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Open AccessJournal ArticleDOI

Akt Promotes Cell Survival by Phosphorylating and Inhibiting a Forkhead Transcription Factor

TLDR
It is demonstrated that Akt also regulates the activity of FKHRL1, a member of the Forkhead family of transcription factors, which triggers apoptosis most likely by inducing the expression of genes that are critical for cell death, such as the Fas ligand gene.
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This article is published in Cell.The article was published on 1999-03-19 and is currently open access. It has received 6481 citations till now. The article focuses on the topics: PI3K/AKT/mTOR pathway & AKT1.

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Journal ArticleDOI

Cell signaling by receptor-tyrosine kinases

TL;DR: Understanding of the complex signaling networks downstream from RTKs and how alterations in these networks are translated into cellular responses provides an important context for therapeutically countering the effects of pathogenic RTK mutations in cancer and other diseases.
Journal ArticleDOI

The phosphatidylinositol 3-Kinase AKT pathway in human cancer.

TL;DR: Small-molecule therapeutics that block PI3K signalling might deal a severe blow to cancer cells by blocking many aspects of the tumour-cell phenotype.
Journal ArticleDOI

AKT/PKB signaling: navigating downstream.

TL;DR: Those Akt substrates that are most likely to contribute to the diverse cellular roles of Akt, which include cell survival, growth, proliferation, angiogenesis, metabolism, and migration are discussed.
PatentDOI

Phosphorylation and regulation of Akt/PKB by the rictor-mTOR complex

TL;DR: In this paper, the rictor-mTOR complex was used to identify compounds which modulate Akt activity mediated by the Rictor mTOR complex and methods for treating or preventing a disorder that is associated with aberrant Akt activation.
Journal ArticleDOI

Cellular survival: a play in three Akts

TL;DR: The mechanisms by which survival factors regulate the PI3K/c-Akt cascade, the evidence that activation of the PI 3K/ c-AKT pathway promotes cell survival, and the current spectrum of c- akt targets and their roles in mediating c- Akt-dependent cell survival are reviewed.
References
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Journal ArticleDOI

Death receptors: signaling and modulation

Avi Ashkenazi, +1 more
- 28 Aug 1998 - 
TL;DR: Apoptosis is a cell suicide mechanism that enables metazoans to control cell number in tissues and to eliminate individual cells that threaten the animal's survival.
Journal ArticleDOI

Akt Phosphorylation of BAD Couples Survival Signals to the Cell-Intrinsic Death Machinery

TL;DR: It is shown that growth factor activation of the PI3'K/Akt signaling pathway culminates in the phosphorylation of the BCL-2 family member BAD, thereby suppressing apoptosis and promoting cell survival.
Journal ArticleDOI

Apoptosis by death factor.

TL;DR: This work was supported in part by Grants-in-Aid from the Ministry of Education, Science, and Culture of Japan and by a Research Grant from the Princess Takamatsu Cancer Research Fund, and performed in part through Special Coordination Funds of the Science and Technology Agency of the Japanese Government.
Journal ArticleDOI

Tumor suppressor p53 is a direct transcriptional activator of the human bax gene

TL;DR: The bax gene promoter region contains four motifs with homology to consensus p53-binding sites and wild-type but not mutant p53 protein bound to oligonucleotides corresponding to this region of the bax promoter, suggesting that bax is a p53 primary-response gene, presumably involved in a p 53-regulated pathway for induction of apoptosis.
Journal ArticleDOI

Regulation of Cell Death Protease Caspase-9 by Phosphorylation

TL;DR: In this paper, the kinase Akt and p21-Ras, an Akt activator, induced phosphorylation of pro-caspase-9 (pro-Casp9) in cells.
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