Fas-associated death domain (FADD) is a negative regulator of T-cell receptor-mediated necroptosis. - Wikidata - wikimedia - TriplyDB

Fas-associated death domain (FADD) is a negative regulator of T-cell receptor-mediated necroptosis.

Fas-associated death domain (FADD) is a negative regulator of T-cell receptor-mediated necroptosis.

http://www.wikidata.org/entity/Q34059345

about

Whole-exome-sequencing-based discovery of human FADD deficiency Regulation of protein kinase C inactivation by Fas-associated protein with death domain Ripped to death Necroptosis in tumorigenesis, activation of anti-tumor immunity, and cancer therapy DED or alive: assembly and regulation of the death effector domain complexes Necroptosis: molecular signalling and translational implications RIP1-dependent and independent effects of necrostatin-1 in necrosis and T cell activation Complementary roles of Fas-associated death domain (FADD) and receptor interacting protein kinase-3 (RIPK3) in T-cell homeostasis and antiviral immunity Mechanisms of necroptosis in T cells The role of FADD in pancreatic cancer cell proliferation and drug resistance A critical role of Fas-associated protein with death domain phosphorylation in intracellular reactive oxygen species homeostasis and aging.Shikonin-induced necroptosis is enhanced by the inhibition of autophagy in non-small cell lung cancer cells Cholecystokinin octapeptide antagonizes apoptosis in human retinal pigment epithelial cells Necroptotic signaling in adaptive and innate immunity.Alternative cell death mechanisms in development and beyond.Synchronized renal tubular cell death involves ferroptosis.Commensal microbiota are required for systemic inflammation triggered by necrotic dendritic cells.Functional complementation between FADD and RIP1 in embryos and lymphocytes.RIP kinases: key decision makers in cell death and innate immunity.Necroptosis takes place in human immunodeficiency virus type-1 (HIV-1)-infected CD4+ T lymphocytes.Requirement of FADD, NEMO, and BAX/BAK for aberrant mitochondrial function in tumor necrosis factor alpha-induced necrosis.Deletion of FADD in macrophages and granulocytes results in RIP3- and MyD88-dependent systemic inflammation Caspase-8 inactivation in T cells increases necroptosis and suppresses autoimmunity in Bim-/- mice.The ubiquitin-modifying enzyme A20 restricts ubiquitination of the kinase RIPK3 and protects cells from necroptosis FADD regulates thymocyte development at the β-selection checkpoint by modulating Notch signaling.RIP3: a molecular switch for necrosis and inflammation.Interferon-induced RIP1/RIP3-mediated necrosis requires PKR and is licensed by FADD and caspases Tubular epithelial cells in renal clear cell carcinoma express high RIPK1/3 and show increased susceptibility to TNF receptor 1-induced necroptosis Regulated necrosis-related molecule mRNA expression in humans and mice and in murine acute tissue injury and systemic autoimmunity leading to progressive organ damage, and progressive fibrosis.Self-renewal and differentiation of muscle satellite cells are regulated by the Fas-associated death domain.Proliferative versus apoptotic functions of caspase-8 Hetero or homo: the caspase-8 dimer controls cell fate.Central role of mitochondria in drug-induced liver injury.RIP1-mediated regulation of lymphocyte survival and death responses.Macroautophagy in T lymphocyte development and function Programmed necrosis and autophagy in immune function.The role of necroptosis, an alternative form of cell death, in cancer therapy.Functions of caspase 8: the identified and the mysterious.Anticancer agents targeted to sirtuins.Emerging Roles for RIPK1 and RIPK3 in Pathogen-Induced Cell Death and Host Immunity.Necroptotic cell death in failing heart: relevance and proposed mechanisms.

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Fas-associated death domain (FADD) is a negative regulator of T-cell receptor-mediated necroptosis.

http://www.wikidata.org/entity/Q34059345

description

2010 nî lūn-bûn

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2010 թուականի Յուլիսին հրատարակուած գիտական յօդուած

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2010 թվականի հուլիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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Fas-associated death domain (F ...... receptor-mediated necroptosis.

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PNAS.1005997107

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Proceedings of the National Academy of Sciences of the United States of America

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Fas-associated death domain (F ...... receptor-mediated necroptosis.

@en

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Astar Winoto

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Dragana Cado

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Ellen A Robey

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Gretchen Diehl

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Kristina Hsieh

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Ling Xue

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Nadia Kurd

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Seong-Ji Han

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Stephanie L Osborn

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P2860

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

Fas triggers an alternative, caspase-8-independent cell death pathway using the kinase RIP as effector molecule

Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha

Phosphorylation-driven assembly of the RIP1-RIP3 complex regulates programmed necrosis and virus-induced inflammation

FADD and caspase-8 control the outcome of autophagic signaling in proliferating T cells

Essential roles of Atg5 and FADD in autophagic cell death: dissection of autophagic cell death into vacuole formation and cell death

FADD: essential for embryo development and signaling from some, but not all, inducers of apoptosis

Phosphorylation of FADD at serine 194 by CKIalpha regulates its nonapoptotic activities

Fas-mediated apoptosis and activation-induced T-cell proliferation are defective in mice lacking FADD/Mort1

RIP3, an energy metabolism regulator that switches TNF-induced cell death from apoptosis to necrosis

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13034-13039

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scholarly article

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10.1073/PNAS.1005997107

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29

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107

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2010-07-06T00:00:00Z

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45113500

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20615958

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2919948

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