The regulation of MLKL function during apoptosis [PDF]
, 2016 细胞凋亡是主动性的细胞死亡过程，半胱氨酸蛋白酶caspase在细胞凋亡中发挥着主要作用，因此细胞凋亡也被称为caspase依赖的细胞死亡过程。与细胞凋亡不同，长期以来细胞坏死都被认为是极端理化因素刺激的结果，是不受调控的被动性细胞死亡过程。然而近些年的研究表明，细胞坏死也是受调控的，在包括机体发育、组织损伤应答和抗病毒免疫的多种生理和病理中发挥着重要作用。RIP3是细胞坏死应答的决定因子，当然还有一些重要的蛋白也参与其中，例如RIP1和MLKL。 细胞凋亡和细胞坏死作为细胞程序性死亡的两种主要途径 ...
江诗浩
core
Linear ubiquitin chain assembly complex coordinates late thymic T-cell differentiation and regulatory T-cell homeostasis. [PDF]
, 2016 The linear ubiquitin chain assembly complex (LUBAC) is essential for innate immunity in mice and humans, yet its role in adaptive immunity is unclear. Here we show that the LUBAC components HOIP, HOIL-1 and SHARPIN have essential roles in late thymocyte ...
Alvarez-Diaz, S +20 more
core +1 more source
Bacillus cereus Induces Necroptosis in Microglia via the RIPK1/3‐MLKL Pathway
MicrobiologyOpen, Volume 15, Issue 2, April 2026.Bacillus cereus induces necroptosis in murine/human microglia via the RIPK1/3‐MLKL pathway, triggering inflammatory cytokine release—uncovering a new pathogenic mechanism for its severe ocular infection. ABSTRACT Bacillus cereus endophthalmitis is a rapidly progressing intraocular infection that often results in poor visual outcomes due to extensive ...
Jing Yang +7 more
wiley +1 more source
The establishment and mechanism research in the mice model of actue liver failure [PDF]
, 2016 背景和目的：急性肝衰竭（acuteliverfailure，ALF）是一个危及生命的严重病理生理状态。它可导致肝脏合成、排泄、解毒、生物转化等功能发生严重障碍或失代偿，出现凝血功能障碍、黄疸以及肝性脑病等主要表现的临床综合征。因其死亡率极高，严重ALF的治疗是当今临床医学中最具有挑战的课题之一。为了有效地治疗ALF，制备与ALF发病经过相同、临床表现类似并可复制的物模型是解决此难题的第一步，而了解各种ALF动物模型的构建机制就显得尤为重要。本课题以氧化偶氮甲烷（azoxymethane，AOM ...
金丽鑫
core
Poly-ubiquitination in TNFR1-mediated necroptosis [PDF]
, 2016 Tumor necrosis factor (TNF) is a master pro-inflammatory cytokine, and inappropriate TNF signaling is implicated in the pathology of many inflammatory diseases.
Henning Walczak +3 more
core +3 more sources
Cerebral Infarction: Epidemiology, Classification, Mechanisms, Diagnosis, and Management
MedComm, Volume 7, Issue 4, April 2026.Within minutes after ischemia onset, deprivation of oxygen and glucose leads to rapid ATP depletion, resulting in failure of Na+/K+‐ATPase activity and membrane depolarization. This ionic imbalance promotes uncontrolled synaptic release of glutamate and excessive activation of postsynaptic NMDA and AMPA receptors.
Meibiao Zhang +4 more
wiley +1 more source
Holding RIPK1 on the Ubiquitin Leash in TNFR1 Signaling [PDF]
, 2016 The kinase RIPK1 is an essential signaling node in various innate immune signaling pathways being most extensively studied in the TNFR1 signaling pathway.
Darding, M, Peltzer, N, Walczak, H
core
The evolving world of pseudoenzymes: proteins, prejudice and zombies [PDF]
, 2016 Pseudoenzymes are catalytically deficient variants of enzymes that are represented in all major enzyme families. Their regulatory functions in signalling pathways are shedding new light on the non-catalytic functions of active enzymes, and are suggesting
Eyers, Patrick A, Murphy, James M
core +1 more source
NEMO regulates a cell death switch in TNF signaling by inhibiting recruitment of RIPK3 to the cell death-inducing complex II [PDF]
, 2016 Incontinentia Pigmenti (IP) is a rare X-linked disease characterized by early male lethality and multiple abnormalities in heterozygous females. IP is caused by NF-κB essential modulator (NEMO) mutations.
Draber, P +4 more
core +1 more source
Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
Journal of Visualized Experiments, 2018 Necroptosis is a programmed cell death pathway triggered by activation of receptor interacting protein kinase 3 (RIPK3), which phosphorylates and activates the mixed lineage kinase-like domain pseudokinase, MLKL, to rupture or permeabilize the plasma membrane.
Dan E, McNamara +4 more
openaire +3 more sources