Fueling the flames: Mammalian programmed necrosis in inflammatory diseases - Test2 - elhamkhani - TriplyDB

Fueling the flames: Mammalian programmed necrosis in inflammatory diseases

Fueling the flames: Mammalian programmed necrosis in inflammatory diseases

http://www.wikidata.org/entity/Q26830515

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Ionic regulation of cell volume changes and cell death after ischemic stroke.Calcineurin Orchestrates Lateral Transfer of Aspergillus fumigatus during Macrophage Cell Death CYLD deubiquitinates RIP1 in the TNFα-induced necrosome to facilitate kinase activation and programmed necrosis.On the translocation of bacteria and their lipopolysaccharides between blood and peripheral locations in chronic, inflammatory diseases: the central roles of LPS and LPS-induced cell death.Receptor-Interacting Protein Kinase 3 Deficiency Delays Cutaneous Wound Healing Therapeutic hypothermia attenuates tissue damage and cytokine expression after traumatic brain injury by inhibiting necroptosis in the rat.Hypothermic machine perfusion increases A20 expression which protects renal cells against ischemia/reperfusion injury by suppressing inflammation, apoptosis and necroptosis.RIP3: a molecular switch for necrosis and inflammation.Understanding the non-canonical pathways involved in p53-mediated tumor suppression.Necrosis-dependent and independent signaling of the RIP kinases in inflammation.Bone and the innate immune system.Mitochondria-mediated apoptosis in mammals.The recent progress of the mechanism and regulation of tumor necrosis in colorectal cancer.Viral RNA at Two Stages of Reovirus Infection Is Required for the Induction of Necroptosis.Docosahexanoic acid antagonizes TNF-α-induced necroptosis by attenuating oxidative stress, ceramide production, lysosomal dysfunction, and autophagic features Necrostatin-1 Attenuates Inflammatory Response and Improves Cognitive Function in Chronic Ischemic Stroke Mice.Positive and negative phosphorylation regulates RIP1- and RIP3-induced programmed necrosis Developmental Coordination of Gamete Differentiation with Programmed Cell Death in Sporulating Yeast.MLKL forms disulfide bond-dependent amyloid-like polymers to induce necroptosis.Necrostatin-1 Protects Against D-Galactosamine and Lipopolysaccharide-Induced Hepatic Injury by Preventing TLR4 and RAGE Signaling.RIPK3-mediated necroptosis promotes donor kidney inflammatory injury and reduces allograft survival.Pravastatin Attenuates Acute Radiation-Induced Enteropathy and Improves Epithelial Cell Function

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Fueling the flames: Mammalian programmed necrosis in inflammatory diseases

http://www.wikidata.org/entity/Q26830515

description

2012 nî lūn-bûn

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2012 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

@hyw

2012 թվականի նոյեմբերին հրատարակված գիտական հոդված

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年论文

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name

Fueling the flames: Mammalian programmed necrosis in inflammatory diseases

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Fueling the flames: Mammalian programmed necrosis in inflammatory diseases

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Fueling the flames: Mammalian programmed necrosis in inflammatory diseases

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Fueling the flames: Mammalian programmed necrosis in inflammatory diseases

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Fueling the flames: Mammalian programmed necrosis in inflammatory diseases

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Fueling the flames: Mammalian programmed necrosis in inflammatory diseases

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Fueling the flames: Mammalian programmed necrosis in inflammatory diseases

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Fueling the flames: Mammalian programmed necrosis in inflammatory diseases

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Fueling the flames: Mammalian programmed necrosis in inflammatory diseases

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CSHPERSPECT.A008805

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Cold Spring Harbor Perspectives in Biology

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Fueling the flames: Mammalian programmed necrosis in inflammatory diseases

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F. K.-M. Chan

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P2860

Cleavage of the death domain kinase RIP by caspase-8 prompts TNF-induced apoptosis

The RIP1/RIP3 necrosome forms a functional amyloid signaling complex required for programmed necrosis

NEMO and RIP1 control cell fate in response to extensive DNA damage via TNF-α feedforward signaling

IAP antagonists induce autoubiquitination of c-IAPs, NF-kappaB activation, and TNFalpha-dependent apoptosis

IAP antagonists target cIAP1 to induce TNFalpha-dependent apoptosis

Mixed lineage kinase domain-like protein mediates necrosis signaling downstream of RIP3 kinase

The mitochondrial phosphatase PGAM5 functions at the convergence point of multiple necrotic death pathways

RIP: a novel protein containing a death domain that interacts with Fas/APO-1 (CD95) in yeast and causes cell death

cIAPs block Ripoptosome formation, a RIP1/caspase-8 containing intracellular cell death complex differentially regulated by cFLIP isoforms

Induction of TNF receptor I-mediated apoptosis via two sequential signaling complexes

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scholarly article

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1688411

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10.1101/CSHPERSPECT.A008805

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23125016

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