The tyrosine kinase Lck is a positive regulator of the mitochondrial apoptosis pathway by controlling Bak expression (Q24317331)

positive regulation of intrinsic apoptotic signaling pathway

GOA release 2020-03-11

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GOA release 2020-03-11

author name string

A K Samraj

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C Stroh

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U Fischer

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K Schulze-Osthoff

Inhibition of Bax channel-forming activity by Bcl-2

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publication date

12 January 2006

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language of work or name

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25

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issue

2

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page(s)

186-97

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cites work

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Nonredundant role of Bax and Bak in Bid-mediated apoptosis

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BAX and BAK mediate p53-independent suppression of tumorigenesis

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The lck SH3 domain is required for activation of the mitogen-activated protein kinase pathway but not the initiation of T-cell antigen receptor signaling

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Bid-induced conformational change of Bax is responsible for mitochondrial cytochrome c release during apoptosis

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Bid induces the oligomerization and insertion of Bax into the outer mitochondrial membrane

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LAT is required for TCR-mediated activation of PLCgamma1 and the Ras pathway

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Induction of cell death by the BH3-only Bcl-2 homolog Nbk/Bik is mediated by an entirely Bax-dependent mitochondrial pathway

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Cell damage-induced conformational changes of the pro-apoptotic protein Bak in vivo precede the onset of apoptosis

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Involvement of tyrosine kinase p56/Lck in apoptosis induction by anticancer drugs

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The Src kinase Lyn is a negative regulator of mast cell proliferation

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Rosmarinic acid induces p56lck-dependent apoptosis in Jurkat and peripheral T cells via mitochondrial pathway independent from Fas/Fas ligand interaction

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The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues

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Cardiomyocyte apoptosis triggered by RAFTK/pyk2 via Src kinase is antagonized by paxillin

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Association of Bax and Bak homo-oligomers in mitochondria. Bax requirement for Bak reorganization and cytochrome c release

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Movement of Bax from the Cytosol to Mitochondria during Apoptosis

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Long-Term Survival But Impaired Homeostatic Proliferation of Naive T Cells in the Absence of p56lck

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