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Open AccessJournal ArticleDOI

Apoptosis Induced by the Kinase Inhibitor BAY 43-9006 in Human Leukemia Cells Involves Down-regulation of Mcl-1 through Inhibition of Translation

TLDR
It is demonstrated that BAY 43-9006 mediates cell death in human leukemia cells, at least in part, through down-regulation of Mcl-1 via inhibition of translation.
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This article is published in Journal of Biological Chemistry.The article was published on 2005-10-21 and is currently open access. It has received 286 citations till now. The article focuses on the topics: Jurkat cells & MG132.

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Discovery and development of sorafenib: a multikinase inhibitor for treating cancer

TL;DR: The discovery and continuing development of sorafenib is described, the first oral multikinase inhibitor that targets Raf and affects tumour signalling and the tumour vasculature.
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Sorafenib Blocks the RAF/MEK/ERK Pathway, Inhibits Tumor Angiogenesis, and Induces Tumor Cell Apoptosis in Hepatocellular Carcinoma Model PLC/PRF/5

TL;DR: The results suggest that the antitumor activity of sorafenib in HCC models may be attributed to inhibition of tumor angiogenesis (VEGFR and PDGFR) and direct effects on tumor cell proliferation/survival (Raf kinase signaling-dependent and signaling-independent mechanisms).
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Preclinical overview of sorafenib, a multikinase inhibitor that targets both Raf and VEGF and PDGF receptor tyrosine kinase signaling

TL;DR: This review highlights the antitumor activity of sorafenib across a variety of tumor types, including renal cell, hepatocellular, breast, and colorectal carcinomas in the preclinical setting.
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The BH3 mimetic ABT-737 targets selective Bcl-2 proteins and efficiently induces apoptosis via Bak/Bax if Mcl-1 is neutralized.

TL;DR: It is shown that resistance reflects ABT-737's inability to target another prosurvival relative, Mcl-1, and should prove efficacious in tumors with low MCl-1 levels, or when combined with agents that inactivate Mcl -1, even to treat those tumors that overexpress Bcl-2.
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Pharmacological inhibition of cystine–glutamate exchange induces endoplasmic reticulum stress and ferroptosis

TL;DR: Dixon, Patel, et al. as mentioned in this paper found that erastin is a very effective inhibitor of system xc− function and that it is over 1000 times more potent than the previously known best inhibitor, sulfasalazine.
References
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Journal ArticleDOI

BCL-2 family members and the mitochondria in apoptosis

TL;DR: As the BCL-2 family members reside upstream of irreversible cellular damage and focus much of their efforts at the level of mitochondria, they play a pivotal role in deciding whether a cell will live or die, and it is argued that the amphipathic a-helical BH3 domain serves as a critical death domain in the pro-apoptotic members.
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BCL-2 FAMILY: Regulators of Cell Death

TL;DR: The BCL-2 family reveals evidence for a cell-autonomous coordination between the opposing pathways of proliferation and cell death, and acts as a checkpoint upstream of CASPASES and mitochondrial dysfunction.
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High frequency of BRAF mutations in nevi.

TL;DR: In this article, the authors evaluated the timing of mutations in BRAF during melanocytic neoplasia and found that mutations resulted in the V599E amino acid substitution in 41 of 60 (68%) melanoma metastases, 4 of 5 (80%) primary melanomas and, unexpectedly, in 63 of 77 (82%) nevi.
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