Cell adhesion molecule IGPR-1 activates AMPK connecting cell adhesion to autophagy.
AMP-Activated Protein Kinases
/ metabolism
Amino Acid Motifs
Animals
Autophagy
/ drug effects
Autophagy-Related Protein-1 Homolog
/ metabolism
Beclin-1
/ metabolism
CD28 Antigens
/ chemistry
Cell Adhesion
/ drug effects
HEK293 Cells
Humans
I-kappa B Kinase
/ deficiency
Intracellular Signaling Peptides and Proteins
/ metabolism
Lipopolysaccharides
/ pharmacology
Microscopy, Fluorescence
Microtubule-Associated Proteins
/ metabolism
Phosphorylation
/ drug effects
Primates
RNA, Guide, Kinetoplastida
/ metabolism
Sirolimus
/ pharmacology
Substrate Specificity
AMP-activated kinase (AMPK)
IGPR-1
IKKβ
autophagy
cell adhesion molecule
cell surface receptor
cell–cell interaction
immunoglobulin-like domain
nutrient deprivation
post-translational modification (PTM)
serine phosphorylation of IGPR-1
serine/threonine protein kinase
Journal
The Journal of biological chemistry
ISSN: 1083-351X
Titre abrégé: J Biol Chem
Pays: United States
ID NLM: 2985121R
Informations de publication
Date de publication:
04 12 2020
04 12 2020
Historique:
received:
11
06
2020
revised:
22
09
2020
pubmed:
27
9
2020
medline:
5
5
2021
entrez:
26
9
2020
Statut:
ppublish
Résumé
Autophagy plays critical roles in the maintenance of endothelial cells in response to cellular stress caused by blood flow. There is growing evidence that both cell adhesion and cell detachment can modulate autophagy, but the mechanisms responsible for this regulation remain unclear. Immunoglobulin and proline-rich receptor-1 (IGPR-1) is a cell adhesion molecule that regulates angiogenesis and endothelial barrier function. In this study, using various biochemical and cellular assays, we demonstrate that IGPR-1 is activated by autophagy-inducing stimuli, such as amino acid starvation, nutrient deprivation, rapamycin, and lipopolysaccharide. Manipulating the IκB kinase β activity coupled with
Identifiants
pubmed: 32978258
pii: S0021-9258(17)50485-8
doi: 10.1074/jbc.RA120.014790
pmc: PMC7864065
pii:
doi:
Substances chimiques
Beclin-1
0
CD28 Antigens
0
Intracellular Signaling Peptides and Proteins
0
Lipopolysaccharides
0
MAP1LC3B protein, human
0
Microtubule-Associated Proteins
0
RNA, Guide
0
TMIGD2 protein, human
0
Autophagy-Related Protein-1 Homolog
EC 2.7.11.1
ULK1 protein, human
EC 2.7.11.1
I-kappa B Kinase
EC 2.7.11.10
AMP-Activated Protein Kinases
EC 2.7.11.31
Sirolimus
W36ZG6FT64
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
16691-16699Subventions
Organisme : NCI NIH HHS
ID : R21 CA191970
Pays : United States
Organisme : NCI NIH HHS
ID : R21 CA193958
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001430
Pays : United States
Informations de copyright
© 2020 Amraei et al.
Déclaration de conflit d'intérêts
Conflict of interest—The authors declare that they have no conflicts of interest with the contents of this article.
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