Results 31 to 40 of about 2,978 (173)

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

MCAO in RIPK3 knockout mice (Ripk3-/-).

open access: yes, 2023
(A). Apoptosis in various mice upon MCAO treatment. Images show the results of CD31 (green) and PI (red) staining in brain sections from MCAO-treated mice. The results indicated that Ripk3 knockout (n = 3) only partially inhibited cell death, in contrast
Yongjiao Wang (2192470)   +4 more
core   +1 more source

Sugar Fix Keeps RIPK3 at Bay [PDF]

open access: yesImmunity, 2019
Immunometabolism is emerging as an important modulator of immune responses. In this issue of Immunity, Li et al. (2019) examine the link between lipopolysaccharide (LPS)-induced glucose metabolism and innate immune signaling and identify how β-N-acetylglucosamine (O-GlcNAc) modification of the RIPK3 RHIM domain limits inflammation and necroptosis.
Cristina, Giogha, Kate E, Lawlor
openaire   +2 more sources

Killing AML: RIPK3 leads the way [PDF]

open access: yesCell Cycle, 2016
Acute myeloid leukemia (AML) is a heterogeneous group of haematopoietic neoplasms driven partly by the loss of differentiation and the blockade of cell death.
Ulrike, Höckendorf   +2 more
openaire   +2 more sources

Loss of Ripk3 attenuated neutrophil accumulation in a lipopolysaccharide-induced zebrafish inflammatory model

open access: yesCell Death Discovery, 2022
Neutrophils are important effector cells during inflammation, which play complex roles. Therefore, investigating the regulation of neutrophil accumulation during inflammation might provide targets for treating related diseases.
Wanying Wen   +4 more
doaj   +1 more source

RIPK3 Is Largely Dispensable for RIG-I-Like Receptor- and Type I Interferon-Driven Transcriptional Responses to Influenza A Virus in Murine Fibroblasts. [PDF]

open access: yesPLoS 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

RIPK3 Slams the Brake on Leukemogenesis [PDF]

open access: yesCancer 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.
openaire   +2 more sources

Necroptosis, The Double-Edged Sword and Its Therapeutic Implications in Cancer [PDF]

open access: yesArchives of Pharmaceutical Sciences Ain Shams University
Necroptosis is a regulated cell death technique that eliminates cancer cells that are resistant to apoptosis, without requiring caspase. Necroptosis is implicated in several physiological and pathological processes.
Amer, Rana A.   +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   +15 more
core   +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   +1 more source

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