TBC1D1 interacting proteins, VPS13A and VPS13C, regulate GLUT4 homeostasis in C2C12 myotubes.
AMP-Activated Protein Kinases
/ metabolism
Animals
Cells, Cultured
Diabetes Mellitus, Type 2
GTPase-Activating Proteins
/ pharmacology
Glucose Transporter Type 4
/ metabolism
HEK293 Cells
Homeostasis
/ drug effects
Humans
Insulin Resistance
Male
Mice, Transgenic
Muscle Fibers, Skeletal
/ metabolism
Proteins
/ pharmacology
Vesicular Transport Proteins
/ pharmacology
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
21 10 2020
21 10 2020
Historique:
received:
28
05
2020
accepted:
07
09
2020
entrez:
22
10
2020
pubmed:
23
10
2020
medline:
10
4
2021
Statut:
epublish
Résumé
Proteins involved in the spaciotemporal regulation of GLUT4 trafficking represent potential therapeutic targets for the treatment of insulin resistance and type 2 diabetes. A key regulator of insulin- and exercise-stimulated glucose uptake and GLUT4 trafficking is TBC1D1. This study aimed to identify proteins that regulate GLUT4 trafficking and homeostasis via TBC1D1. Using an unbiased quantitative proteomics approach, we identified proteins that interact with TBC1D1 in C2C12 myotubes including VPS13A and VPS13C, the Rab binding proteins EHBP1L1 and MICAL1, and the calcium pump SERCA1. These proteins associate with TBC1D1 via its phosphotyrosine binding (PTB) domains and their interactions with TBC1D1 were unaffected by AMPK activation, distinguishing them from the AMPK regulated interaction between TBC1D1 and AMPKα1 complexes. Depletion of VPS13A or VPS13C caused a post-transcriptional increase in cellular GLUT4 protein and enhanced cell surface GLUT4 levels in response to AMPK activation. The phenomenon was specific to GLUT4 because other recycling proteins were unaffected. Our results provide further support for a role of the TBC1D1 PTB domains as a scaffold for a range of Rab regulators, and also the VPS13 family of proteins which have been previously linked to fasting glycaemic traits and insulin resistance in genome wide association studies.
Identifiants
pubmed: 33087848
doi: 10.1038/s41598-020-74661-1
pii: 10.1038/s41598-020-74661-1
pmc: PMC7578007
doi:
Substances chimiques
GTPase-Activating Proteins
0
Glucose Transporter Type 4
0
Proteins
0
TBC1D1 protein, human
0
VPS13A protein, human
0
VPS13C protein, human
0
Vesicular Transport Proteins
0
AMP-Activated Protein Kinases
EC 2.7.11.31
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
17953Subventions
Organisme : British Heart Foundation
ID : PG/10/008/28186
Pays : United Kingdom
Organisme : Diabetes UK
ID : 14/0004877
Pays : United Kingdom
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