Results 11 to 20 of about 6,382 (183)
HSP70 promotes MLKL polymerization and necroptosis [PDF]
Mixed lineage kinase domain-like protein (MLKL) is the proposed executioner of necroptosis. Our recent findings identify a novel inhibitor necroptosis-blocking compound 1 (NBC1) which specifically conjugates to two cysteines of heat shock protein 70 ...
Andrea N. Johnston, Zhigao Wang
doaj +3 more sources
Interferons Transcriptionally Up-Regulate MLKL Expression in Cancer Cells
Interferons (IFNs) are key players in the tumor immune response and act by inducing the expression of IFN-stimulated genes (ISGs). Here, we identify the mixed-lineage kinase domain-like pseudokinase (MLKL) as an ISG in various cancer cell lines.
Anne-Kathrin Knuth +5 more
doaj +5 more sources
The molecular mechanisms of MLKL-dependent and MLKL-independent necrosis [PDF]
AbstractNecrosis, a type of unwanted and passive cell demise, usually occurs under the excessive external stress and is considered to be unregulated. However, under some special conditions such as caspase inhibition, necrosis is regulable in a well-orchestrated way.
Li, Lu +4 more
openaire +2 more sources
Cytotoxicity of crystals involves RIPK3-MLKL-mediated necroptosis [PDF]
AbstractCrystals cause injury in numerous disorders, and induce inflammation via the NLRP3 inflammasome, however, it remains unclear how crystals induce cell death. Here we report that crystals of calcium oxalate, monosodium urate, calcium pyrophosphate dihydrate and cystine trigger caspase-independent cell death in five different cell types, which is ...
et al,, Liapis, Helen
core +8 more sources
MLKL D144K mutation activates the necroptotic activity of the N-terminal MLKL domain [PDF]
AbstractMixed-lineage kinase domain-like protein (MLKL) is an essential effector protein of necroptotic cell death. The four-helix bundle domain (4HB) presented by the first 125 amino acids of the N-terminal domain is sufficient for its necroptotic activity. However, it has been proposed that the subsequent helix H6 of the brace region has a regulatory
Katja Hrovat-Schaale +4 more
openaire +1 more source
Abstract Background and Aims Intrahepatic cholangiocarcinoma (ICC) is a deadly but poorly understood disease, and its treatment options are very limited. The aim of this study was to identify the molecular drivers of ICC and search for therapeutic targets.
Yuto Shiode +16 more
wiley +1 more source
Macrophage‐derived MLKL in alcohol‐associated liver disease: Regulation of phagocytosis
EtOH causes leaky gut allowing bacteria and PAMPs into the liver, resulting in hepatic inflammation and injury. We demonstrate that LPS induces STAT1‐mediated expression and phosphorylation of MLKL in macrophages and identify a novel function that myeloid MLKL translocates to phagosomes and lysosomes and regulates phagocytosis, which contributes to the
Xiaoqin Wu +16 more
wiley +1 more source
RIPK3 dampens mitochondrial bioenergetics and lipid droplet dynamics in metabolic liver disease
RIPK3 dampens mitochondrial bioenergetics and lipid droplet dynamics in metabolic liver disease. Abstract Background and Aims Receptor‐interacting protein kinase 3 (RIPK3) mediates NAFLD progression, but its metabolic function is unclear. Here, we aimed to investigate the role of RIPK3 in modulating mitochondria function, coupled with lipid droplet (LD)
Marta B. Afonso +16 more
wiley +1 more source
MLKL regulates necrotic plasma membrane permeabilization [PDF]
Recent data from two independent laboratories have shed new light on the molecular mechanisms by which mixed lineage kinase domain-like (MLKL) promotes a peculiar form of regulated necrosis known as necroptosis. Upon phosphorylation by receptor-interacting protein kinase 3 (RIPK3), MLKL appears indeed to form oligomers that localize to the plasma ...
Lorenzo, Galluzzi +2 more
openaire +2 more sources
Phosphorylated MLKL causes plasma membrane rupture [PDF]
Necroptosis, cell death caused by uncontrolled swelling (oncosis) and rapid plasma membrane rupture, exerts detrimental pathogenic effects.1,2 According to recent reports by Wang et al.3 in Molecul...
Linkermann, Andreas +2 more
openaire +2 more sources

