Dataset Information

Mitochondrial CaMKII phosphoproteome.

ABSTRACT: Mice overexpressing CaMKII in myocardial mitochondria have dilated cardiomyopathy that appears to be exclusively driven by metabolic defects that lead to reduced ATP production. Phosphoproteomics study of mitochondrial proteins supports the metabolomics data.

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Heart

DISEASE(S): Cardiovascular System Disease

SUBMITTER: Eleonora Corradini

LAB HEAD: Albert J.R. Heck

PROVIDER: PXD004631 | Pride | 2020-07-31

REPOSITORIES: pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	OR9_20130310_EC_CK_ISO_mix_TiIMAC.msf	Msf
	OR9_20130310_EC_CK_ISO_mix_TiIMAC.raw	Raw
	OR9_20130310_EC_CK_ISO_mix_TiIMAC.zip	Other
	OR9_20130310_EC_CK_ISO_mix_TiIMAC_rerun.raw	Raw

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Publications

Mitochondrial CaMKII causes adverse metabolic reprogramming and dilated cardiomyopathy.

Luczak Elizabeth D ED Wu Yuejin Y Granger Jonathan M JM Joiner Mei-Ling A MA Wilson Nicholas R NR Gupta Ashish A Umapathi Priya P Murphy Kevin R KR Reyes Gaido Oscar E OE Sabet Amin A Corradini Eleonora E Tseng Wen-Wei WW Wang Yibin Y Heck Albert J R AJR Wei An-Chi AC Weiss Robert G RG Anderson Mark E ME

Nature communications 20200904 1

Despite the clear association between myocardial injury, heart failure and depressed myocardial energetics, little is known about upstream signals responsible for remodeling myocardial metabolism after pathological stress. Here, we report increased mitochondrial calmodulin kinase II (CaMKII) activation and left ventricular dilation in mice one week after myocardial infarction (MI) surgery. By contrast, mice with genetic mitochondrial CaMKII inhibition are protected from left ventricular dilation ...[more]

PMID: 32887881

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