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a(MESH:Cathepsins)

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Entity

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

Appears in Networks 1

The Ubiquitin–Proteasome System and the Autophagic–Lysosomal System in Alzheimer Disease v1.0.0

In-Edges 3

p(HGNC:IGF2R) increases tloc(a(MESH:Cathepsins), fromLoc(GO:"trans-Golgi network"), toLoc(GO:"multivesicular body")) View Subject | View Object

Acid hydrolases, including cathepsins, are delivered from the trans-Golgi network (TGN) to MVBs/late endosomes by either of two mannose-6- phosphate receptors: cation-dependent 46 kDa MPR (CD-MPR) and cation-independent 215 kDa MPR (CI-MPR; Mullins et al. 2001). PubMed:22908190

Appears in Networks:

p(HGNC:M6PR) increases tloc(a(MESH:Cathepsins), fromLoc(GO:"trans-Golgi network"), toLoc(GO:"multivesicular body")) View Subject | View Object

Acid hydrolases, including cathepsins, are delivered from the trans-Golgi network (TGN) to MVBs/late endosomes by either of two mannose-6- phosphate receptors: cation-dependent 46 kDa MPR (CD-MPR) and cation-independent 215 kDa MPR (CI-MPR; Mullins et al. 2001). PubMed:22908190

Appears in Networks:

p(HGNC:PSEN1) increases act(a(MESH:Cathepsins)) View Subject | View Object

Beyond its role as a component of g-secretase, Presenilin 1 (PS1) is required for lysosome acidification, which is needed to activate cathepsins and other hydrolases that carry out digestion during autophagy (Lee et al. 2010). PubMed:22908190

Appears in Networks:
Annotations
MeSH
Lysosomes

Out-Edges 2

a(MESH:Cathepsins) regulates deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

Although less well studied as “Ab degrading proteases” than the zinc metallopeptidase family (Guenette 2003; Eckman et al. 2005), cathepsins are considered an important route for Ab/amyloid clearance (Mueller-Steiner et al. 2006; Nixon 2007; Butler et al. 2011) and human neurons may be particularly dependent on this mechanism (LeBlanc et al. 1999; reviewed in Saido and Leissring 2011). PubMed:22908190

Appears in Networks:

sec(a(MESH:Cathepsins)) increases bp(GO:"apoptotic process") View Subject | View Object

Cataclysmic disruption of lysosomal membranes releases hydrolases that act as both the trigger and executioner in rapid necrosis (Syntichaki et al. 2003; Kroemer et al. 2005), whereas slow release of cathepsins more likely operates through signaling pathways to trigger apoptosis (Kroemer et al. 2005). PubMed:22908190

Appears in Networks:

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.