Results 51 to 60 of about 15,294 (209)

Roles of RIPK3 in necroptosis, cell signaling, and disease

open access: yesExperimental & Molecular Medicine, 2022
AbstractReceptor-interacting protein kinase-3 (RIPK3, or RIP3) is an essential protein in the “programmed” and “regulated” cell death pathway called necroptosis. Necroptosis is activated by the death receptor ligands and pattern recognition receptors of the innate immune system, and the findings of many reports have suggested that necroptosis is highly
Michael J. Morgan, You-Sun Kim
openaire   +2 more sources

Identification of TRIM proteins as novel RIPK3 binding partners

open access: yes, 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   +7 more
core   +1 more source

Genomic locus proteomic screening identifies the NF-κB signaling pathway components NFκB1 and IKBKG as transcriptional regulators of Ripk3 in endothelial cells.

open access: yesPLoS ONE, 2021
The receptor-interacting protein kinase 3 (RIPK3) is a multi-functional protein best known for facilitating cellular necroptosis and inflammation. Recent evidence from our lab indicates that RIPK3 expression must be tightly regulated in endothelial cells
Siqi Gao   +3 more
doaj   +1 more source

NET formation can occur independently of RIPK3 and MLKL signaling [PDF]

open access: yes, 2016
The importance of neutrophil extracellular traps (NETs) in innate immunity is well established but the molecular mechanisms responsible for their formation are still a matter of scientific dispute.
Kaufmann, Thomas   +23 more
core   +2 more sources

Supplementary Figure 1C from Somatic Epigenetic Silencing of RIPK3 Inactivates Necroptosis and Contributes to Chemoresistance in Malignant Mesothelioma

open access: yes, 2021
Immunoblot analysis demonstrating re-expression of wild type (WT) or kinase dead (KD) RIPK3 in four RIPK3-negative human MM cell lines after infection with lentivirus for 24 h.
Eleonora Sementino (14916552)   +14 more
core   +1 more source

RIPK3 promotes adenovirus type 5 activity [PDF]

open access: yesCell Death & Disease, 2017
AbstractOncolytic adenoviral mutants infect human malignant cells and replicate selectively within them. This induces direct cytotoxicity that can also trigger profound innate and adaptive immune responses. However, the mechanism by which adenoviruses produce cell death remains uncertain.
Melanie Weigert   +12 more
openaire   +4 more sources

RIPK1-RIPK3 mediates myocardial fibrosis in type 2 diabetes mellitus by impairing autophagic flux of cardiac fibroblasts

open access: yesCell Death and Disease, 2022
Receptor-interacting protein kinase 1 (RIPK1) and 3 (RIPK3) are critical regulators of programmed necrosis or necroptosis. However, the role of the RIPK1/RIPK3 signaling pathway in myocardial fibrosis and related diabetic cardiomyopathy is still unclear.
Shigang Qiao   +9 more
doaj   +1 more source

Role of RIPK3 in IAV-activated transcriptional responses.

open access: yes, 2016
(A) Heatmap depicting behavior of IAV-regulated genes in ripk3+/+ MEFs (columns 1–4) or ripk3+/+ MEFs treated with the RIPK3 inhibitor (GSK’872 at 5μM, columns 5–8) or ripk3-/- MEFs (columns 9–12) following PR8-ΔNS1 infection for the indicated times. All
Shoko Nogusa (347948)   +4 more
core   +1 more source

RIPK3—a predictive marker for personalized immunotherapy? [PDF]

open access: yesOncoImmunology, 2016
Cancer immunotherapy is an attractive therapeutic option but it is currently unclear which patient may benefit from such approaches. Using the model of cervical cancer, we have demonstrated that PolyIC-driven immunogenicity strictly depends on the necroptosis regulator RIPK3 in the neoplastic cells.
openaire   +3 more sources

SR‐A3 Promotes USP18‐Mediated deISGylation of STING to Protect Against Myocardial Ischemia‐Reperfusion Injury

open access: yesAdvanced Science, EarlyView.
MI/RI is a major clinical challenge with high morbidity and mortality. This study demonstrates that SR‐A3 expression is downregulated in MI/RI, and its deletion exacerbates damage via the USP18/ISG15/STING axis, revealing SR‐A3 as a potential therapeutic target.
Yufei Han   +24 more
wiley   +1 more source

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