Cytokine G-protein signaling crosstalk in cardiomyocytes: attenuation of Jak-STAT activation by endothelin-1 (Q78677543)

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:12487370%20AND%20SRC:MED&resulttype=core&format=json

15 December 2019

title

Cytokine G-protein signaling crosstalk in cardiomyocytes: attenuation of Jak-STAT activation by endothelin-1 (English)

1 reference

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15 December 2019

author name string

George W Booz

1

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15 December 2019

Jonathan N E Day

2

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15 December 2019

Robert Speth

3

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15 December 2019

Kenneth M Baker

4

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15 December 2019

publication date

1 November 2002

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Molecular and Cellular Biochemistry

15 December 2019

published in

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15 December 2019

volume

240

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15 December 2019

issue

1-2

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15 December 2019

page(s)

39-46

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https://scigraph.springernature.com/pub.10.1023/a:1020648425895

15 December 2019

exact match

0 references

cites work

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Activation of gp130 transduces hypertrophic signals via STAT3 in cardiac myocytes

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Inhibition of myocardial endothelin pathway improves long-term survival in heart failure

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Interleukin-6 family of cytokines mediate angiotensin II-induced cardiac hypertrophy in rodent cardiomyocytes

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Signal transducer and activator of transcription 3 in the heart transduces not only a hypertrophic signal but a protective signal against doxorubicin-induced cardiomyopathy

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Ischemia-induced STAT-1 Expression and Activation Play a Critical Role in Cardiomyocyte Apoptosis

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Extracellular Signal-regulated Kinase Plays an Essential Role in Hypertrophic Agonists, Endothelin-1 and Phenylephrine-induced Cardiomyocyte Hypertrophy

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STAT3 serine phosphorylation by ERK-dependent and -independent pathways negatively modulates its tyrosine phosphorylation

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Cardiotrophin-1 activates a distinct form of cardiac muscle cell hypertrophy. Assembly of sarcomeric units in series VIA gp130/leukemia inhibitory factor receptor-dependent pathways

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