Abstract

The function of the Gene Transfer Core is to provide a facility for the construction, screening, large-scale purification, and tittering of replication-defective recombinant adenoviruses. Recombinant adenoviruses provide a reliable method for high efficiency gene transfer into adult cardiocytes and for directly altering the phenotype. Specifically, the core will 1) maintain 293 kidney cells in culture, 2) amplify and maintain purified stocks of the pdeltaE1sp1A shuttle plasmid and the pJM17 adenovirus plasmid, 3) construct recombinant adenoviruses by the homologous recombination procedure in 293 kidney cells, 4) propagate recombinant adenoviruses in 293 cells with large-scale purifications, and 5) titer purified adenoviruses by plaque assays in 293 cells. The core will also be responsible for long-term storage of recombinant adenoviruses and will assist individual investigators in carrying out gene transfer protocols in adult cardiocytes.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
5P01HL048788-07
Application #
6202359
Study Section
Project Start
1999-08-01
Project End
2000-07-31
Budget Start
1997-10-01
Budget End
1998-09-30
Support Year
7
Fiscal Year
1999
Total Cost
Indirect Cost

  Institution

Name
Medical University of South Carolina
Department
Type
DUNS #
183710748
City
Charleston
State
SC
Country
United States
Zip Code
29425

  Publications

Palanisamy, Arun P; Suryakumar, Geetha; Panneerselvam, Kavin et al. (2015) A Kinase-Independent Function of c-Src Mediates p130Cas Phosphorylation at the Serine-639 Site in Pressure Overloaded Myocardium. J Cell Biochem 116:2793-803
McDermott, Paul J; Baicu, Catalin F; Wahl, Shaun R et al. (2012) In vivo measurements of the contributions of protein synthesis and protein degradation in regulating cardiac pressure overload hypertrophy in the mouse. Mol Cell Biochem 367:205-13
Baicu, Catalin F; Li, Jiayu; Zhang, Yuhua et al. (2012) Time course of right ventricular pressure-overload induced myocardial fibrosis: relationship to changes in fibroblast postsynthetic procollagen processing. Am J Physiol Heart Circ Physiol 303:H1128-34
Mukherjee, Rupak; Snipes, Jonathan M; Saunders, Stuart M et al. (2012) Discordant activation of gene promoters for matrix metalloproteinases and tissue inhibitors of the metalloproteinases following myocardial infarction. J Surg Res 172:59-67
Baicu, Catalin F; Zhang, Yuhua; Van Laer, An O et al. (2012) Effects of the absence of procollagen C-endopeptidase enhancer-2 on myocardial collagen accumulation in chronic pressure overload. Am J Physiol Heart Circ Physiol 303:H234-40
McCurdy, Sarah M; Dai, Qiuxia; Zhang, Jianhua et al. (2011) SPARC mediates early extracellular matrix remodeling following myocardial infarction. Am J Physiol Heart Circ Physiol 301:H497-505
Bradshaw, Amy D; Baicu, Catalin F; Rentz, Tyler J et al. (2010) Age-dependent alterations in fibrillar collagen content and myocardial diastolic function: role of SPARC in post-synthetic procollagen processing. Am J Physiol Heart Circ Physiol 298:H614-22
Mukherjee, Rupak; Zavadzkas, Juozas A; Rivers, William T et al. (2010) Short-term disruption in regional left ventricular electrical conduction patterns increases interstitial matrix metalloproteinase activity. Am J Physiol Heart Circ Physiol 299:H217-24
Chinnakkannu, Panneerselvam; Samanna, Venkatesababa; Cheng, Guangmao et al. (2010) Site-specific microtubule-associated protein 4 dephosphorylation causes microtubule network densification in pressure overload cardiac hypertrophy. J Biol Chem 285:21837-48
Mukherjee, Rupak; Rivers, William T; Ruddy, Jean Marie et al. (2010) Long-term localized high-frequency electric stimulation within the myocardial infarct: effects on matrix metalloproteinases and regional remodeling. Circulation 122:20-32

Showing the most recent 10 out of 136 publications