Results 1 to 10 of about 15,294 (209)

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   +12 more sources

Ripk3 induces mitochondrial apoptosis via inhibition of FUNDC1 mitophagy in cardiac IR injury

open access: yesRedox Biology, 2017
Ripk3-required necroptosis and mitochondria-mediated apoptosis are the predominant types of cell death that largely account for the development of cardiac ischemia reperfusion injury (IRI). Here, we explored the effect of Ripk3 on mitochondrial apoptosis.
Hao Zhou   +9 more
doaj   +4 more sources

RIPK3 Mediates Necroptosis during Embryonic Development and Postnatal Inflammation in Fadd-Deficient Mice

open access: yesCell Reports, 2017
RIPK3 mediates cell death and regulates inflammatory responses. Although genetic studies have suggested that RIPK3-MLKL-mediated necroptosis leads to embryonic lethality in Fadd or Caspase-8-deficient mice, the exact mechanisms are not fully understood ...
Qun Zhao   +9 more
doaj   +4 more sources

TREM-1 deficiency attenuates RIPK3/MLKL-associated epithelial injury in Klebsiella pneumoniae-induced acute lung injury [PDF]

open access: yesFrontiers in Cell and Developmental Biology
BackgroundKlebsiella pneumoniae (KP)-induced acute lung injury involves excessive myeloid inflammation, epithelial barrier disruption, and inflammatory cell death.
Wei Zhang   +6 more
doaj   +2 more sources

RIPK3 Promotes JEV Replication in Neurons via Downregulation of IFI44L

open access: yesFrontiers 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   +3 more sources

Therapeutic contribution of melatonin to the treatment of septic cardiomyopathy: A novel mechanism linking Ripk3-modified mitochondrial performance and endoplasmic reticulum function

open access: yesRedox Biology, 2019
The basic pathophysiological mechanisms underlying septic cardiomyopathy have not yet been completely clarified. Disease-specific treatments are lacking, and care is still based on supportive modalities.
Jiankai Zhong   +10 more
doaj   +3 more sources

Structure-Based Virtual Screening of Cinnamic Acid Analogs Against RIPK3: Implications for Anti-Inflammatory Drug Discovery [PDF]

open access: yesAvicenna Journal of Medical Biochemistry, 2023
Background: A common oral inflammatory disease known as apical periodontitis (AP) is caused by the intrusion of microorganisms into the dental pulp, resulting in an inflammatory response and bone degradation in periapical tissues.
Elham Khoshbin   +4 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: A Novel Pathway in Neuroinflammation

open access: yesFrontiers in Pharmacology, 2021
Neuroinflammation is a complex inflammatory process in the nervous system that is expected to play a significant role in neurological diseases. Necroptosis is a kind of necrosis that triggers innate immune responses by rupturing dead cells and releasing ...
Ziyu Yu   +4 more
doaj   +1 more source

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

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