1. Catalog
  2. Nodes
  3. p(MGI:Mapt, var("p.P301L"))

p(MGI:Mapt, var("p.P301L"))

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

Entity

Name
Mapt
Namespace
mgi
Namespace Version
20181021
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/f2f993e599694ab5ce989cc39d789a499f75db99/external/mgi-names.belns

Appears in Networks 1

Tau clearance mechanisms and their possible role in the pathogenesis of Alzheimer disease v1.0.0

In-Edges 4

p(HGNC:NPEPPS) positiveCorrelation p(MGI:Mapt, var("p.P301L")) View Subject | View Object

Interestingly, PSA was found to be elevated in the cerebellum of these TAUP301L mice (10). The levels of PSA are also higher in human cerebellum compared to cortex in both controls and FTD cases. A slight elevation in PSA was also observed in FTD cortices compared to controls. PubMed:24027553

Appears in Networks:
Annotations
MeSH
Cerebellum
Text Location
Review

p(HGNC:NPEPPS) decreases p(MGI:Mapt, var("p.P301L")) View Subject | View Object

In addition, a non-functional PSA mutant exacerbated tau pathology in a Drosophila model of tauopathy, while overexpressing PSA ameliorated the tau phenotype and diminished tau levels (10). Overexpressing PSA had a similar effect in the TAUP301L mice, reducing the pathologic phenotype (delaying paralysis, increasing motor neuron density in the spinal cord, decreasing gliosis) and decreasing tau levels (12). PubMed:24027553

Appears in Networks:
Annotations
Text Location
Review

p(MGI:Mapt) hasVariant p(MGI:Mapt, var("p.P301L")) View Subject | View Object

Appears in Networks:

path(HBP:Neurodegeneration) association p(MGI:Mapt, var("p.P301L")) View Subject | View Object

PSA was identified as a potential player in tau pathology through a microarray analysis of gene expression in disease-vulnerable vs. disease-resistant brain regions in JNPL3 mice that overexpress a mutant form of tau (P301L) found in the disease frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). These mice develop neurodegeneration in the cortex while the cerebellum is relatively spared [although in the original description of these animals pathology was found in the deep cerebellar nuclei (27)]. PubMed:24027553

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
Text Location
Review

Out-Edges 2

p(MGI:Mapt, var("p.P301L")) association path(HBP:Neurodegeneration) View Subject | View Object

PSA was identified as a potential player in tau pathology through a microarray analysis of gene expression in disease-vulnerable vs. disease-resistant brain regions in JNPL3 mice that overexpress a mutant form of tau (P301L) found in the disease frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). These mice develop neurodegeneration in the cortex while the cerebellum is relatively spared [although in the original description of these animals pathology was found in the deep cerebellar nuclei (27)]. PubMed:24027553

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
Text Location
Review

p(MGI:Mapt, var("p.P301L")) positiveCorrelation p(HGNC:NPEPPS) View Subject | View Object

Interestingly, PSA was found to be elevated in the cerebellum of these TAUP301L mice (10). The levels of PSA are also higher in human cerebellum compared to cortex in both controls and FTD cases. A slight elevation in PSA was also observed in FTD cortices compared to controls. PubMed:24027553

Appears in Networks:
Annotations
MeSH
Cerebellum
Text Location
Review

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.