Targeting PANoptosis in Bacterial-Induced Inflammatory Diseases: Mechanisms and Therapeutic Interventions. [PDF]
Wang T, Lu Y, Zhang X, Yu F.
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The TNFR-RIPK1/RIPK3 signalling pathway mediates the effect of lanthanum on necroptosis of nerve cells. [PDF]
Jin B +7 more
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O-GlcNAcylation in novel regulated cell death: ferroptosis, pyroptosis, and necroptosis. [PDF]
Wang YZ, Zhao HY, Nyima T, Ma Z.
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RIPK1 Drives JAK1-STAT3 Signaling to Promote CXCL1-Mediated Neutrophil Recruitment in Sepsis-Induced Lung Injury. [PDF]
Sun H +15 more
europepmc +1 more source
TAK1 activates PANoptosis through the NF-κB signalling pathway to delay diabetic wound healing. [PDF]
Wang X +8 more
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Design, Optimization, and Development of RIPK1 Degraders with Improved Pharmacokinetic and Pharmacodynamic Properties. [PDF]
Lu D +9 more
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Genetic Regulation of RIPK1 and Necroptosis
Annual Review of Genetics, 2021The receptor-interacting protein kinase 1 (RIPK1) is recognized as a master upstream regulator that controls cell survival and inflammatory signaling as well as multiple cell death pathways, including apoptosis and necroptosis. The activation of RIPK1 kinase is extensively modulated by ubiquitination and phosphorylation, which are mediated by multiple
Daichao, Xu, Chengyu, Zou, Junying, Yuan
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RIPK1 and RIPK3 in antibacterial defence
Biochemical Society Transactions, 2022Upon sensing pathogenic bacterial infection, host cells activate a multitude of inflammatory and immunogenic responses to promote bacterial clearance and restore tissue homeostasis. RIPK1 and RIPK3 are two key players in antimicrobial defence, by either driving inflammatory signalling or inducing programmed cell death activation, ranging from apoptosis,
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RIPK1 ubiquitination: Evidence, correlations and the undefined
Seminars in Cell & Developmental Biology, 2021Over the last two decades the mechanisms that underpin cell survival and cell death have been intensively studied. One molecule in particular, Receptor Interacting Protein Kinase 1 (RIPK1), has gained interest due to the ability to function upstream of both NF-κB signaling and caspase-dependent and -independent cell death.
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