necroptosis

necroptosis

A more recent term for regulated cell necrosis, which is carried out by so-called death receptors—e.g., tumour necrosis factor receptor 1, which requires receptor-interacting protein kinase 1 (encoded by RIPK1) and receptor-interacting protein kinase 3 (encoded by RIPK3). Necroptosis requires the active disintegration of mitochondrial, lysosomal and plasma membranes, and it is pathogenetically linked to ischaemic injury, neurodegeneration and viral infection, making the process an attractive therapeutic target in the future. It contrasts to apoptosis (formerly regarded as the only form of programmed cell death to be carried out during development, homeostasis and disease) and to necrosis (which is regarded as an unregulated and uncontrollable process).
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Autophagy, necroptosis, and mitoptosis may be induced instead or in parallel to apoptosis upon challenge of cells with toxic insults Gain et al.
Artesunate (5) induced cell death in cancer cells by both the intrinsic and extrinsic pathways of apoptosis as well as autophagy and necroptosis (Button et al.
In conclusion, the present investigation demonstrated that artemisinin derivatives do not only kill tumor cells by induction of apoptosis, autophagy or necroptosis as shown in the past, but also by ferroptosis.
Yuan's research has uncovered many significant distinctions in the multiple cell death mechanisms, including programmed cell death (apoptosis) and necroptosis elicited by external factors such as infection, toxins or trauma (necrosis).
Among specific topics are detecting apoptosis in cell-free systems, analyze cellular necroptosis, the transglutamination of proteins involved in apoptosis, fluorometric methods for detecting mitochondrial membrane permeabilization during apoptosis, the genetic mapping of anti-apoptosis pathways in myoloid progenitor cells, and a reliable method for detecting programmed cell death in yeast.
Their studies provided insight into regulation of two forms of programmed cell-death pathways known as apoptosis and necroptosis.
Jude Department of Immunology, highlighted the protein FLIP as a key regulator of both apoptosis and necroptosis.