Results 31 to 40 of about 15,502 (223)

Depletion of RIPK3 or MLKL blocks TNF-driven necroptosis and switches towards a delayed RIPK1 kinase-dependent apoptosis [PDF]

open access: yes, 2014
In human cells, the RIPK1-RIPK3-MLKL-PGAM5-Drp1 axis drives tumor necrosis factor (TNF)-induced necroptosis through mitochondrial fission, but whether this pathway is conserved among mammals is not known. To answer this question, we analyzed the presence
Baekelandt, V   +13 more
core   +3 more sources

Molecular Insights into the Mechanism of Necroptosis: The Necrosome As a Potential Therapeutic Target

open access: yesCells, 2019
Necroptosis, or regulated necrosis, is an important type of programmed cell death in addition to apoptosis. Necroptosis induction leads to cell membrane disruption, inflammation and vascularization.
Jing Chen   +3 more
doaj   +1 more source

Inhibition of MLKL-dependent necroptosis via downregulating interleukin-1R1 contributes to neuroprotection of hypoxic preconditioning in transient global cerebral ischemic rats

open access: yesJournal of Neuroinflammation, 2021
Background Our previous study indicated that hypoxic preconditioning reduced receptor interacting protein (RIP) 3-mediated necroptotic neuronal death in hippocampal CA1 of adult rats after transient global cerebral ischemia (tGCI). Although mixed lineage
Lixuan Zhan   +4 more
doaj   +1 more source

PUMA amplifies necroptosis signaling by activating cytosolic DNA sensors. [PDF]

open access: yes, 2018
Necroptosis, a form of regulated necrotic cell death, is governed by RIP1/RIP3-mediated activation of MLKL. However, the signaling process leading to necroptotic death remains to be elucidated.
Chen, Dongshi   +7 more
core   +2 more sources

Essential versus accessory aspects of cell death: recommendations of the NCCD 2015 [PDF]

open access: yes, 2014
Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ‘accidental cell death’ (ACD).
A Ciechanover   +438 more
core   +21 more sources

Enhanced nuclear localization of phosphorylated MLKL predicts adverse events in patients with dilated cardiomyopathy

open access: yesESC Heart Failure, 2022
Aims The role of necroptosis in dilated cardiomyopathy (DCM) remains unclear. Here, we examined whether phosphorylation of mixed lineage kinase domain‐like protein (MLKL), an indispensable event for execution of necroptosis, is associated with the ...
Yugo Fujita   +15 more
doaj   +1 more source

The brain protection of MLKL inhibitor necrosulfonamide against focal ischemia/reperfusion injury associating with blocking the nucleus and nuclear envelope translocation of MLKL and RIP3K

open access: yesFrontiers in Pharmacology, 2023
Mixed lineage kinase like protein (MLKL) is a key mediator of necroptosis. While previous studies highlighted the important role of MLKL as one of the central regulators of brain damage against acute ischemic neuronal injury, how the activation of MLKL ...
Xian-Yong Zhou   +8 more
doaj   +1 more source

Evolutionary divergence of the necroptosis effector MLKL [PDF]

open access: yesCell Death & Differentiation, 2016
The pseudokinase, MLKL (mixed-lineage kinase domain-like), is the most terminal obligatory component of the necroptosis cell death pathway known. Phosphorylation of the MLKL pseudokinase domain by the protein kinase, receptor interacting protein kinase-3 (RIPK3), is known to be the key step in MLKL activation.
M C, Tanzer   +12 more
openaire   +2 more sources

Triad3a induces the degradation of early necrosome to limit RipK1-dependent cytokine production and necroptosis. [PDF]

open access: yes, 2018
Understanding the molecular signaling in programmed cell death is vital to a practical understanding of inflammation and immune cell function. Here we identify a previously unrecognized mechanism that functions to downregulate the necrosome, a central ...
A Degterev   +67 more
core   +2 more sources

MLKL polymerization-induced lysosomal membrane permeabilization promotes necroptosis

open access: yesCell Death & Differentiation, 2023
AbstractMixed lineage kinase-like protein (MLKL) forms amyloid-like polymers to promote necroptosis; however, the mechanism through which these polymers trigger cell death is not clear. We have determined that activated MLKL translocates to the lysosomal membrane during necroptosis induction.
Shuzhen Liu   +6 more
openaire   +2 more sources

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