This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The purpose of this core is to provide neonatal myocyte cultures for COBRE researchers. Neonatal cultures are available on a routine schedule for all COBRE projects and several other projects by CRI faculty. The Cell Culture Core also isolates adult mouse cardiac myocytes, providing these cultures on demand.

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
Exploratory Grants (P20)
Project #
5P20RR017662-08
Application #
8168336
Study Section
National Center for Research Resources Initial Review Group (RIRG)
Project Start
2010-07-01
Project End
2011-06-30
Budget Start
2010-07-01
Budget End
2011-06-30
Support Year
8
Fiscal Year
2010
Total Cost
$192,888
Indirect Cost
Name
Sanford Research/Usd
Department
Type
DUNS #
050113252
City
Sioux Falls
State
SD
Country
United States
Zip Code
57104
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Kobayashi, Satoru; Liang, Qiangrong (2015) Autophagy and mitophagy in diabetic cardiomyopathy. Biochim Biophys Acta 1852:252-61
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Savinova, Olga V; Fillaus, Kristi; Jing, Linhong et al. (2014) Reduced apolipoprotein glycosylation in patients with the metabolic syndrome. PLoS One 9:e104833
Jensen, Brian C; O?Connell, Timothy D; Simpson, Paul C (2014) Alpha-1-adrenergic receptors in heart failure: the adaptive arm of the cardiac response to chronic catecholamine stimulation. J Cardiovasc Pharmacol 63:291-301
Wu, Steven C; Dahl, Erika F; Wright, Casey D et al. (2014) Nuclear localization of a1A-adrenergic receptors is required for signaling in cardiac myocytes: an “inside-out” a1-AR signaling pathway. J Am Heart Assoc 3:e000145
Xu, Xianmin; Kobayashi, Satoru; Chen, Kai et al. (2013) Diminished autophagy limits cardiac injury in mouse models of type 1 diabetes. J Biol Chem 288:18077-92

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