Results 71 to 80 of about 2,978 (173)

Identification of TRIM proteins as novel RIPK3 binding partners

, 2022
Receptor interacting protein kinase-3 (RIP3 or RIPK3) is serine threonine kinase largely essential protein in tumor necrosis factor (TNF)-induced necroptosis. It also plays a role in some inflammatory diseases.
Noh, Hyun Jin, Kim, You Sun, Park, Se Yeon, Park, Han Hee, Ha, Yu Jin, Lee, You Sang, Lee, Eun Ji, Kim, Min Kyoung   +7 more
core   +1 more source

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

Ca2+/Calmodulin-Dependent Protein Kinase II Regulation by RIPK3 Alleviates Necroptosis in Transverse Arch Constriction-Induced Heart Failure

Frontiers in Cardiovascular Medicine, 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, Jingjing Zhang, Jingjing Zhang, Jianan Qian, Xue Wang, Wei Zhang, Wei Zhang, Xiangfan Chen   +7 more
doaj   +1 more source

D4F‐Functionalized Ceria Nanozyme‐CasRx Platform Suppresses STING and Reprograms the Renal Immune Niche in Acute Kidney Injury

Advanced Science, EarlyView.
D4F‐functionalized ceria nanozyme–CasRx nanoparticles preferentially target renal macrophages through SR‐B1‐mediated uptake in ischemia–reperfusion injury. Ceria scavenges excessive ROS, while CasRx silences STING signaling, shifting macrophages toward a less inflammatory, pro‐resolving state and increasing the proportion of regulatory T cells.
Weibo Chen, Ming Li, Xuesheng Wang, Jiajia Sun, Ziyuan Zhang, Yongfeng Gong, Benkang Shi, Nengwang Yu, Yunuo Mao, Shengtian Zhao, Xiulin Zhang, Liqiang Guo   +11 more
wiley   +1 more source

RIPK1 both positively and negatively regulates RIPK3 oligomerization and necroptosis

, 2014
Necroptosis is a form of programmed cell death that depends on the activation of receptor interacting protein kinase-1 (RIPK1) and RIPK3 by receptors such as tumor necrosis factor (TNF) receptor-1.
Green, D.R., Tait, S.W.G., M L Albert, Orozco, S, Green, D R, N Yatim, Werner, M R, Oberst, A, S Orozco, A Oberst, S Y Gunja, Yatim, N, S WG Tait, M R Werner, H Tran, Werner, M.R., Gunja, S.Y., Albert, A, Albert, M.L., Oberst, A., D R Green, Tran, H., Tran, H, Tait, S Wg, Gunja, S y   +24 more
core   +1 more source

Impact of RIPK3 on tissue cytokine levels.

, 2022
(A) Heat map comparing mRNA patterns of immune-related genes in brain from WT and Ripk3−/− mice (n = 3 for each group) at 5 dpi, where mean fold-change of each transcript was compared to normalized expression of all WT immune-related transcripts.
Edward S. Mocarski (8628189), Richard D. Dix (9611146), Hongyan Guo (74519), Heather S. Koehler (13822874)   +3 more
core   +1 more source

A viable kinase-inactive RIPK3 D143N mouse model reveals its scaffold function in driving TNF-induced inflammatory disorder

Cell Death Discovery
RIPK3 is a key regulator of necroptosis, but the specific roles of its kinase-dependent and -independent functions in disease pathogenesis remain poorly understood.
Yayun Du, Jingjing Li, Cong Zhao, Shouqiao Hou, Qiuye Li, Xiangping Xu, Zhanhui Li, Jiaying Qiu, Changyu Zhuang, Lifen Xie, Feng Ma, Xiaohu Zhang, Xiaoliang Yu, Sudan He   +13 more
doaj   +1 more source

Autophagy-Related LC3 Accumulation Interacted Directly With LIR Containing RIPK1 and RIPK3, Stimulating Necroptosis in Hypoxic Cardiomyocytes

Frontiers in Cell and Developmental Biology, 2021
The exact relationships and detailed mechanisms between autophagy and necroptosis remain obscure. Here, we demonstrated the link between accumulated autophagosome and necroptosis by intervening with autophagic flux.
Yao Huang, Yanhai Feng, Lin Cui, Lei Yang, Qiong Zhang, Junhui Zhang, Xupin Jiang, Xingyue Zhang, Yanling Lv, Jie-Zhi Jia, Dong-Xia Zhang, Yue-Sheng Huang, Yue-Sheng Huang   +12 more
doaj   +1 more source

A Rare RIPK3 Variant Enhances Necroptosis and Promotes Inflammation in a Still Disease–Like Autoinflammatory Syndrome

Arthritis &Rheumatology, EarlyView.
Objective Still disease represents a prototypical polygenic systemic autoinflammatory disease, characterized by recurrent systemic inflammation and dysregulation of innate immunity. Despite extensive clinical characterization, familial clustering Still disease remains unreported.
Longfang Chen, Qihua Dai, Yu Xiao, Jialin Dai, Mengyan Wang, Yuning Ma, Yujie Shen, Zhimo Xu, Jianfen Meng, Xia Chen, Da Yi, Yue Sun, Hui Shi, Honglei Liu, Xiaobing Cheng, Yutong Su, Junna Ye, Huihui Chi, Zhuochao Zhou, Tingting Liu, Jialin Teng, Chengde Yang, Jinchao Jia, Qiongyi Hu   +23 more
wiley   +1 more source

Human Monocytic Models Reveal Genotype‐Dependent Inflammatory Programs in VEXAS Syndrome

Arthritis &Rheumatology, Accepted Article.
Objectives VEXAS syndrome is a severe X‐linked autoinflammatory disorder caused by somatic mutations in ubiquitin‐like modifier activating enzyme 1 (UBA1), with clinical outcomes that vary by UBA1 genotype. We aimed to elucidate genotype‐specific inflammatory programs and identify potential therapeutic targets.
Kana Higashitani, Tatsuma Ban, Yohei Kirino, Go R Sato, Soichiro Adachi, Yuki Iizuka, Kayo Harita, Ayaka Maeda, Osamu Ohara, Hideaki Nakajima, Tomohiko Tamura   +10 more
wiley   +1 more source