1. Catalog
  2. Nodes
  3. p(HGNC:MAPT, pmod(HBP:misfolded))

p(HGNC:MAPT, pmod(HBP:misfolded))

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

Entity

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

Appears in Networks 2

Carboxy terminus heat shock protein 70 interacting protein reduces tau-associated degenerative changes v1.0.0

Alzheimer's disease pathological lesions activate the spleen tyrosine kinase. v1.0.0

In-Edges 7

a(MESH:"HSP70 Heat-Shock Proteins") increases deg(p(HGNC:MAPT, pmod(HBP:misfolded))) View Subject | View Object

Several publications suggest that molecular chaperones, e.g., heat shock protein 70 and 90 (Hsp70, Hsp90) play a fundamental role in the clearance of misfolded proteins including tau [12]. PubMed:25374103

Appears in Networks:

bp(GO:"chaperone-mediated autophagy") increases deg(p(HGNC:MAPT, pmod(HBP:misfolded))) View Subject | View Object

Misfolded tau proteins, like other natively unfolded molecules, can be detected and cleared by chaperone assisted mechanisms [13]. PubMed:25374103

Appears in Networks:

complex(a(GO:microtubule), p(HGNC:MAPT)) decreases p(HGNC:MAPT, pmod(HBP:misfolded)) View Subject | View Object

In the pathological case of Alzheimer’s disease (AD) tau becomes hyperphosphorylated, detaches from the microtubules, misfolds, and mislocalizes to the somatodendritic compartment where it aggregates into neurofibrillary tangles. PubMed:25374103

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:MAPT) hasVariant p(HGNC:MAPT, pmod(HBP:misfolded)) View Subject | View Object

Appears in Networks:

p(FPLX:HSP90) increases deg(p(HGNC:MAPT, pmod(HBP:misfolded))) View Subject | View Object

Several publications suggest that molecular chaperones, e.g., heat shock protein 70 and 90 (Hsp70, Hsp90) play a fundamental role in the clearance of misfolded proteins including tau [12]. PubMed:25374103

Appears in Networks:

act(p(HGNC:SYK)) increases p(HGNC:MAPT, pmod(HBP:misfolded)) View Subject | View Object

Altogether, these data suggest that only certain pathogenic forms of tau (MC1, Y18) promote Syk activation, whereas Syk activation appears to directly in- duce tau phosphorylation at Y18 and to indirectly regulate tau phosphorylation at multiple epitopes (S396/404, S202) as well as tau misfolding (MC1, TOC1). PubMed:28877763

Appears in Networks:

act(p(HGNC:SYK)) positiveCorrelation p(HGNC:MAPT, pmod(HBP:misfolded)) View Subject | View Object

We found an increase in Syk activation in DNs surrounding A β deposits as well as in neurons displaying an accumu- lation of phosphorylated Tau at Y18 and elevated levels of MC1 pathogenic tau conformers in AD brain sections whereas only weak immunoreactivity for pSyk was ob- served in brain sections from a non-demented control (Figs. 15, 16 and 17). PubMed:28877763

Appears in Networks:
Annotations
MeSH
Neurites
MeSH
Brain
MeSH
Alzheimer Disease

Out-Edges 1

p(HGNC:MAPT, pmod(HBP:misfolded)) positiveCorrelation act(p(HGNC:SYK)) View Subject | View Object

We found an increase in Syk activation in DNs surrounding A β deposits as well as in neurons displaying an accumu- lation of phosphorylated Tau at Y18 and elevated levels of MC1 pathogenic tau conformers in AD brain sections whereas only weak immunoreactivity for pSyk was ob- served in brain sections from a non-demented control (Figs. 15, 16 and 17). PubMed:28877763

Appears in Networks:
Annotations
MeSH
Neurites
MeSH
Brain
MeSH
Alzheimer 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.