Results 61 to 70 of about 52,832 (305)

RIP1-HAT1-SirT complex identification and targeting in treatment and prevention of cancer [PDF]

open access: yes, 2018
Purpose: Alteration in cell death is a hallmark of cancer. A functional role regulating survival, apoptosis, and necroptosis has been attributed to RIP1/3 complexes.Experimental Design: We have investigated the role of RIP1 and the effects of MC2494 in ...
A. Baldi   +23 more
core   +2 more sources

Necroptosis in development and diseases [PDF]

open access: yesGenes & Development, 2018
Necroptosis, a form of regulated necrotic cell death mediated by RIPK1 (receptor-interacting protein kinase 1) kinase activity, RIPK3, and MLKL (mixed-lineage kinase domain-like pseudokinase), can be activated under apoptosis-deficient conditions. Modulating the activation of RIPK1 by ubiquitination and phosphorylation is critical to control both ...
Shan, Bing   +3 more
openaire   +2 more sources

Kinase-independent function of RIP1, critical for mature T-cell survival and proliferation. [PDF]

open access: yes, 2016
The death receptor, Fas, triggers apoptotic death and is essential for maintaining homeostasis in the peripheral lymphoid organs. RIP1 was originally cloned when searching for Fas-binding proteins and was later shown to associate also with the signaling ...
Bertin, John   +4 more
core   +2 more sources

An Inflammatory Perspective on Necroptosis [PDF]

open access: yesMolecular Cell, 2017
Necroptosis (programmed necrosis) occurs in response to TNF, Fas, or TRAIL, as well as certain TLR ligands, when caspase activity required for apoptosis is blocked. Necroptosis is typically considered a highly pro-inflammatory mode of cell death, due to release of intracellular "danger signals" that promote inflammation.
Conor J, Kearney, Seamus J, Martin
openaire   +2 more sources

Aging Is a Key Driver for Adult Acute Myeloid Leukemia

open access: yesAging and Cancer, EarlyView.
Acute myeloid leukemia (AML) is a classical age‐related hematologic malignancy, and a key driver of AML is aging, which profoundly regulates intrinsic factors such as genomic instability, epigenetic reprogramming, and metabolic dysregulation, and alters bone marrow microenvironment.
Rong Yin, Haojian Zhang
wiley   +1 more source

TNF receptor–related factor 3 inactivation promotes the development of intrahepatic cholangiocarcinoma through NF‐κB‐inducing kinase–mediated hepatocyte transdifferentiation

open access: yesHepatology, EarlyView., 2022
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

4-Hydroxy-2-Nonenal Promotes Cardiomyocyte Necroptosis via Stabilizing Receptor-Interacting Serine/Threonine-Protein Kinase 1

open access: yesFrontiers in Cell and Developmental Biology, 2021
Background: Necroptosis is a vital regulator of myocardial ischemia/reperfusion (MI/R) injury. Meanwhile, 4-hydroxy-2-nonenal (4-HNE) is abundantly increased during MI/R injury. However, whether 4-HNE induces cardiomyocyte necroptosis during MI/R remains
Xiaoxuan Zhai   +72 more
doaj   +1 more source

Optineurin functions for optimal immunity [PDF]

open access: yes, 2018
Optineurin (OPTN) was identified 20 years ago in a yeast-two-hybrid screen with a viral protein known to inhibit the cytolytic effects of tumor necrosis factor.
Slowicka, Karolina, van Loo, Geert
core   +1 more source

Super‐Refractory Status Epilepticus (SRSE) in a Patient With Compound Heterozygous OPA1 Variants: Case Report and Literature Review

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
ABSTRACT Objective Super‐Refractory Status Epilepticus (SRSE) is a rare, life‐threatening neurological emergency with unclear etiology in many cases. Mitochondrial dysfunction, often due to disease‐causing genetic variants, is increasingly recognized as a cause, with each gene producing distinct pathophysiological mechanisms.
Pouria Mohammadi   +2 more
wiley   +1 more source

Macrophage‐derived MLKL in alcohol‐associated liver disease: Regulation of phagocytosis

open access: yesHepatology, EarlyView., 2022
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

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