Inhibition of Bcl-2/Bcl-xL and c-MET causes synthetic lethality in model systems of glioblastoma.

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Inhibition of Bcl-2/Bcl-xL and c-MET causes synthetic lethality in model systems of glioblastoma.

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2018 nî lūn-bûn

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2018年の論文

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2018年学术文章

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2018年学术文章

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2018年学术文章

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2018年学术文章

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2018年学术文章

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Inhibition of Bcl-2/Bcl-xL and ...... model systems of glioblastoma.

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Inhibition of Bcl-2/Bcl-xL and ...... model systems of glioblastoma.

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Item

label

Inhibition of Bcl-2/Bcl-xL and ...... model systems of glioblastoma.

@en

Inhibition of Bcl-2/Bcl-xL and ...... model systems of glioblastoma.

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Inhibition of Bcl-2/Bcl-xL and ...... model systems of glioblastoma.

@en

Inhibition of Bcl-2/Bcl-xL and ...... model systems of glioblastoma.

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P1476

Inhibition of Bcl-2/Bcl-xL and ...... model systems of glioblastoma

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Catarina M Quinzii

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Chang Shu

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Chiaki Tsuge Ishida

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Elena Bianchetti

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Georg Karpel-Massler

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Markus D Siegelin

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Yiru Zhang

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P2860

BH3 domains other than Bim and Bid can directly activate Bax/Bak

An integrated genomic analysis of human glioblastoma multiforme

IDH1 and IDH2 mutations in gliomas

Noxa, a BH3-only member of the Bcl-2 family and candidate mediator of p53-induced apoptosis

ERAD inhibitors integrate ER stress with an epigenetic mechanism to activate BH3-only protein NOXA in cancer cells

Acquired resistance to ABT-737 in lymphoma cells that up-regulate MCL-1 and BFL-1.

Utilization of the cellular stress response to sensitize cancer cells to TRAIL-mediated apoptosis.

c-Met signaling induces a reprogramming network and supports the glioblastoma stem-like phenotype.

Multiple BH3 mimetics antagonize antiapoptotic MCL1 protein by inducing the endoplasmic reticulum stress response and up-regulating BH3-only protein NOXA.

Assessment of ABT-263 activity across a cancer cell line collection leads to a potent combination therapy for small-cell lung cancer.

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7373

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scholarly article

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10.1038/S41598-018-25802-0

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English

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Mike-Andrew Westhoff

Giulio Kleiner

Maria J Sanchez-Quintero

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2018-05-09T00:00:00Z

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29743557

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5943348

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