Results 21 to 30 of about 43,311 (200)

Aβ oligomers trigger necroptosis-mediated neurodegeneration via microglia activation in Alzheimer’s disease [PDF]

open access: yes, 2022
Alzheimer’s disease (AD) is a major adult-onset neurodegenerative condition with no available treatment. Compelling reports point amyloid-β (Aβ) as the main etiologic agent that triggers AD.
Court, Felipe A   +19 more
core   +1 more source

Necroptosis and neutrophil-associated disorders. [PDF]

open access: yes, 2018
Necroptosis is a form of regulated necrosis and is dependent on a signaling pathway involving receptor interacting protein kinase-3 (RIPK3) and mixed lineage kinase domain-like protein (MLKL).
Simon, Hans-Uwe   +5 more
core   +3 more sources

Necroptosis in the Pathophysiology of Disease [PDF]

open access: yesThe American Journal of Pathology, 2020
Over the past 15 years, elegant studies have demonstrated that in certain conditions, programed cell death resembles necrosis and depends on a unique molecular pathway with no overlap with apoptosis. This form of regulated necrosis is represented by necroptosis, in which the receptor-interacting protein kinase-3 and its substrate mixed-lineage kinase ...
Mitri K. Khoury   +3 more
openaire   +2 more sources

Staurosporine induces necroptotic cell death under caspase-compromised conditions in U937 cells [PDF]

open access: yes, 2012
For a long time necrosis was thought to be an uncontrolled process but evidences recently have revealed that necrosis can also occur in a regulated manner.
Gabor Barna (146087)   +20 more
core   +2 more sources

Phenytoin inhibits necroptosis [PDF]

open access: yesCell Death & Disease, 2018
AbstractReceptor-interacting protein kinases 1 and 3 (RIPK1/3) have best been described for their role in mediating a regulated form of necrosis, referred to as necroptosis. During this process, RIPK3 phosphorylates mixed lineage kinase domain-like (MLKL) to cause plasma membrane rupture.
von Mässenhausen, Anne   +27 more
openaire   +3 more sources

Necroptosis in Intestinal Inflammation and Cancer: New Concepts and Therapeutic Perspectives

open access: yesBiomolecules, 2020
Necroptosis is a caspases-independent programmed cell death displaying intermediate features between necrosis and apoptosis. Albeit some physiological roles during embryonic development such tissue homeostasis and innate immune response are documented ...
Anna Negroni   +3 more
doaj   +1 more source

RIPK1-dependent necroptosis promotes vasculogenic mimicry formation via eIF4E in triple-negative breast cancer

open access: yesCell Death and Disease, 2023
Necroptosis is a caspase-independent form of programmed cell death. Receptor interacting protein kinase 1 (RIPK1) is a key molecule in the initiation of necroptosis and the formation of the necrotic complex.
Fan Li   +9 more
doaj   +1 more source

Exposure to the complement C5b-9 complex sensitizes 661W photoreceptor cells to both apoptosis and necroptosis. [PDF]

open access: yes, 2015
The loss of photoreceptors is the defining characteristic of many retinal degenerative diseases, but the mechanisms that regulate photoreceptor cell death are not fully understood.
Dimitrios Stampoulis   +11 more
core   +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

Identification of necroptosis-related features in diabetic nephropathy and analysis of their immune microenvironent and inflammatory response

open access: yesFrontiers in Cell and Developmental Biology, 2023
Background: Diabetic nephropathy (DN) was considered a severe microvascular complication of diabetes, which was recognized as the second leading cause of end-stage renal diseases.
Kaibo Hu   +32 more
doaj   +1 more source

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