Human RIPK3 C-lobe phosphorylation is essential for necroptotic signaling
Cell Death and Disease, 2022 Necroptosis is a caspase-independent, pro-inflammatory mode of programmed cell death which relies on the activation of the terminal effector, MLKL, by the upstream protein kinase RIPK3.
Yanxiang Meng +7 more
doaj +1 more source
RIPK3 Promotes JEV Replication in Neurons via Downregulation of IFI44L
Frontiers in Microbiology, 2020 Japanese encephalitis virus (JEV), the leading cause of viral encephalitis in Asia, is neurovirulent and neuroinvasive. Neurons are the main target of JEV infection and propagation.
Peiyu Bian +13 more
doaj +1 more source
Viruses, 2022 Receptor interacting protein kinase 3 (RIPK3) is a vital serine/threonine kinase in regulating the programmed destruction of infected cells to defend against RNA viruses.
Guanming Tian +12 more
doaj +1 more source
Brainiac Caspases: Beyond the Wall of Apoptosis [PDF]
, 2019 For the last two decades, caspases, a family of cysteine-aspartic proteases, have evolved from being considered solely as regulators of apoptosis or inflammation to having a wider range of functions.
Alonso Bellido, Isabel María +3 more
core +1 more source
Caspase-1 engagement and TLR-induced c-FLIP expression suppress ASC/caspase-8-dependent apoptosis by inflammasome sensors NLRP1b and NLRC4 [PDF]
, 2017 The caspase activation and recruitment domain (CARD)-based inflammasome sensors NLRP1b and NLRC4 induce caspase-1-dependent pyroptosis independent of the inflammasome adaptor ASC.
D'Hont, Jinke +14 more
core +6 more sources
RIPK3 Is Largely Dispensable for RIG-I-Like Receptor- and Type I Interferon-Driven Transcriptional Responses to Influenza A Virus in Murine Fibroblasts. [PDF]
PLoS ONE, 2016 The kinase RIPK3 is a key regulator of cell death responses to a growing number of viral and microbial agents. We have found that influenza A virus (IAV)-mediated cell death is largely reliant on RIPK3 and that RIPK3-deficient mice are notably more ...
Shoko Nogusa +4 more
doaj +1 more source
The CCL11-CCR3 Axis Regulates the Aggravation of Neuroinflammation in Astrocytic Necroptosis After Cerebral Ischemia. [PDF]
FASEB JSchematic diagram of the triggering mechanism of necroptosis after cerebral ischemia. First, CCL11 targetedly binds to CCR3 on the surface of astrocytes and upregulates the expression of CCR3. After CCR3 activation, it triggers the transcriptional activation of necroptosis.
Yin H +10 more
europepmc +2 more sources
Ischemia and reperfusion injury in kidney transplantation : relevant mechanisms in injury and repair [PDF]
, 2020 Ischemia and reperfusion injury (IRI) is a complex pathophysiological phenomenon, inevitable in kidney transplantation and one of the most important mechanisms for non- or delayed function immediately after transplantation.
Berger, Stefan P. +7 more
core +2 more sources
Kinase domain dimerization drives RIPK3-dependent necroptosis [PDF]
Science Signaling, 2018 Necroptotic cell death is promoted by the dimerization-dependent activation of the kinase RIPK3.
Saravanan Raju +8 more
openaire +2 more sources
RIPK3 Contributes to Lyso-Gb3-Induced Podocyte Death [PDF]
Cells, 2021 Fabry disease is a lysosomal storage disease with an X-linked heritage caused by absent or decreased activity of lysosomal enzymes named alpha-galactosidase A (α-gal A). Among the various manifestations of Fabry disease, Fabry nephropathy significantly affects patients’ morbidity and mortality.
So-Young Kim +10 more
openaire +3 more sources