Results 91 to 100 of about 15,294 (209)

Cytotoxicity of crystals involves RIPK3-MLKL-mediated necroptosis [PDF]

Nature Communications, 2016
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 ...
Mulay, Shrikant R., Desai, Jyaysi, Kumar, Santhosh V., Eberhard, Jonathan N., Thomasova, Dana, ROMOLI, SIMONE, Grigorescu, Melissa, Kulkarni, Onkar P., Popper, Bastian, Vielhauer, Volker, Zuchtriegel, Gabriele, Reichel, Christoph, Bräsen, Jan Hinrich, ROMAGNANI, PAOLA, Bilyy, Rostyslav, Munoz, Luis E., Herrmann, Martin, Liapis, Helen, Krautwald, Stefan, Linkermann, Andreas, ANDERS, HANS JOACHIM   +20 more
openaire   +5 more sources

RIPK3 impacts antibody generation in an induced model of murine lupus through mechanisms other than necroptosis and antigen presentation

Frontiers in Immunology
IntroductionReceptor-interacting protein kinase 3 (RIPK3) is a protein involved in cell death and inflammatory processes. The most recognized function of RIPK3 is the induction of necroptosis, an inflammatory type of cell death that is dependent on RIPK3
Céleste Pilon, Elena Lonina, Jerrold S. Levine, Jerrold S. Levine, Sylvie Lesage, Sylvie Lesage, Joyce Rauch   +6 more
doaj   +1 more source

Photoactivated iridium(III) complexes drive pyroptosis–necroptosis synergy for multi‐network photoimmunotherapy of renal cell carcinoma

Smart Molecules, EarlyView.
Photoactivated iridium(III) complexes trigger mitochondrial DNA leakage and Ca²⁺ efflux, simultaneously driving pyroptosis and necroptosis to synergistically enhance immunogenic cell death. This multi‐network cascade promotes dendritic cell maturation and CD8⁺ T cell activation, achieving potent photoimmunotherapy of renal cell carcinoma.
Xin Qin, Meng‐Di Chen, Wenqi Gao, Yiping Wang, Lin‐Qing Liu, Zhen Teng, Tienan Qi, Qiyuan Wang, Yuxuan Wang, Daoxiang Li, Keqiang Yan, Ling Pan, Zhongwei Zhao, Shuo Zhao, Kang‐Nan Wang, Shuai Fu, Nengwang Yu   +16 more
wiley   +1 more source

Deciphering diverse cell‐death patterns to predict the prognosis and potential therapy target of hepatocellular carcinoma patients

VIEW, EarlyView.
Abstract Ninety percent of all primary liver malignancies are hepatocellular carcinomas (HCC), making liver cancer the third most common cause of cancer‐associated mortality. Different patterns of programmed cell death (PCD) are crucial for the survival of tumors, and they might serve as a prognostic marker for HCC.
Lin Ding, Qian Li, Wenjing Yang, Te Liu, Tongtong Tian, Yu Liu, Chunyan Zhang, Baishen Pan, Beili Wang, Fan Wu, Wei Guo   +10 more
wiley   +1 more source

Data_Sheet_1_Ca2+/Calmodulin-Dependent Protein Kinase II Regulation by RIPK3 Alleviates Necroptosis in Transverse Arch Constriction-Induced Heart Failure.XLSX

, 2022
Some studies have reported that the activation of Ca2+/calmodulin dependent protein kinase (CaMKII) plays a vital role in the pathogenesis of cardiovascular disease.
Ji Cao (237887), Xue Wang (102830), Wei Zhang (405), Jianan Qian (12471321), Xiangfan Chen (3345482), Jingjing Zhang (163589)   +5 more
core   +1 more source

Ammonia Accumulation Drives Intervertebral Disc Degeneration by Triggering Ammonia‐Induced Cell Death Through Lysosome–Mitochondria Crosstalk

Cell Proliferation, EarlyView.
Mechanical strain disrupts the lysosome‐mitochondria axis via GLS1‐mediated ammonia toxicity, causing NP cell death and ECM breakdown in IVDD. CB839‐mediated GLS1 inhibition effectively rescues cellular homeostasis and alleviates disc degeneration.
Yang Zhang, Yucheng Gao, Shuhang Dong, Shuanggong Liu, Lei Liu, Ziyi Song, Jie Xu, Yijun Rong, Guangxu Song, Yingze Zhang, Dongjin Wu, Zengxin Gao   +11 more
wiley   +1 more source

The ubiquitin-modifying enzyme A20 restricts ubiquitination of the kinase RIPK3 and protects cells from necroptosis [PDF]

, 2015
A20 is a deubiquitinating enzyme that restrict inflammation by various mechanisms. Ma and colleagues show that A20 inhibits necroptosis by inhibiting the ubiquitination of RIPK3 and formation of the RIPK1-RIPK3 ...
Rita Tavares, Barbara A Malynn, Malynn, Barbara A, Hao Wu, Averil Ma, Onizawa, Michio, Rommel Advincula, Schulze-Topphoff, Ulf, Duong, Bao, Ma, Averil, Agelidis, Alex, Shigeru Oshima, Timothy Lu, Alma Burlingame, Barrera, Julio, Burlingame, Alma, Alex Agelidis, Michio Onizawa, Wu, Hao, Julio Barrera, Tavares, Rita, Oshima, Shigeru, Prodhomme, Thomas, Whang, Michael I, Advincula, Rommel, Oses-Prieto, Juan A, Juan A Oses-Prieto, Michael I Whang, Thomas Prodhomme, Scott S Zamvil, Zamvil, Scott S, Lu, Timothy, Ulf Schulze-Topphoff, Bao Duong   +33 more
core   +1 more source

A comparative analysis of cell death signalling in RNA and DNA virus infections and potential inhibitory strategies

The FEBS Journal, EarlyView.
RNA and DNA viruses can manipulate host cell death through various mechanisms. RNA viruses (H1N1, SARS‐CoV‐2) induce acute apoptosis, necroptosis, and pyroptosis to promote rapid viral transmission and epithelial barrier damage. In contrast, DNA viruses (HSV‐1, EBV) regulate these mechanisms to sustain a lytic‐latency cycle, evade immune response and ...
Panagiotis Keramidas, Maria Pitou, Amalia Aggeli, Sotiris Varlamis, Theodora Choli‐Papadopoulou   +4 more
wiley   +1 more source

Data_Sheet_1_Catecholamine Surges Cause Cardiomyocyte Necroptosis via a RIPK1–RIPK3-Dependent Pathway in Mice.PDF

, 2021
Background: Catecholamine surges and resultant excessive β-adrenergic stimulation occur in a broad spectrum of diseases. Excessive β-adrenergic stimulation causes cardiomyocyte necrosis, but the underlying mechanism remains obscure.
Xuejun Wang (174299), Mingqi Cai (9911052), Jinbao Liu (292973), Penglong Wu (9592058)   +3 more
core   +1 more source

Intercellular propagation of RIPK1/RIPK3 amyloid fibrils

Proceedings of the National Academy of Sciences
The canonical necrosome formed by receptor-interacting protein kinase 1 (RIPK1) and RIPK3 is a functional amyloid fibril structure critical to intracellularly drive necroptosis. Since necroptosis leads to the release of intracellular content, the fate of RIPK1/RIPK3 fibrils after necroptotic cell death has not been investigated.
Yeyang Ma, Qiuyuan Zhang, Dekang Li, Kun Zhao, Zefei Li, Yuan Liu, Chu Wang, Bo Sun, Dan Li, Junying Yuan, Cong Liu   +10 more
openaire   +2 more sources