Heart failure is a major cause of death and disability. Impairments
in blood circulation that accompany heart failure can be traced,
in part, to alterations in the activity of the sarcoplasmic reticulum
Ca$^2+$ pump that are induced by its interactions with phospholamban,
a reversible inhibitor. If phospholamban becomes superinhibitory
or chronically inhibitory, contractility is diminished, inducing
dilated cardiomyopathy in mice and humans. In mice, phospholamban
seems to encumber an otherwise healthy heart, but humans with a phospholamban-null
genotype develop early-onset dilated cardiomyopathy.
%0 Journal Article
%1 MacL_2003_566
%A MacLennan, David H
%A Kranias, Evangelia G
%D 2003
%J Nat. Rev. Mol. Cell Biol.
%K 12838339 ATPase, Animals, Calcium-Binding Cardiomyopathy, Contraction, Dilated, Gov't, Humans, Knockout, Mice, Myocardial Non-U.S. P.H.S., Proteins, Research Reticulum, Sarcoplasmic Support, U.S. {C}a$^{2+}$-Transporting
%N 7
%P 566--577
%R 10.1038/nrm1151
%T Phospholamban: a crucial regulator of cardiac contractility.
%U http://dx.doi.org/10.1038/nrm1151
%V 4
%X Heart failure is a major cause of death and disability. Impairments
in blood circulation that accompany heart failure can be traced,
in part, to alterations in the activity of the sarcoplasmic reticulum
Ca$^2+$ pump that are induced by its interactions with phospholamban,
a reversible inhibitor. If phospholamban becomes superinhibitory
or chronically inhibitory, contractility is diminished, inducing
dilated cardiomyopathy in mice and humans. In mice, phospholamban
seems to encumber an otherwise healthy heart, but humans with a phospholamban-null
genotype develop early-onset dilated cardiomyopathy.
@article{MacL_2003_566,
abstract = {Heart failure is a major cause of death and disability. Impairments
in blood circulation that accompany heart failure can be traced,
in part, to alterations in the activity of the sarcoplasmic reticulum
{C}a$^{2+}$ pump that are induced by its interactions with phospholamban,
a reversible inhibitor. If phospholamban becomes superinhibitory
or chronically inhibitory, contractility is diminished, inducing
dilated cardiomyopathy in mice and humans. In mice, phospholamban
seems to encumber an otherwise healthy heart, but humans with a phospholamban-null
genotype develop early-onset dilated cardiomyopathy.},
added-at = {2009-06-03T11:20:58.000+0200},
author = {MacLennan, David H and Kranias, Evangelia G},
biburl = {https://www.bibsonomy.org/bibtex/2bcd3cbda46f74cfb1ce0aa0a00c6e19c/hake},
description = {The whole bibliography file I use.},
doi = {10.1038/nrm1151},
file = {MacL_2003_566.pdf:MacL_2003_566.pdf:PDF},
interhash = {ef83282fe329fb270a917b10b6df1ec6},
intrahash = {bcd3cbda46f74cfb1ce0aa0a00c6e19c},
journal = {Nat. Rev. Mol. Cell Biol.},
keywords = {12838339 ATPase, Animals, Calcium-Binding Cardiomyopathy, Contraction, Dilated, Gov't, Humans, Knockout, Mice, Myocardial Non-U.S. P.H.S., Proteins, Research Reticulum, Sarcoplasmic Support, U.S. {C}a$^{2+}$-Transporting},
month = Jul,
number = 7,
pages = {566--577},
pii = {nrm1151},
pmid = {12838339},
timestamp = {2009-06-03T11:21:21.000+0200},
title = {Phospholamban: a crucial regulator of cardiac contractility.},
url = {http://dx.doi.org/10.1038/nrm1151},
volume = 4,
year = 2003
}