GLIPR2 is a negative regulator of autophagy and the BECN1-ATG14-containing phosphatidylinositol 3-kinase complex.
Autophagy
BECN1
GLIPR2
Golgi
PtdIns3k-C1 complex
Tat-BECN1 peptide
Journal
Autophagy
ISSN: 1554-8635
Titre abrégé: Autophagy
Pays: United States
ID NLM: 101265188
Informations de publication
Date de publication:
10 2021
10 2021
Historique:
pubmed:
24
11
2020
medline:
8
4
2022
entrez:
23
11
2020
Statut:
ppublish
Résumé
A key mediator of macroautophagy/autophagy induction is the class III phosphatidylinositol 3-kinase complex I (PtdIns3K-C1) consisting of PIK3C3/VPS34, PIK3R4/VPS15, BECN1, and ATG14. Although several proteins are known to enhance or decrease PtdIns3K-C1 activity, our understanding of the molecular regulation of PtdIns3K-C1 is still incomplete. Previously, we identified a Golgi-associated protein, GLIPR2, in a screen for proteins that interact with amino acids 267-284 of BECN1, a region of BECN1 sufficient to induce autophagy when fused to a cell penetrating leader sequence. In this study, we used CRISPR-Cas9-mediated depletion of GLIPR2 in cells and mice to investigate the role of GLIPR2 in the regulation of autophagy and PtdIns3K-C1 activity. Depletion of GLIPR2 in HeLa cells increased autelophagic flux and generation of phosphatidylinositol 3-phosphate (PtdIns3P).
Identifiants
pubmed: 33222586
doi: 10.1080/15548627.2020.1847798
pmc: PMC8526008
doi:
Substances chimiques
ATG14 protein, human
0
Adaptor Proteins, Vesicular Transport
0
Autophagy-Related Proteins
0
BECN1 protein, human
0
Beclin-1
0
Becn1 protein, mouse
0
GLIPR2 protein, human
0
Membrane Proteins
0
Class III Phosphatidylinositol 3-Kinases
EC 2.7.1.137
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
2891-2904Subventions
Organisme : NIGMS NIH HHS
ID : R15 GM122035
Pays : United States
Organisme : NIAID NIH HHS
ID : U19 AI109725
Pays : United States
Organisme : NIAID NIH HHS
ID : U19 AI142784
Pays : United States
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