Results 51 to 60 of about 14,072 (183)

Human RIPK3 maintains MLKL in an inactive conformation prior to cell death by necroptosis [PDF]

, 2021
The ancestral origins of the lytic cell death mode, necroptosis, lie in host defense. However, the dysregulation of necroptosis in inflammatory diseases has led to widespread interest in targeting the pathway therapeutically.
Garnier, Jean Marc, Cowan, Angus D.; id_orcid, Luo, Cindy, Fitzgibbon, Cheree, Garnish, Sarah E., Sandow, Jarrod J., Murphy, James M., Horne, Christopher R., Czabotar, Peter E., Liang, Lung Yu, Davies, Katherine A., Lessene, Guillaume, Samson, Andre L., Meng, Yanxiang, Young, Samuel N., Meng, Y, Liang, LY, Samson, AL, Horne, CR, Fitzgibbon, C, Lessene, G, Garnier, JM, Cowan, AD, Young, SN, Murphy, JM, Davies, KA, Czabotar, PE, Sandow, JJ, Garnish, SE, Luo, C, James M. Murphy, Katherine A. Davies, Andre L. Samson, Cindy Luo, Guillaume Lessene, Christopher R. Horne, Peter E. Czabotar, Samuel N. Young, Yanxiang Meng, Lung-Yu Liang, Jean-Marc Garnier, Cheree Fitzgibbon, Jarrod J. Sandow, Sarah E. Garnish, Angus D. Cowan   +44 more
core   +1 more source

A RIPK3-independent role of MLKL in suppressing parthanatos promotes immune evasion in hepatocellular carcinoma

Cell Discovery, 2023
Mixed lineage kinase domain-like (MLKL) is widely accepted as an executioner of necroptosis, in which MLKL mediates necroptotic signaling and triggers cell death in a receptor-interacting protein kinase 3 (RIPK3)-dependent manner.
Xifei Jiang, Wenjia Deng, Siyao Tao, Zheng Tang, Yuehong Chen, Mengxin Tian, Ting Wang, Chenyang Tao, Yize Li, Yuan Fang, Congying Pu, Jun Gao, Xiaomin Wang, Weifeng Qu, Xiameng Gai, Zhenbin Ding, Yixian Fu, Ying Zheng, Siyuwei Cao, Jian Zhou, Min Huang, Weiren Liu, Jun Xu, Jia Fan, Yinghong Shi   +24 more
doaj   +1 more source

Mixed lineage kinase-like protein protects against Clostridium perfringens infection by enhancing NLRP3 inflammasome-extracellular traps axis

iScience, 2022
Summary: Despite intense research in understanding Clostridium perfringens (C. perfringens) pathogenesis, the mechanisms by which it is cleared from the host are largely unclarified. In C.
Yang Liu, Li-Hua Xing, Fen-Xin Li, Na Wang, Yu-Ze Ma, Jian-Wei Li, Yu-Jing Wu, Jing Liang, Yu-Xin Lei, Xue-Yin Wang, Fan-Hua Meng, Yong-Jun Yang, Guang-Peng Li, Xiao Wang, Shui-Xing Yu   +14 more
doaj   +1 more source

Structural Insights into RIP3-Mediated Necroptotic Signaling

Cell Reports, 2013
RIP3 is an essential upstream kinase in necroptosis. The pseudokinase MLKL functions as a substrate of RIP3 to mediate downstream signaling. The molecular mechanism by which RIP3 recognizes and phosphorylates MLKL remains unknown.
Tian Xie, Wei Peng, Chuangye Yan, Jianping Wu, Xinqi Gong, Yigong Shi   +5 more
doaj   +1 more source

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

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, Toshiyuki Yano, Hiromitsu Kanamori, Daigo Nagahara, Atsuko Muranaka, Hidemichi Kouzu, Atsushi Mochizuki, Masayuki Koyama, Nobutaka Nagano, Takefumi Fujito, Ryo Nishikawa, Naoyuki Kamiyama, Marenao Tanaka, Atsushi Kuno, Masaya Tanno, Tetsuji Miura   +15 more
doaj   +1 more source

The necroptosis-inducing pseudokinase mixed lineage kinase domain-like regulates the adipogenic differentiation of pre-adipocytes

iScience, 2022
Summary: Receptor-interacting protein kinase-3 (RIPK3) and mixed lineage kinase domain-like (MLKL) proteins are key regulators of necroptosis, a highly pro-inflammatory mode of cell death, which has been involved in various human diseases.
Julie Magusto, Carine Beaupère, Marta B. Afonso, Martine Auclair, Jean-Louis Delaunay, Pierre-Antoine Soret, Gilles Courtois, Tounsia Aït-Slimane, Chantal Housset, Isabelle Jéru, Bruno Fève, Vlad Ratziu, Cecilia M.P. Rodrigues, Jérémie Gautheron   +13 more
doaj   +1 more source

MLKL variant call files- place holder

, 2023
Variant call files for MLKL p.Ser132Pro polymorphism ...
Hildebrand, Joanne
core   +1 more source

A Plug Release Mechanism for Membrane Permeation by MLKL [PDF]

Structure, 2014
MLKL is crucial for necroptosis, permeabilizing membranes through its N-terminal region upon phosphorylation of its kinase-like domain by RIP3. However, the mechanism underlying membrane permeabilization is unknown. The solution structure of the MLKL N-terminal region determined by nuclear magnetic resonance spectroscopy reveals a four-helix bundle ...
Su, Lijing, Quade, Bradley, Wang, Huayi, Sun, Liming, Wang, Xiaodong, Rizo, Josep   +5 more
openaire   +2 more sources

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

Frontiers 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, Bo Lin, Wei Chen, Rui-Qi Cao, Yi Guo, Ali Said, Taous Khan, Hui-Ling Zhang, Yong-Ming Zhu   +8 more
doaj   +1 more source

Necroptosis induced by RIPK3 requires MLKL but not Drp1 [PDF]

Cell Death & Disease, 2014
Necroptosis is a mechanism by which cells can kill themselves that does not require caspase activity or the presence of the pro-apoptotic Bcl-2 family members Bax or Bak. It has been reported that RIPK3 (receptor interacting protein kinase 3) activates MLKL (mixed lineage kinase domain-like) to cause cell death that requires dynamin-related protein 1 ...
Moujalled, DM, Cook, WD, Murphy, JM, Vaux, DL   +3 more
openaire   +3 more sources