Muscle calcium stress cleaves junctophilin1, unleashing a gene regulatory program predicted to correct glucose dysregulation.
Animals
Humans
Calcium
/ metabolism
Calcium, Dietary
Disease Susceptibility
Glucose
/ metabolism
Glycogen Synthase Kinase 3 beta
/ genetics
Hyperglycemia
/ metabolism
Malignant Hyperthermia
/ metabolism
Mammals
/ metabolism
Muscle, Skeletal
/ metabolism
Ryanodine Receptor Calcium Release Channel
/ metabolism
glucose transport
human
immunocytochemistry
molecular biophysics
mouse
phosphorylation
protein kinase
structural biology
transcription factors
Journal
eLife
ISSN: 2050-084X
Titre abrégé: Elife
Pays: England
ID NLM: 101579614
Informations de publication
Date de publication:
01 02 2023
01 02 2023
Historique:
received:
23
03
2022
accepted:
11
01
2023
entrez:
1
2
2023
pubmed:
2
2
2023
medline:
4
2
2023
Statut:
epublish
Résumé
Calcium ion movements between cellular stores and the cytosol govern muscle contraction, the most energy-consuming function in mammals, which confers skeletal myofibers a pivotal role in glycemia regulation. Chronic myoplasmic calcium elevation ("calcium stress"), found in malignant hyperthermia-susceptible (MHS) patients and multiple myopathies, has been suggested to underlie the progression from hyperglycemia to insulin resistance. What drives such progression remains elusive. We find that muscle cells derived from MHS patients have increased content of an activated fragment of GSK3β - a specialized kinase that inhibits glycogen synthase, impairing glucose utilization and delineating a path to hyperglycemia. We also find decreased content of junctophilin1, an essential structural protein that colocalizes in the couplon with the voltage-sensing Ca
Identifiants
pubmed: 36724092
doi: 10.7554/eLife.78874
pii: 78874
pmc: PMC9891728
doi:
pii:
Substances chimiques
Calcium
SY7Q814VUP
Calcium, Dietary
0
Glucose
IY9XDZ35W2
Glycogen Synthase Kinase 3 beta
EC 2.7.11.1
Ryanodine Receptor Calcium Release Channel
0
junctophilin
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIAMS NIH HHS
ID : R01AR071381
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR071381
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01AR072602
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR072602
Pays : United States
Organisme : NCRR NIH HHS
ID : S10 RR024707
Pays : United States
Organisme : NCRR NIH HHS
ID : S1055024707
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01GM111254
Pays : United States
Informations de copyright
© 2023, Tammineni et al.
Déclaration de conflit d'intérêts
ET, LF, CM, DV, NK, CI, AK, SR, ER No competing interests declared
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