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David H. MacLennan

Researcher at University of Toronto

Publications -  241
Citations -  24877

David H. MacLennan is an academic researcher from University of Toronto. The author has contributed to research in topics: Endoplasmic reticulum & Phospholamban. The author has an hindex of 84, co-authored 241 publications receiving 24173 citations. Previous affiliations of David H. MacLennan include University of Cape Town & National Institute for Medical Research.

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Amino-acid sequence of a Ca2+ + Mg2+-dependent ATPase from rabbit muscle sarcoplasmic reticulum, deduced from its complementary DNA sequence.

TL;DR: A model of the Ca2+-ATPase of rabbit muscle sarcoplasmic reticulum which has 3 cytoplasmic domains joined to a set of 10 transmembrane helices by a narrow, penta-helical stalk is proposed.
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Phospholamban: a crucial regulator of cardiac contractility

TL;DR: In mice, phospholamban seems to encumber an otherwise healthy heart, but humans with a phosphol amban-null genotype develop early-onset dilated cardiomyopathy, a major cause of death and disability.
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Purification and properties of an adenosine triphosphatase from sarcoplasmic reticulum

TL;DR: An adenosine triphosphatase has been purified approximately 6-fold from sarcoplasmic reticulum through the use of deoxycholate and salt fractionation and the rate of ATP-ADP exchange and the level of phosphorylation are both increased by a factor commensurate with the increase in ATPase activity.
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Molecular cloning of cDNA encoding human and rabbit forms of the Ca2+ release channel (ryanodine receptor) of skeletal muscle sarcoplasmic reticulum.

TL;DR: Analysis of the cDNAs encoding the rabbit and human forms of the Ca2+ release channel of sarcoplasmic reticulum indicates that 10 potential transmembrane sequences in the COOH-terminal fifth of the molecule and two additional, potential trans membrane sequences nearer to the center of the molecules could contribute to the formation of theCa2+ conducting pore.
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Dilated cardiomyopathy and heart failure caused by a mutation in phospholamban.

TL;DR: It is reported that an inherited human dilated cardiomyopathy with refractory congestive heart failure is caused by a dominant Arg → Cys missense mutation at residue 9 (R9C) in phospholamban (PLN), a transmembrane phosphoprotein that inhibits the cardiac sarcoplasmic reticular Ca2–adenosine triphosphatase (SERCA2a) pump.