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Necroptosis and its role in infectious diseases | Apoptosis
Description:
Necroptosis is a noncaspase-dependent and precisely regulated mechanism of cell death. Necroptosis is mainly initiated by members of the tumor necrosis factor receptor (TNFR) and Toll-like receptor (TLR) families, interferon, intracellular RNA and DNA sensors and other mediators. Subsequently, the protein kinase RIPK1 (receptor-interacting protein kinase 1) and RIPK3 interact with the receptor protein, which transduces death signals and further recruits and phosphorylates MLKL (mixed lineage kinase domain-like protein). MLKL serves as the initiator of cell death and eventually induces necroptosis. It was found that necroptosis is not only involved in the physiological regulation but also in the occurrence, development and prognosis of some necrotic diseases, especially infectious diseases. Intervention in the necroptosis signaling pathway is helpful for removing pathogens, inhibiting the development of lesions, and promoting the remodeling of tissue. In-depth study of the molecular regulation mechanism of necroptosis and its relationship with the pathogenesis of infectious diseases will help to provide new ideas and directions for research of the pathological mechanisms and clinical prevention of infectious diseases.
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pubmed, article, google, scholar, cas, cell, necroptosis, central, death, necrosis, protein, rip, receptor, kinase, nature, sci, apoptosis, ripk, mlkl, wang, programmed, usa, biol, httpsdoiorgnature, proc, natl, acad, httpsdoiorgpnas, inflammation, science, role, zhang, necrotic, httpsdoiorgs, nat, mol, cells, china, research, diseases, xia, molecular, access, galluzzi, host, privacy, cookies, content, infectious, song,
Topics {āļø}
receptor-interacting kinase-3āmediated pathway tnf-induced nf-Īŗb signal t-cell receptorāmediated necroptosis month download article/chapter pattern-recognition receptor signalling lipopolysaccharide-induced hepatic injury dai/zbp1/dlm-1 complexes nad-dependent deacetylase sirt2 naturally-occurring shikonin analogues mlkl-mediated pore formation mycobacterium tuberculosis-induced inflammation receptor-interacting protein innate immune defense rip3/mlkl-dependent necrosis full article pdf protein kinase ripk1 murine cytomegalovirus vira bone marrow failure article apoptosis aims receptor 3-mediated necrosis tnf-induced necrosis related subjects necrotic cell death kaiser wj salmonella outer protein tnf-induced necroptosis privacy choices/manage cookies eventually induces necroptosis article xia toxin-induced necroptosis chan fkm ischemic brain injury ischemia-reperfusion injury tumor necrosis factor upton jw caspase-2 mediated apoptotic interferon induces necroptosis plasma membrane leads trimerized mlkl protein virus-induced inflammation primary murine microglia jianhe hu programmed cell death rip1 kinase activity proinflammatory cell death cell death subroutines nonapoptotic cell death apoptotic cell death transduces death signals rip1/rip3 binding
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headline:Necroptosis and its role in infectious diseases
description:Necroptosis is a noncaspase-dependent and precisely regulated mechanism of cell death. Necroptosis is mainly initiated by members of the tumor necrosis factor receptor (TNFR) and Toll-like receptor (TLR) families, interferon, intracellular RNA and DNA sensors and other mediators. Subsequently, the protein kinase RIPK1 (receptor-interacting protein kinase 1) and RIPK3 interact with the receptor protein, which transduces death signals and further recruits and phosphorylates MLKL (mixed lineage kinase domain-like protein). MLKL serves as the initiator of cell death and eventually induces necroptosis. It was found that necroptosis is not only involved in the physiological regulation but also in the occurrence, development and prognosis of some necrotic diseases, especially infectious diseases. Intervention in the necroptosis signaling pathway is helpful for removing pathogens, inhibiting the development of lesions, and promoting the remodeling of tissue. In-depth study of the molecular regulation mechanism of necroptosis and its relationship with the pathogenesis of infectious diseases will help to provide new ideas and directions for research of the pathological mechanisms and clinical prevention of infectious diseases.
datePublished:2020-01-07T00:00:00Z
dateModified:2020-01-07T00:00:00Z
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Infection
RIPK1
RIPK3
MLKL
Cancer Research
Cell Biology
Oncology
Biochemistry
general
Virology
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description:Necroptosis is a noncaspase-dependent and precisely regulated mechanism of cell death. Necroptosis is mainly initiated by members of the tumor necrosis factor receptor (TNFR) and Toll-like receptor (TLR) families, interferon, intracellular RNA and DNA sensors and other mediators. Subsequently, the protein kinase RIPK1 (receptor-interacting protein kinase 1) and RIPK3 interact with the receptor protein, which transduces death signals and further recruits and phosphorylates MLKL (mixed lineage kinase domain-like protein). MLKL serves as the initiator of cell death and eventually induces necroptosis. It was found that necroptosis is not only involved in the physiological regulation but also in the occurrence, development and prognosis of some necrotic diseases, especially infectious diseases. Intervention in the necroptosis signaling pathway is helpful for removing pathogens, inhibiting the development of lesions, and promoting the remodeling of tissue. In-depth study of the molecular regulation mechanism of necroptosis and its relationship with the pathogenesis of infectious diseases will help to provide new ideas and directions for research of the pathological mechanisms and clinical prevention of infectious diseases.
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RIPK1
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