Sequential Engagement of Distinct MLKL Phosphatidylinositol-Binding Sites Executes Necroptosis.
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Questions and controversies: the role of necroptosis in liver diseaseNoncanocial cell death program independent of caspase activation cascade and necroptotic modules is elicited by loss of TGFβ-activated kinase 1.Necroptosis Is an Important Severity Determinant and Potential Therapeutic Target in Experimental Severe Pancreatitis.Pyroptosis is driven by non-selective gasdermin-D pore and its morphology is different from MLKL channel-mediated necroptosis.Viral RNA at Two Stages of Reovirus Infection Is Required for the Induction of Necroptosis.Evidence of necroptosis in hearts subjected to various forms of ischemic insults.Regulating the balance between necroptosis, apoptosis and inflammation by inhibitors of apoptosis proteins.Insane in the membrane: a structural perspective of MLKL function in necroptosis.Complex Pathologic Roles of RIPK1 and RIPK3: Moving Beyond Necroptosis.The MLKL Channel in Necroptosis Is an Octamer Formed by Tetramers in a Dyadic Process.RIPK3-driven cell death during virus infections.Initiation and execution mechanisms of necroptosis: an overview.Thioredoxin-1 actively maintains the pseudokinase MLKL in a reduced state to suppress disulfide bond-dependent MLKL polymer formation and necroptosis.Decidual Stromal Cell Necroptosis Contributes to Polyinosinic-Polycytidylic Acid-Triggered Abnormal Murine Pregnancy.Necroptosis: Mechanisms and Relevance to Disease.Electrophysiologist shows a cation channel function of MLKL.The lure of the lipids: how defensins exploit membrane phospholipids to induce cytolysis in target cells.Chemically different non-thermal plasmas target distinct cell death pathways.Necroptosis Execution Is Mediated by Plasma Membrane Nanopores Independent of Calcium.MLKL Activation Triggers NLRP3-Mediated Processing and Release of IL-1β Independently of Gasdermin-D.ESCRT-III Acts Downstream of MLKL to Regulate Necroptotic Cell Death and Its Consequences.Necroptotic cell death in anti-cancer therapy.MLKL forms disulfide bond-dependent amyloid-like polymers to induce necroptosis.Plasma membrane changes during programmed cell deaths.The brace helices of MLKL mediate interdomain communication and oligomerisation to regulate cell death by necroptosis.MLKL Requires the Inositol Phosphate Code to Execute Necroptosis.Conformational switching of the pseudokinase domain promotes human MLKL tetramerization and cell death by necroptosis.Nuclear RIPK3 and MLKL contribute to cytosolic necrosome formation and necroptosisCharacterization of MLKL-mediated Plasma Membrane Rupture in NecroptosisNecroptosis: MLKL PolymerizationA FRET biosensor for necroptosis uncovers two different modes of the release of DAMPs
P2860
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P2860
Sequential Engagement of Distinct MLKL Phosphatidylinositol-Binding Sites Executes Necroptosis.
description
2016 nî lūn-bûn
@nan
2016年の論文
@ja
2016年論文
@yue
2016年論文
@zh-hant
2016年論文
@zh-hk
2016年論文
@zh-mo
2016年論文
@zh-tw
2016年论文
@wuu
2016年论文
@zh
2016年论文
@zh-cn
name
Sequential Engagement of Disti ...... ng Sites Executes Necroptosis.
@ast
Sequential Engagement of Disti ...... ng Sites Executes Necroptosis.
@en
type
label
Sequential Engagement of Disti ...... ng Sites Executes Necroptosis.
@ast
Sequential Engagement of Disti ...... ng Sites Executes Necroptosis.
@en
prefLabel
Sequential Engagement of Disti ...... ng Sites Executes Necroptosis.
@ast
Sequential Engagement of Disti ...... ng Sites Executes Necroptosis.
@en
P2093
P2860
P50
P1433
P1476
Sequential Engagement of Disti ...... ng Sites Executes Necroptosis.
@en
P2093
Amanda Nourse
Christy R Grace
Cliff S Guy
Diego A Rodriguez
Fabien Llambi
Randall Wakefield
Sharon Frase
P2860
P304
P356
10.1016/J.MOLCEL.2016.01.011
P577
2016-02-03T00:00:00Z