LRRK2 and the "LRRKtosome" at the Crossroads of Programmed Cell Death: Clues from RIP Kinase Relatives.

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LRRK2 and the "LRRKtosome" at the Crossroads of Programmed Cell Death: Clues from RIP Kinase Relatives.

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2017 nî lūn-bûn

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2017年学术文章

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2017年学术文章

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LRRK2 and the "LRRKtosome" at ...... ues from RIP Kinase Relatives.

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LRRK2 and the "LRRKtosome" at ...... ues from RIP Kinase Relatives.

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LRRK2 and the "LRRKtosome" at ...... ues from RIP Kinase Relatives.

@en

LRRK2 and the "LRRKtosome" at ...... ues from RIP Kinase Relatives.

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LRRK2 and the "LRRKtosome" at ...... ues from RIP Kinase Relatives.

@en

LRRK2 and the "LRRKtosome" at ...... ues from RIP Kinase Relatives.

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P1476

LRRK2 and the "LRRKtosome" at ...... ues from RIP Kinase Relatives.

@en

P2093

Hardy J Rideout

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P2860

Dopaminergic neuronal loss, reduced neurite complexity and autophagic abnormalities in transgenic mice expressing G2019S mutant LRRK2.

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

Parkinson's disease-associated mutations in leucine-rich repeat kinase 2 augment kinase activity

The RIP1/RIP3 necrosome forms a functional amyloid signaling complex required for programmed necrosis

Expression of leucine-rich repeat kinase 2 (LRRK2) inhibits the processing of uMtCK to induce cell death in a cell culture model system

Leucine-rich repeat kinase 2 (LRRK2) interacts with parkin, and mutant LRRK2 induces neuronal degeneration.

LRRK2 kinase activity and biology are not uniformly predicted by its autophosphorylation and cellular phosphorylation site status

Phosphorylation by polo-like kinase 1 induces the tumor-suppressing activity of FADD

Kinase activity of mutant LRRK2 mediates neuronal toxicity

Threonine 56 phosphorylation of Bcl-2 is required for LRRK2 G2019S-induced mitochondrial depolarization and autophagy

P304

193-208

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scholarly article

P356

10.1007/978-3-319-49969-7_10

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P478

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P50

Diane B Re

P577

2017-01-01T00:00:00Z

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P698

28353285

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