The basic approach is to establish molecular-structural and structural-functional correlations, under the premise that structure can be best understood by observing its changes following specific molecular perturbations, and that function cannot be fully modeled without knowledge of the underlying structure. Past and planned projects in which changes in structural parameters due to perturbation of protein expression relate to the functional effects of the same perturbation offer examples of such correlations. A second approach, which was initiated with the current funding is to relate phylogeny with structure and protein expression in the critical transition from low chordates to vertebrates

National Institute of Health (NIH)
National Heart, Lung, and Blood Institute (NHLBI)
Method to Extend Research in Time (MERIT) Award (R37)
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Special Emphasis Panel (NSS)
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Krull, Holly
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University of Pennsylvania
Anatomy/Cell Biology
Schools of Medicine
United States
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Franzini-Armstrong, Clara (2014) Memories of Annemarie Weber. Anat Rec (Hoboken) 297:1543-7
Park, Chang Sik; Chen, Shan; Lee, Hoyong et al. (2013) Targeted ablation of the histidine-rich Ca(2+)-binding protein (HRC) gene is associated with abnormal SR Ca(2+)-cycling and severe pathology under pressure-overload stress. Basic Res Cardiol 108:344
Schredelseker, Johann; Dayal, Anamika; Schwerte, Thorsten et al. (2009) Proper restoration of excitation-contraction coupling in the dihydropyridine receptor beta1-null zebrafish relaxed is an exclusive function of the beta1a subunit. J Biol Chem 284:1242-51
Di Maio, Alessandro; Block, Barbara A (2008) Ultrastructure of the sarcoplasmic reticulum in cardiac myocytes from Pacific bluefin tuna. Cell Tissue Res 334:121-34
Snopko, Rose M; Ramos-Franco, Josefina; Di Maio, Alessandro et al. (2008) Ca2+ sparks and cellular distribution of ryanodine receptors in developing cardiomyocytes from rat. J Mol Cell Cardiol 44:1032-44
Di Maio, Alessandro; Karko, Kimberly; Snopko, Rose M et al. (2007) T-tubule formation in cardiacmyocytes: two possible mechanisms? J Muscle Res Cell Motil 28:231-41
Di Maio, Alessandro; Ter Keurs, H E; Franzini-Armstrong, Clara (2007) T-tubule profiles in Purkinje fibres of mammalian myocardium. J Muscle Res Cell Motil 28:115-21
Chopra, Nagesh; Kannankeril, Prince J; Yang, Tao et al. (2007) Modest reductions of cardiac calsequestrin increase sarcoplasmic reticulum Ca2+ leak independent of luminal Ca2+ and trigger ventricular arrhythmias in mice. Circ Res 101:617-26
Knollmann, Bjorn C; Chopra, Nagesh; Hlaing, Thinn et al. (2006) Casq2 deletion causes sarcoplasmic reticulum volume increase, premature Ca2+ release, and catecholaminergic polymorphic ventricular tachycardia. J Clin Invest 116:2510-20
Tijskens, Pierre; Jones, Larry R; Franzini-Armstrong, Clara (2003) Junctin and calsequestrin overexpression in cardiac muscle: the role of junctin and the synthetic and delivery pathways for the two proteins. J Mol Cell Cardiol 35:961-74

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