(Q43572770)

24 November 2017

title

Phenylarsine oxide induces mitochondrial permeability transition, hypercontracture, and cardiac cell death (English)

1 reference

24 November 2017

1 reference

Korge P

1

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24 November 2017

Goldhaber JI

series ordinal

2

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24 November 2017

Weiss JN

series ordinal

3

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24 November 2017

language of work or name

1 reference

1 May 2001

1 reference

American Journal of Physiology Heart and Circulatory Physiology

24 November 2017

published in

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24 November 2017

volume

280

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24 November 2017

issue

5

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24 November 2017

page(s)

H2203-13

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Okadaic acid, vanadate, and phenylarsine oxide stimulate 2-deoxyglucose transport in insulin-resistant human skeletal muscle.

24 November 2017

cites work

1 reference

https://api.crossref.org/works/10.1152%2FAJPHEART.2001.280.5.H2203

Mitochondrial function as a determinant of recovery or death in cell response to injury.

21 January 2018

1 reference

https://api.crossref.org/works/10.1152%2FAJPHEART.2001.280.5.H2203

Effects of acidosis on resting cytosolic and mitochondrial Ca2+ in mammalian myocardium

21 January 2018

1 reference

https://api.crossref.org/works/10.1152%2FAJPHEART.2001.280.5.H2203

Mitochondrial non-specific pores remain closed during cardiac ischaemia, but open upon reperfusion

21 January 2018

1 reference

https://api.crossref.org/works/10.1152%2FAJPHEART.2001.280.5.H2203

Elucidating the molecular mechanism of the permeability transition pore and its role in reperfusion injury of the heart

21 January 2018

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MgADP- increases maximum tension and Ca2+ sensitivity in skinned rabbit soleus fibers

21 January 2018

1 reference

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Mitochondrial calcium in relaxed and tetanized myocardium

21 January 2018

1 reference

https://api.crossref.org/works/10.1152%2FAJPHEART.2001.280.5.H2203

Mitochondria are excitable organelles capable of generating and conveying electrical and calcium signals.

21 January 2018

1 reference

https://api.crossref.org/works/10.1152%2FAJPHEART.2001.280.5.H2203

The mitochondrial permeability transition in cell death: a common mechanism in necrosis, apoptosis and autophagy

21 January 2018

1 reference

https://api.crossref.org/works/10.1152%2FAJPHEART.2001.280.5.H2203

The relationship between mitochondrial state, ATP hydrolysis, [Mg2+]i and [Ca2+]i studied in isolated rat cardiomyocytes.

21 January 2018

1 reference

https://api.crossref.org/works/10.1152%2FAJPHEART.2001.280.5.H2203

Transient and long-lasting openings of the mitochondrial permeability transition pore can be monitored directly in intact cells by changes in mitochondrial calcein fluorescence

21 January 2018

1 reference

https://api.crossref.org/works/10.1152%2FAJPHEART.2001.280.5.H2203

Sarcolemmal phospholipid asymmetry and Ca fluxes on metabolic inhibition of neonatal rat heart cells

21 January 2018

1 reference

https://api.crossref.org/works/10.1152%2FAJPHEART.2001.280.5.H2203

Endocytosis of the rat somatostatin receptors: subtype discrimination, ligand specificity, and delineation of carboxy-terminal positive and negative sequence motifs

21 January 2018

1 reference

https://api.crossref.org/works/10.1152%2FAJPHEART.2001.280.5.H2203

Protein-tyrosine phosphatase inhibitors block tumor necrosis factor-dependent activation of the nuclear transcription factor NF-kappa B.

21 January 2018

1 reference

https://api.crossref.org/works/10.1152%2FAJPHEART.2001.280.5.H2203

Selective loading of Rhod 2 into mitochondria shows mitochondrial Ca2+ transients during the contractile cycle in adult rabbit cardiac myocytes.

21 January 2018

1 reference

https://api.crossref.org/works/10.1152%2FAJPHEART.2001.280.5.H2203

What we can learn from the effects of thiol reagents on transport proteins

21 January 2018

1 reference

https://api.crossref.org/works/10.1152%2FAJPHEART.2001.280.5.H2203

10.1152/AJPHEART.2001.280.5.H2203

21 January 2018

Identifiers

DOI

0 references

1 reference