Core C is the Mouse Resources Core. All three Projects will make extensive use of genetically modified mice for their proposed experiments. The purpose of Core C is to provide a centralized localization of the animals, sharing of common breeding stocks, and uniform performance of genotype analyses, which will maximize efficiency and minimize costs associated with the production and maintenance of the mice needed for the proposed experiments. Specific activities of the Core C include (1) assistance in the generation of new genetically modified mouse models; (2) establishment and maintenance of breeding stocks; (3) generation of timed pregnancies; (4) generation of postnatal experimental animals; (5) delivery of experimental animals to the appropriate laboratory for use; (6) distribution of genetically modified mouse models. Core C personnel are well-trained in all aspects of the services to be provided. Given the heavy reliance on genetically modified animals and the proven performance of the Core personnel, the importance of Core C to the success of the Program Project Grant application cannot be overstated.

Public Health Relevance

The major benefit of this Mouse Resources Core to these three Projects is to facilitate development of new animal models and efficient usage of existing animal models of human disease thereby accelerating basic discovery. The benefit of this Core to society is to maximize efficiency and minimize the costs associated with usage of animal models of human disease.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
5P01HL134599-03
Application #
9640228
Study Section
Heart, Lung, and Blood Initial Review Group (HLBP)
Program Officer
Schramm, Charlene A
Project Start
Project End
Budget Start
2019-02-01
Budget End
2020-01-31
Support Year
3
Fiscal Year
2019
Total Cost
Indirect Cost
Name
Indiana University-Purdue University at Indianapolis
Department
Type
DUNS #
603007902
City
Indianapolis
State
IN
Country
United States
Zip Code
46202
Liu, Ying; Chen, Vincent H S; Shou, Weinian (2018) LUMA in cardiac development and function. Cardiovasc Res 114:347-348
Shi, Jianjian; Surma, Michelle; Wei, Lei (2018) Disruption of ROCK1 gene restores autophagic flux and mitigates doxorubicin-induced cardiotoxicity. Oncotarget 9:12995-13008
Miao, Lianjie; Li, Jingjing; Li, Jun et al. (2018) Notch signaling regulates Hey2 expression in a spatiotemporal dependent manner during cardiac morphogenesis and trabecular specification. Sci Rep 8:2678
Xiao, Deyong; Wang, Huijun; Hao, Lili et al. (2018) The roles of SMYD4 in epigenetic regulation of cardiac development in zebrafish. PLoS Genet 14:e1007578
Liu, Ying; Chen, Hanying; Shou, Weinian (2018) Potential Common Pathogenic Pathways for the Left Ventricular Noncompaction Cardiomyopathy (LVNC). Pediatr Cardiol 39:1099-1106
Xiao, Yun-Fei; Zeng, Zhi-Xiong; Guan, Xiao-Hui et al. (2018) FKBP12.6 protects heart from AngII-induced hypertrophy through inhibiting Ca2+ /calmodulin-mediated signalling pathways in vivo and in vitro. J Cell Mol Med 22:3638-3651
Wang, Jun; Shen, Tao; Zhu, Wuqiang et al. (2018) Protein phosphatase 5 and the tumor suppressor p53 down-regulate each other's activities in mice. J Biol Chem 293:18218-18229
Vincentz, Joshua W; Toolan, Kevin P; Zhang, Wenjun et al. (2017) Hand factor ablation causes defective left ventricular chamber development and compromised adult cardiac function. PLoS Genet 13:e1006922
Firulli, Beth A; Toolan, Kevin P; Harkin, Jade et al. (2017) The HAND1 frameshift A126FS mutation does not cause hypoplastic left heart syndrome in mice. Cardiovasc Res 113:1732-1742
Martinez, Hugo R; Ware, Stephanie M; Schamberger, Marcus S et al. (2017) Noncompaction cardiomyopathy and heterotaxy syndrome. Prog Pediatr Cardiol 46:23-27

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