View Subject | View Object

Mutations in α-synuclein that are causative of familial Parkinson’s disease are poorly transferred to the lysosomal lumen and accumulate on the lysosomal surface, resulting in blockade of receptor-mediated translocation. PubMed:18930136

Appears in Networks:

path(MESH:"Psychotic Disorders") association p(HGNC:SNCA, var("?")) View Subject | View Object

In addition, the occurrence of alpha synuclein gene (SNCA) polymorphisms is associated with human METH psychosis [166]. PubMed:30061532

Appears in Networks:

Out-Edges 10

p(HGNC:SNCA, var("?")) association path(MESH:"Parkinsonian Disorders") View Subject | View Object

It is important to note that while mutations in the nonglycosylated 14 kDa form of alphaSYN have been linked to the pathogenesis of PD (see below), to date, they have not been linked with Parkin-associated AR-JP. PubMed:14556719

Appears in Networks:

p(HGNC:SNCA, var("?")) increases bp(GO:"apoptotic process") View Subject | View Object

Overexpression of wild-type, but in particular mutant alphaSYN in many cell types but not in all, induces apoptosis or sensitizes the cells to toxic agents, including proteasome inhibitors (see, for example, Lee et al.,2001a). PubMed:14556719

Appears in Networks:

p(HGNC:SNCA, var("?")) decreases bp(GO:"autophagosome assembly") View Subject | View Object

Third, α-synuclein mutations, triplications or excesses amplify the ALN burden, interfere with auto phagosome formation and irreversibly disrupt the lysosomal mem- brane 1,3,44,56 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Parkinson Disease

p(HGNC:SNCA, var("?")) decreases a(GO:"lysosomal membrane") View Subject | View Object

Third, α-synuclein mutations, triplications or excesses amplify the ALN burden, interfere with auto phagosome formation and irreversibly disrupt the lysosomal mem- brane 1,3,44,56 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Parkinson Disease

p(HGNC:SNCA, var("?")) association path(HP:Neurodegeneration) View Subject | View Object

Early studies demonstrated that overexpression of a specific human HSP70 (HSPA1L) in a Drosophila disease model suppressed neurodegeneration associated with expression of polyQ-containing forms of both ataxin 3 or androgen receptor, and α -synuclein (Warrick et al., 1999; Chan et al., 2000, 2002; Auluck et al., 2002). PubMed:27491084

Appears in Networks:

p(HGNC:SNCA, var("?")) association bp(GO:"chaperone-mediated autophagy") View Subject | View Object

Cuervo et al. have revealed a distinct interaction of wild-type and mutant α-synuclein proteins with CMA [64] PubMed:29758300

Appears in Networks:

p(HGNC:SNCA, var("?")) increases path(MESH:"Parkinson Disease") View Subject | View Object

Mutations in α-synuclein that are causative of familial Parkinson’s disease are poorly transferred to the lysosomal lumen and accumulate on the lysosomal surface, resulting in blockade of receptor-mediated translocation. PubMed:18930136

Appears in Networks:

p(HGNC:SNCA, var("?")) decreases tloc(p(HGNC:SNCA, var("?")), fromLoc(GO:cytoplasm), toLoc(GO:"lysosomal lumen")) View Subject | View Object

Mutations in α-synuclein that are causative of familial Parkinson’s disease are poorly transferred to the lysosomal lumen and accumulate on the lysosomal surface, resulting in blockade of receptor-mediated translocation. PubMed:18930136

Appears in Networks:

p(HGNC:SNCA, var("?")) increases path(MESH:"Parkinson Disease") View Subject | View Object

The mutation in the SNCA gene causes PD. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Parkinson Disease

p(HGNC:SNCA, var("?")) association path(MESH:"Psychotic Disorders") View Subject | View Object

In addition, the occurrence of alpha synuclein gene (SNCA) polymorphisms is associated with human METH psychosis [166]. PubMed:30061532

Appears in Networks:

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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.