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p(MGI:Atg7)

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Entity

Name
Atg7
Namespace
mgi
Namespace Version
20181021
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/f2f993e599694ab5ce989cc39d789a499f75db99/external/mgi-names.belns

Appears in Networks 2

The Biology of Proteostasis in Aging and Disease v1.0.0

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

In-Edges 0

Out-Edges 6

p(MGI:Atg7) decreases bp(HP:Neurodegeneration) View Subject | View Object

Mice deficient for the autophagy-related genes Atg5 and Atg7 exhibit severe neurodegeneration (84, 85), and the expression of disease- associated proteins is reported to exert differential inhibitory effects on autophagic pathways. PubMed:25784053

Appears in Networks:

p(MGI:Atg7) decreases path(HBP:Neurodegeneration) View Subject | View Object

Mice in which the critical autophagy gene Atg7 is knocked out in forebrain neurons develop age-dependent neurodegeneration with accumulation of phosphorylated tau within intracellular inclusions (99). These inclusions specifically contained tau phosphorylated at AT8, AT100, and TG3 epitopes, but not PHF1. Significantly, if tau was also knocked out in these autophagy-deficient mice, neurodegeneration was reduced (99). PubMed:24027553

Appears in Networks:
Annotations
MeSH
Neurons
Text Location
Review

p(MGI:Atg7) decreases p(MGI:Mapt, pmod(Ph)) View Subject | View Object

Mice in which the critical autophagy gene Atg7 is knocked out in forebrain neurons develop age-dependent neurodegeneration with accumulation of phosphorylated tau within intracellular inclusions (99). These inclusions specifically contained tau phosphorylated at AT8, AT100, and TG3 epitopes, but not PHF1. Significantly, if tau was also knocked out in these autophagy-deficient mice, neurodegeneration was reduced (99). PubMed:24027553

Appears in Networks:
Annotations
MeSH
Neurons
Text Location
Review

p(MGI:Atg7) decreases p(MGI:Mapt, pmod(Ph, Ser, 214), pmod(Ph, Thr, 212)) View Subject | View Object

Mice in which the critical autophagy gene Atg7 is knocked out in forebrain neurons develop age-dependent neurodegeneration with accumulation of phosphorylated tau within intracellular inclusions (99). These inclusions specifically contained tau phosphorylated at AT8, AT100, and TG3 epitopes, but not PHF1. Significantly, if tau was also knocked out in these autophagy-deficient mice, neurodegeneration was reduced (99). PubMed:24027553

Appears in Networks:
Annotations
MeSH
Neurons
Text Location
Review

p(MGI:Atg7) decreases p(MGI:Mapt, pmod(Ph, Ser, 202), pmod(Ph, Thr, 205)) View Subject | View Object

Mice in which the critical autophagy gene Atg7 is knocked out in forebrain neurons develop age-dependent neurodegeneration with accumulation of phosphorylated tau within intracellular inclusions (99). These inclusions specifically contained tau phosphorylated at AT8, AT100, and TG3 epitopes, but not PHF1. Significantly, if tau was also knocked out in these autophagy-deficient mice, neurodegeneration was reduced (99). PubMed:24027553

Appears in Networks:
Annotations
MeSH
Neurons
Text Location
Review

p(MGI:Atg7) decreases p(MGI:Mapt, pmod(Ph, Thr, 231)) View Subject | View Object

Mice in which the critical autophagy gene Atg7 is knocked out in forebrain neurons develop age-dependent neurodegeneration with accumulation of phosphorylated tau within intracellular inclusions (99). These inclusions specifically contained tau phosphorylated at AT8, AT100, and TG3 epitopes, but not PHF1. Significantly, if tau was also knocked out in these autophagy-deficient mice, neurodegeneration was reduced (99). PubMed:24027553

Appears in Networks:
Annotations
MeSH
Neurons
Text Location
Review

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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.