JNK3 phosphorylates Bax protein and induces ability to form pore on bilayer lipid membrane.

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JNK3 phosphorylates Bax protein and induces ability to form pore on bilayer lipid membrane.

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2017 nî lūn-bûn

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2017年の論文

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年學術文章

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JNK3 phosphorylates Bax protei ...... ore on bilayer lipid membrane.

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JNK3 phosphorylates Bax protei ...... ore on bilayer lipid membrane.

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JNK3 phosphorylates Bax protei ...... ore on bilayer lipid membrane.

@en

JNK3 phosphorylates Bax protei ...... ore on bilayer lipid membrane.

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JNK3 phosphorylates Bax protei ...... ore on bilayer lipid membrane.

@en

JNK3 phosphorylates Bax protei ...... ore on bilayer lipid membrane.

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P1476

JNK3 phosphorylates Bax protei ...... ore on bilayer lipid membrane.

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P2093

Rajeev Gupta

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Subhendu Ghosh

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P2860

Endophilin B1/Bif-1 stimulates BAX activation independently from its capacity to produce large scale membrane morphological rearrangements

The Bax subfamily of Bcl2-related proteins is essential for apoptotic signal transduction by c-Jun NH(2)-terminal kinase

A new view of the lethal apoptotic pore

Structure of Bax: coregulation of dimer formation and intracellular localization

Mono- or double-site phosphorylation distinctly regulates the proapoptotic function of Bax

The regulation of Bax by c-Jun N-terminal protein kinase (JNK) is a prerequisite to the mitochondrial-induced apoptotic pathway

Bax increases the pore size of rat brain mitochondrial voltage-dependent anion channel in the presence of tBid

The N-terminus and alpha-5, alpha-6 helices of the pro-apoptotic protein Bax, modulate functional interactions with the anti-apoptotic protein Bcl-xL.

P38α MAPK underlies muscular dystrophy and myofiber death through a Bax-dependent mechanism.

Bax channel inhibitors prevent mitochondrion-mediated apoptosis and protect neurons in a model of global brain ischemia.

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41-46

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scholarly article

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10.1016/J.BIOPEN.2017.02.001

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P478

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P577

2017-02-11T00:00:00Z

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P698

29450140

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P921

phosphorylation

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5801821

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