Results 41 to 50 of about 15,125 (218)
MLKL polymerization-induced lysosomal membrane permeabilization promotes necroptosis
Cell 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
ESC 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
Triad3a induces the degradation of early necrosome to limit RipK1-dependent cytokine production and necroptosis. [PDF]
, 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
Detection of necroptosis by phospho-MLKL immunohistochemical labeling
STAR Protocols, 2021 TNF-induced necroptosis is involved in many physiological and pathological processes. Phospho-MLKL is a hallmark of necroptosis. Cecum is a sensitive organ with extensive necroptosis responses to TNF in vivo. Here, taking advantage of commercially available mouse TNF and easily accessible reagents and materials, we systematically provide a detailed and
Peng He +4 more
openaire +3 more sources
Viral RNA at two stages of reovirus infection is required for the induction of necroptosis [PDF]
, 2017 Necroptosis, a regulated form of necrotic cell death, requires the activation of the RIP3 kinase. Here, we identify that infection of host cells with reovirus can result in necroptosis.
Berger, Angela K +6 more
core +2 more sources
Flicking the molecular switch underlying MLKL-mediated necroptosis [PDF]
Molecular & Cellular Oncology, 2015 The pseudokinase domain of the necroptosis effector mixed lineage kinase domain-like (MLKL) functions as a latch to restrain the unleashing of its N-terminal 4-helix bundle (4HB) domain. Cell death mediated by the 4HB domain relies on membrane association and oligomerization, which can be inhibited by an ATP-mimetic small molecule that binds the ...
Hildebrand, JM, Lucet, IS, Murphy, JM
openaire +3 more sources
MLKL inhibits intestinal tumorigenesis by suppressing STAT3 signaling pathway [PDF]
International Journal of Biological Sciences, 2021 Mixed lineage kinase domain-like protein (MLKL) plays an important role in necroptosis, but the role and mechanism of MLKL in intestinal tumorigenesis remain unclear. Here, we found that hematopoietic- and nonhematopoietic-derived MLKL affected intestinal inflammation, but nonhematopoietic-derived MLKL primarily inhibited intestinal tumorigenesis. Loss
Zhao, Qun +13 more
openaire +2 more sources
Neoplasia: An International Journal for Oncology Research, 2021 Burkitt's lymphoma (BL) is a highly aggressive form of B-cell non-Hodgkin's lymphoma. The clinical outcome in children with BL has improved over the last years but the prognosis for adults is still poor, highlighting the need for novel treatment ...
Annkathrin Koch +5 more
doaj +1 more source
Brainiac Caspases: Beyond the Wall of Apoptosis [PDF]
, 2019 For the last two decades, caspases, a family of cysteine-aspartic proteases, have evolved from being considered solely as regulators of apoptosis or inflammation to having a wider range of functions.
Alonso Bellido, Isabel María +3 more
core +1 more source
The pseudokinase MLKL mediates programmed hepatocellular necrosis independently of RIPK3 during hepatitis [PDF]
, 2016 Although necrosis and necroinflammation are central features of many liver diseases, the role of programmed necrosis in the context of inflammation-dependent hepatocellular death remains to be fully determined.
Andreas E. Kremer +24 more
core +1 more source