Dysbindin deficiency Alters Cardiac BLOC-1 Complex and Myozap Levels in Mice.
Animals
Cardiomegaly
/ genetics
Cytosol
/ metabolism
Dysbindin
/ genetics
Gene Expression Regulation
Hypertrophy
/ physiopathology
Intracellular Signaling Peptides and Proteins
/ metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Muscle Proteins
/ metabolism
Myocytes, Cardiac
/ metabolism
Organelle Biogenesis
Protein Binding
Schizophrenia
/ genetics
Serum Response Factor
/ metabolism
Signal Transduction
Vesicular Transport Proteins
/ metabolism
rhoA GTP-Binding Protein
/ metabolism
Dysbindin
Muted
Myozap
Pallidin
cardiac hypertrophy
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
31 10 2020
31 10 2020
Historique:
received:
24
09
2020
revised:
30
10
2020
accepted:
30
10
2020
entrez:
4
11
2020
pubmed:
5
11
2020
medline:
22
6
2021
Statut:
epublish
Résumé
Dysbindin, a schizophrenia susceptibility marker and an essential constituent of BLOC-1 (biogenesis of lysosome-related organelles complex-1), has recently been associated with cardiomyocyte hypertrophy through the activation of Myozap-RhoA-mediated SRF signaling. We employed sandy mice (
Identifiants
pubmed: 33142804
pii: cells9112390
doi: 10.3390/cells9112390
pmc: PMC7692170
pii:
doi:
Substances chimiques
Bloc1s6 protein, mouse
0
Dtnbp1 protein, mouse
0
Dysbindin
0
Intracellular Signaling Peptides and Proteins
0
Muscle Proteins
0
Myozap protein, mouse
0
Serum Response Factor
0
Vesicular Transport Proteins
0
muted protein, mouse
0
rhoA GTP-Binding Protein
EC 3.6.5.2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
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