MCP-1-induced protein attenuates endotoxin-induced myocardial dysfunction by suppressing cardiac NF-кB activation via inhibition of IкB kinase activation (Q28504691)

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English	MCP-1-induced protein attenuates endotoxin-induced myocardial dysfunction by suppressing cardiac NF-кB activation via inhibition of IкB kinase activation	scientific journal article

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scholarly article

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PubMed publication ID

24 January 2017

MCP-1-induced protein attenuates endotoxin-induced myocardial dysfunction by suppressing cardiac NF-кB activation via inhibition of IкB kinase activation (English)

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PubMed publication ID

24 January 2017

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based on heuristic

inferred from title

Zinc finger CCCH type containing 12A

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GOA release 2020-03-11

author name string

Jianli Niu

1

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PubMed publication ID

24 January 2017

Kangkai Wang

2

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PubMed publication ID

24 January 2017

Sarabeth Graham

3

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PubMed publication ID

24 January 2017

Asim Azfer

4

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PubMed publication ID

24 January 2017

Pappachan E. Kolattukudy

5

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PubMed publication ID

24 January 2017

publication date

1 August 2011

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PubMed publication ID

24 January 2017

Journal of Molecular and Cellular Cardiology

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PubMed publication ID

24 January 2017

51

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PubMed publication ID

24 January 2017

2

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PubMed publication ID

24 January 2017

177–186

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PubMed publication ID

24 January 2017

The epidemiology of sepsis in the United States from 1979 through 2000

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Cardiac dysfunction in severe sepsis and septic shock

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Myocardial dysfunction in the patient with sepsis

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Mechanisms of sepsis-induced cardiac dysfunction

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Molecular mechanisms of NF-kappaB activation induced by bacterial lipopolysaccharide through Toll-like receptors

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Innate immunity and myocardial adaptation to ischemia

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NF-kappaB action in sepsis: the innate immune system and the heart

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Overexpression of cardiac I-kappaBalpha prevents endotoxin-induced myocardial dysfunction

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Parthenolide, an inhibitor of the nuclear factor-kappaB pathway, ameliorates cardiovascular derangement and outcome in endotoxic shock in rodents

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Cardiomyocyte Toll-like receptor 4 is involved in heart dysfunction following septic shock or myocardial ischemia

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Early activation of IKKbeta during in vivo myocardial ischemia

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Inhibitor-kappaB kinase-beta regulates LPS-induced TNF-alpha production in cardiac myocytes through modulation of NF-kappaB p65 subunit phosphorylation

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IKKbeta inhibition attenuates myocardial injury and dysfunction following acute ischemia-reperfusion injury

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Absence of NF-kappaB subunit p50 improves heart failure after myocardial infarction

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Blockade of NF-kappaB by pyrrolidine dithiocarbamate attenuates myocardial inflammatory response and ventricular dysfunction following coronary microembolization induced by homologous microthrombi in rats

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Monocyte chemoattractant protein-1 induces a novel transcription factor that causes cardiac myocyte apoptosis and ventricular dysfunction

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A novel CCCH-zinc finger protein family regulates proinflammatory activation of macrophages

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Interleukin-1-inducible MCPIP protein has structural and functional properties of RNase and participates in degradation of IL-1beta mRNA

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Regulatory feedback loop between NF-kappaB and MCP-1-induced protein 1 RNase

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Zc3h12a is an RNase essential for controlling immune responses by regulating mRNA decay

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Protection against lipopolysaccharide-induced myocardial dysfunction in mice by cardiac-specific expression of soluble Fas.

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Endotoxin-induced myocardial dysfunction: effects of macrophage migration inhibitory factor neutralization

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Cardiac-targeted expression of soluble fas attenuates doxorubicin-induced cardiotoxicity in mice

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Toll-like receptor 4, nitric oxide, and myocardial depression in endotoxemia

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Enhanced NO and superoxide generation in dysfunctional hearts from endotoxemic rats

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Cytokine-induced nitric oxide inhibits mitochondrial energy production and induces myocardial dysfunction in endotoxin-treated rat hearts

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Peroxynitrite is a major contributor to cytokine-induced myocardial contractile failure

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The apoptotic pathway as a therapeutic target in sepsis

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Apoptosis and caspases regulate death and inflammation in sepsis

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Tumor necrosis factor-alpha-induced caspase activation mediates endotoxin-related cardiac dysfunction.

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Ventricular Myocyte Caspases Are Directly Responsible for Endotoxin-Induced Cardiac Dysfunction

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Signal transduction through NF-kappa B.

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Molecular events in the cardiomyopathy of sepsis

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CD14-deficient mice are protected against lipopolysaccharide-induced cardiac inflammation and left ventricular dysfunction.

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Escherichia coli LPS-induced LV dysfunction: role of toll-like receptor-4 in the adult heart.

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Negative inotropic effects of tumour necrosis factor-alpha and interleukin-1beta are ameliorated by alfentanil in rat ventricular myocytes

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Changes in cellular contractility and cytokines profile during Trypanosoma cruzi infection in mice

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Nitric oxide and cardiac function: ten years after, and continuing

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Rapid increase in inducible nitric oxide synthase gene expression in the heart during endotoxemia.

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Cytokine-induced nitric oxide production inhibits mitochondrial energy production and impairs contractile function in rat cardiac myocytes

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Inducible nitric oxide synthase expression and cardiomyocyte dysfunction during sustained moderate ischemia in pigs.

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Deletion of inducible nitric oxide synthase provides cardioprotection in mice with 2-kidney, 1-clip hypertension

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Direct activation of protein kinases by unanchored polyubiquitin chains

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MCP-induced protein 1 deubiquitinates TRAF proteins and negatively regulates JNK and NF-kappaB signaling

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10.1016/J.YJMCC.2011.04.018

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PubMed publication ID

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PubMed publication ID

24 January 2017

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