Mixed lineage kinase domain-like protein mediates necrosis signaling downstream of RIP3 kinase (Q24302381)

Mixed lineage kinase domain like pseudokinase

ChEBI release 2020-05-28

ChEBI ID

63770

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Receptor interacting serine/threonine kinase 3

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Receptor interacting serine/threonine kinase 1

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tumor necrosis factor

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necroptotic signaling pathway

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Receptor-interacting serine-threonine kinase 3

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Mixed lineage kinase domain-like

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author name string

Liming Sun

1

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Huayi Wang

2

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Zhigao Wang

3

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Sudan He

4

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She Chen

5

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Daohong Liao

6

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Lai Wang

7

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Jiacong Yan

8

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Weilong Liu

9

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Xiaoguang Lei

10

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Xiaodong Wang

Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha

11

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language of work or name

English

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publication date

20 January 2012

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published in

Cell

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volume

148

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issue

1-2

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page(s)

213-27

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cites work

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Phosphorylation-driven assembly of the RIP1-RIP3 complex regulates programmed necrosis and virus-induced inflammation

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RIP kinases at the crossroads of cell death and survival

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The mitochondrial phosphatase PGAM5 functions at the convergence point of multiple necrotic death pathways

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Cleavage of RIP3 inactivates its caspase-independent apoptosis pathway by removal of kinase domain.

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Virus inhibition of RIP3-dependent necrosis

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Smac, a mitochondrial protein that promotes cytochrome c-dependent caspase activation by eliminating IAP inhibition

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Identification of DIABLO, a mammalian protein that promotes apoptosis by binding to and antagonizing IAP proteins

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Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade

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Apoptosis control by death and decoy receptors

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Polyproline-rod approach to isolating protein targets of bioactive small molecules: isolation of a new target of indomethacin

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Apoptosis: A Basic Biological Phenomenon with Wideranging Implications in Tissue Kinetics

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Catalytic activity of the caspase-8-FLIP(L) complex inhibits RIPK3-dependent necrosis

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RIP3 mediates the embryonic lethality of caspase-8-deficient mice

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Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury

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Identification of RIP1 kinase as a specific cellular target of necrostatins

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Caspase inhibition causes hyperacute tumor necrosis factor-induced shock via oxidative stress and phospholipase A2.

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Caspase-independent cell death

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Mixed-lineage kinase control of JNK and p38 MAPK pathways

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Receptor interacting protein kinases mediate retinal detachment-induced photoreceptor necrosis and compensate for inhibition of apoptosis

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An APAF-1.cytochrome c multimeric complex is a functional apoptosome that activates procaspase-9

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Smac/DIABLO selectively reduces the levels of c-IAP1 and c-IAP2 but not that of XIAP and livin in HeLa cells

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Inhibition of caspases increases the sensitivity of L929 cells to necrosis mediated by tumor necrosis factor.

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Two CD95 (APO-1/Fas) signaling pathways

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Cleavage of the death domain kinase RIP by caspase-8 prompts TNF-induced apoptosis

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A small molecule Smac mimic potentiates TRAIL- and TNFalpha-mediated cell death

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RIP3, an energy metabolism regulator that switches TNF-induced cell death from apoptosis to necrosis

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Caspases: enemies within

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Mechanisms and Functions of Cell Death

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The role of mitochondria in apoptosis*.

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