Necroptosis is a programmed form of necrosis, and is an alternative mode of regulated cell death mimicking features of apoptosis and necrosis.
Generally, cell demise and its survival are the fundamental features of metazoans to maintain the tissue homeostasis. On morphological basis, cell death is achieved by apoptosis, necrosis, and autophagy.
A plenty of studies has been performed on apoptosis and autophagy and reveals a clear picture of molecular mechanisms of apoptosis and autophagy which is recognized as a highly regulated process. Hence, apoptosis and autophagy are usually regarded as “programmed cell death”, but necrosis is considered as “un-programmed” due to deregulated activity.
Necroptosis is specific to vertebrates and may have originated as an additional defense to pathogens. Necroptosis also acts as an alternative "fail-safe" cell death pathway in cases where cells are unable to undergo apoptosis, such as during viral infection in which apoptosis signaling proteins are blocked by the virus.
Additionally, recent studies implicate it in a variety of disease states. In myocardial infarction and stroke, atherosclerosis, ischemia-reperfusion injury, pancreatitis, inflammatory bowel disease and a number of other clinically common disorders, necroptosis is of central pathophysiological relevance.
Necroptosis is a newly discovered pathway of regulated necrosis. It can be initiated by different stimuli, such as tumor necrosis factor (TNF), TNF-related apoptosis-inducing ligand (TRAIL), Fas ligand (FasL), interferon (IFN), LPS, viral DNA or RNA, DNA-damage agent and requires the kinase activity of receptor-interacting protein 1 (RIPK1) and RIPK3.
RIPK1 has important kinase-dependent and scaffolding functions that inhibit or trigger necroptosis and apoptosis. Its execution involves ROS generation, calcium overload, the opening of the mitochondrial permeability transition pore, mitochondrial fission, inflammatory response and chromatinolysis. Necroptosis participates in many pathogenesis of diseases, including neurological diseases, retinal disorders, acute kidney injury, inflammatory diseases and microbial infections.
|STAT5A||STAT5A Antibody||STAT5A Protein||STAT5A cDNA||STAT5A ELISA Kit|
|STAT5B||STAT5B Antibody||STAT5B Protein||STAT5B cDNA||STAT5B ELISA Kit|
|STAT6||STAT6 Antibody||STAT6 Protein||STAT6 cDNA||STAT6 ELISA Kit|
|TICAM1||TICAM1 Antibody||TICAM1 Protein||TICAM1 cDNA||TICAM1 ELISA Kit|
|TLR3||TLR3 Antibody||TLR3 Protein||TLR3 cDNA||TLR3 ELISA Kit|
|TLR4||TLR4 Antibody||TLR4 Protein||TLR4 cDNA||TLR4 ELISA Kit|
|TNF||TNF Antibody||TNF Protein||TNF cDNA||TNF ELISA Kit|
|TNFAIP3||TNFAIP3 Antibody||TNFAIP3 Protein||TNFAIP3 cDNA||TNFAIP3 ELISA Kit|
|TNFRSF10A||TNFRSF10A Antibody||TNFRSF10A Protein||TNFRSF10A cDNA||TNFRSF10A ELISA Kit|
|TNFRSF10B||TNFRSF10B Antibody||TNFRSF10B Protein||TNFRSF10B cDNA||TNFRSF10B ELISA Kit|
|TNFRSF10C||TNFRSF10C Antibody||TNFRSF10C Protein||TNFRSF10C cDNA||TNFRSF10C ELISA Kit|
|TNFRSF10D||TNFRSF10D Antibody||TNFRSF10D Protein||TNFRSF10D cDNA||TNFRSF10D ELISA Kit|
|TNFRSF1A||TNFRSF1A Antibody||TNFRSF1A Protein||TNFRSF1A cDNA||TNFRSF1A ELISA Kit|
|TNFSF10||TNFSF10 Antibody||TNFSF10 Protein||TNFSF10 cDNA||TNFSF10 ELISA Kit|
|TRADD||TRADD Antibody||TRADD Protein||TRADD cDNA||TRADD ELISA Kit|
|TRAF2||TRAF2 Antibody||TRAF2 Protein||TRAF2 cDNA||TRAF2 ELISA Kit|
|TRAF5||TRAF5 Antibody||TRAF5 Protein||TRAF5 cDNA||TRAF5 ELISA Kit|
|TRPM7||TRPM7 Antibody||TRPM7 Protein||TRPM7 cDNA||TRPM7 ELISA Kit|
|TYK2||TYK2 Antibody||TYK2 Protein||TYK2 cDNA||TYK2 ELISA Kit|
|USP21||USP21 Antibody||USP21 Protein||USP21 cDNA||USP21 ELISA Kit|