1. Catalog
  2. Nodes
  3. path(MESH:"Acidosis, Lactic")

path(MESH:"Acidosis, Lactic")

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

Entity

Name
Acidosis, Lactic
Namespace
MeSH
Namespace Version
20181007
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/01c9daa61012b37dd0a1bc962521ba51a15b38f1/external/mesh-names.belns

Appears in Networks 1

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

In-Edges 1

bp(MESH:"Oxidative Stress") causesNoChange path(MESH:"Acidosis, Lactic") View Subject | View Object

Only middle-aged Tet-mev-1 mice showed JNK/MARK activation and Ca2+ overload, particularly in astrocytes with decreased hippocampal GFAP and S100ß, but without pathological features such as apoptosis, amyloidosis, and lactic acidosis in neurons and astrocytes. This led to decreasing levels of glial fibrillary acidic protein and S100β in the hippocampal area. PubMed:27623715

Appears in Networks:
Annotations
Uberon
hippocampal formation
Cell Ontology (CL)
astrocyte
Cell Ontology (CL)
neuron

Out-Edges 0

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.