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Epithelial–mesenchymal transition in development and cancer: role of phosphatidylinositol 3′ kinase/AKT pathways
TLDR
The role of PI3K/AKT pathways in EMT during development and cancer with a focus on E-cadherin regulation is discussed, along with a discussion of the therapeutic implications of modulating EMT in order to achieve cancer control.
The protein kinase Akt induces epithelial mesenchymal transition and promotes enhanced motility and invasiveness of squamous cell carcinoma lines.
TLDR
Squamous cell carcinoma lines engineered to express constitutively active Akt underwent EMT, characterized by down-regulation of the epithelial markers desmoplakin, E-cadherin, and beta-catenin and up- regulation of the mesenchymal marker vimentin.
A retroviral oncogene, akt, encoding a serine-threonine kinase containing an SH2-like region.
TLDR
Sequence analysis of v-akt and biochemical characterization of its product revealed that it codes for a protein kinase C-related serine-threonine kinase whose cellular homolog is expressed in most tissues, with the highest amount found in thymus, suggesting that Akt may form a functional link between tyrosine and serinesine phosphorylation pathways.
The PI 3-kinase/Akt signaling pathway delivers an anti-apoptotic signal.
TLDR
The results suggest that uncoupling of survival and mitogenesis can be explained by differing abilities of distinct mitogens to efficiently induce the PI 3-kinase/Akt signaling pathway.
Cytoplasmic relocalization and inhibition of the cyclin-dependent kinase inhibitor p27Kip1 by PKB/Akt-mediated phosphorylation in breast cancer
TLDR
It is demonstrated that the serine/threonine kinase Akt regulates cell proliferation in breast cancer cells by preventing p27kip1-mediated growth arrest and cytoplasmic relocalization of p27Kip1, secondary to Akt-mediated phosphorylation, is a novel mechanism whereby the growth inhibitory properties of p 27kip 1 are functionally inactivated and the proliferation of breast cancer Cells is sustained.
Akt activation by growth factors is a multiple-step process: the role of the PH domain
TLDR
The proposed model provided a framework for a comprehensive understanding of the temporal and spatial requirements for Akt activation by growth factors and found that T308D/S473D double mutant is constitutively active.
AKT plays a central role in tumorigenesis
  • J. Testa, A. Bellacosa
  • Biology, Chemistry
    Proceedings of the National Academy of Sciences…
  • 25 September 2001
TLDR
This issue of PNAS, Mayo and Donner report on yet another function of AKT, involving regulation of the Mdm2/p53 pathway, and define a family of closely related, highly conserved cellular homologues.
Transformation of hematopoietic cells by BCR/ABL requires activation of a PI‐3k/Akt‐dependent pathway
TLDR
In complementation assays using mouse marrow progenitor cells, the ability of transformation‐defective SH2 domain BCR/ABL mutants to induce growth factor‐independent colony formation and leukemia in SCID mice was markedly enhanced by expression of constitutively active Akt.
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