Results 11 to 20 of about 17,129 (242)

Ubiquitylation of RIPK3 beyond-the-RHIM can limit RIPK3 activity and cell death [PDF]

open access: yesiScience, 2022
Summary: Pathogen recognition and TNF receptors signal via receptor interacting serine/threonine kinase-3 (RIPK3) to cause cell death, including MLKL-mediated necroptosis and caspase-8-dependent apoptosis. However, the post-translational control of RIPK3
Daniel Frank   +23 more
doaj   +6 more sources

RIPK3 and kidney disease

open access: yesNefrología
Receptor interacting protein kinase 3 (RIPK3) is an intracellular kinase at the crossroads of cell death and inflammation. RIPK3 contains a RIP homotypic interaction motif (RHIM) domain which allows interactions with other RHIM-containing proteins and a ...
Juan Guerrero-Mauvecin   +4 more
doaj   +6 more sources

PRMT5-mediated regulatory arginine methylation of RIPK3 [PDF]

open access: yesCell Death Discovery, 2023
The TNF receptor-interacting protein kinases (RIPK)-1 and 3 are regulators of extrinsic cell death response pathways, where RIPK1 makes the cell survival or death decisions by associating with distinct complexes mediating survival signaling, caspase ...
Chanchal Chauhan   +7 more
doaj   +4 more sources

RIPK3 Slams the Brake on Leukemogenesis [PDF]

open access: bronzeCancer Cell, 2016
Evasion of cell death is a key hallmark of cancers. In this issue of Cancer Cell, Höckendorf and colleagues identified RIPK3, an essential kinase for necroptosis, as having a key role in inhibiting acute myeloid leukemia development.
Francis K.L. Chan
openalex   +3 more sources

Comparative and evolutionary analysis of RIP kinases in immune responses

open access: yesFrontiers in Genetics, 2022
The group of receptor-interacting protein (RIP) kinases has seven members (RIPK1–7), with one homologous kinase domain but distinct non-kinase regions.
Shangge Lv   +8 more
doaj   +1 more source

Low-Dose Resveratrol Inhibits RIPK3-Mediated Necroptosis and Delays the Onset of Age-Related Hearing Loss

open access: yesFrontiers in Pharmacology, 2022
Background: To investigate the pathophysiology of age-related hearing loss (ARHL) and the mechanism of resveratrol (RSV) in prevention and treatment of ARHL.Methods: C57BL/6 mice of different ages were used in this study. Auditory brainstem response (ABR)
Zeyin Yang   +5 more
doaj   +1 more source

Necroptosis in Pulmonary Diseases: A New Therapeutic Target

open access: yesFrontiers in Pharmacology, 2021
In the past decades, apoptosis has been the most well-studied regulated cell death (RCD) that has essential functions in tissue homeostasis throughout life.
Lingling Wang   +6 more
doaj   +1 more source

RIPK3: Beyond Necroptosis [PDF]

open access: yesImmunity, 2019
In this issue of Immunity, Daniels et al. (2019) demonstrate that RIPK3 signaling limits Zika virus (ZIKV) infection in the central nervous system independently of its function in necroptosis by promoting itaconate production in infected neurons, thereby revealing a neuron-specific mechanism of metabolite-mediated ZIKV control.
Evans, Azia S, Coyne, Carolyn B
openaire   +2 more sources

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

open access: yesNature 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 ...
et al,, Liapis, Helen
core   +8 more sources

Cpd-42 protects against calcium oxalate nephrocalcinosis-induced renal injury and inflammation by targeting RIPK3-mediated necroptosis

open access: yesFrontiers in Pharmacology, 2022
Calcium oxalate (CaOx) crystals, as the predominant component of human kidney stones, can trigger excessive cell death and inflammation of renal tubular epithelial cells, involved in the pathogenesis of nephrocalcinosis.
Bingbing Hou   +18 more
doaj   +1 more source

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