Post-translational control of RIPK3 and MLKL mediated necroptotic cell death.
about
Questions and controversies: the role of necroptosis in liver diseaseThe intersection of cell death and inflammasome activationBiogenic selenium nanoparticles induce ROS-mediated necroptosis in PC-3 cancer cells through TNF activation.Evolutionary divergence of the necroptosis effector MLKL.Active MLKL triggers the NLRP3 inflammasome in a cell-intrinsic manner.Necrostatin-1 Protects Against D-Galactosamine and Lipopolysaccharide-Induced Hepatic Injury by Preventing TLR4 and RAGE Signaling.Non-Hematopoietic MLKL Protects Against Salmonella Mucosal Infection by Enhancing Inflammasome Activation.The brace helices of MLKL mediate interdomain communication and oligomerisation to regulate cell death by necroptosis.
P2860
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P2860
Post-translational control of RIPK3 and MLKL mediated necroptotic cell death.
description
2015 nî lūn-bûn
@nan
2015年の論文
@ja
2015年論文
@yue
2015年論文
@zh-hant
2015年論文
@zh-hk
2015年論文
@zh-mo
2015年論文
@zh-tw
2015年论文
@wuu
2015年论文
@zh
2015年论文
@zh-cn
name
Post-translational control of RIPK3 and MLKL mediated necroptotic cell death.
@en
type
label
Post-translational control of RIPK3 and MLKL mediated necroptotic cell death.
@en
prefLabel
Post-translational control of RIPK3 and MLKL mediated necroptotic cell death.
@en
P2860
P1433
P1476
Post-translational control of RIPK3 and MLKL mediated necroptotic cell death.
@en
P2093
James E Vince
P2860
P356
10.12688/F1000RESEARCH.7046.1
P577
2015-11-19T00:00:00Z