Mitochondrial death protein Nix is induced in cardiac hypertrophy and triggers apoptotic cardiomyopathy (Q44020107)

29 November 2017

Mitochondrial death protein Nix is induced in cardiac hypertrophy and triggers apoptotic cardiomyopathy (English)

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29 November 2017

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7

Bruce J Aronow

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29 November 2017

Martin G Yussman

1

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29 November 2017

Tsuyoshi Toyokawa

2

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29 November 2017

Amy Odley

3

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29 November 2017

Roy A Lynch

4

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29 November 2017

Guangyu Wu

5

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29 November 2017

Melissa C Colbert

6

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29 November 2017

John N Lorenz

8

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29 November 2017

Gerald W Dorn

9

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29 November 2017

language of work or name

English

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publication date

10 June 2002

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29 November 2017

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29 November 2017

8

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29 November 2017

725-730

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29 November 2017

7

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https://scigraph.springernature.com/pub.10.1038/nm719

29 November 2017

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cites work

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Enhanced Galphaq signaling: a common pathway mediates cardiac hypertrophy and apoptotic heart failure

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Loss of a gp130 cardiac muscle cell survival pathway is a critical event in the onset of heart failure during biomechanical stress

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Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study

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Apoptosis and heart failure

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Caspases: enemies within

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Genetic dissection of cardiac growth control pathways

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Transgenic Galphaq overexpression induces cardiac contractile failure in mice

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Embryonic cardiomyocyte hypoplasia and craniofacial defects in G alpha q/G alpha 11-mutant mice

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Calcineurin-mediated hypertrophy protects cardiomyocytes from apoptosis in vitro and in vivo: An apoptosis-independent model of dilated heart failure

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Nix and Nip3 form a subfamily of pro-apoptotic mitochondrial proteins

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Cardiomyocyte apoptosis induced by Galphaq signaling is mediated by permeability transition pore formation and activation of the mitochondrial death pathway.

21 January 2018

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A structural view of mitochondria-mediated apoptosis

21 January 2018

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BNIP3 heterodimerizes with Bcl-2/Bcl-X(L) and induces cell death independent of a Bcl-2 homology 3 (BH3) domain at both mitochondrial and nonmitochondrial sites

21 January 2018

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The E1B 19K/Bcl-2-binding protein Nip3 is a dimeric mitochondrial protein that activates apoptosis

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Left Ventricular Stresses in the Intact Human Heart

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Cardiomyopathy of overload. A major determinant of prognosis in congestive heart failure

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Stretch-mediated release of angiotensin II induces myocyte apoptosis by activating p53 that enhances the local renin-angiotensin system and decreases the Bcl-2-to-Bax protein ratio in the cell

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A mouse model of familial hypertrophic cardiomyopathy

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Neonatal cardiomyopathy in mice homozygous for the Arg403Gln mutation in the alpha cardiac myosin heavy chain gene

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Expression of the gene encoding the proapoptotic Nip3 protein is induced by hypoxia

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Evidence of Apoptosis in Arrhythmogenic Right Ventricular Dysplasia

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Apoptosis in myocytes in end-stage heart failure

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7 January 2021

Apoptosis in the failing human heart

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7 January 2021

Chips ahoy: gene expression in failing hearts surveyed by high-density microarrays

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7 January 2021

Targeting the receptor-Gq interface to inhibit in vivo pressure overload myocardial hypertrophy

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7 January 2021

Absence of pressure overload induced myocardial hypertrophy after conditional inactivation of Gαq/Gα11 in cardiomyocytes

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7 January 2021

Decompensation of pressure-overload hypertrophy in G alpha q-overexpressing mice

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7 January 2021

Divergent transcriptional responses to independent genetic causes of cardiac hypertrophy

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7 January 2021

TAK1 is activated in the myocardium after pressure overload and is sufficient to provoke heart failure in transgenic mice.

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7 January 2021

Regulation of bcl-2 family proteins during development and in response to oxidative stress in cardiac myocytes: association with changes in mitochondrial membrane potential

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7 January 2021

Expression of bcl-2 protein, an inhibitor of apoptosis, and Bax, an accelerator of apoptosis, in ventricular myocytes of human hearts with myocardial infarction

1 reference

7 January 2021

Dimensions Publication ID

Identifiers

DOI

10.1038/NM719

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