Phosphoinositide 3-Kinase Pathway Activation in Phosphate and Tensin Homolog (PTEN)-deficient Prostate Cancer Cells Is Independent of Receptor Tyrosine Kinases and Mediated by the p110β and p110δ Catalytic Subunits-Reference-Cited by-同舟云学术

Phosphoinositide 3-Kinase Pathway Activation in Phosphate and Tensin Homolog (PTEN)-deficient Prostate Cancer Cells Is Independent of Receptor Tyrosine Kinases and Mediated by the p110β and p110δ Catalytic Subunits

Published:2010-05 Issue:20 Volume:285 Page:14980-14989
ISSN:0021-9258
Container-title:Journal of Biological Chemistry
language:en
Short-container-title:Journal of Biological Chemistry

Author:

Jiang Xinnong,Chen Sen,Asara John M.,Balk Steven P.

Publisher

Elsevier BV

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference42 articles.

1. The evolution of phosphatidylinositol 3-kinases as regulators of growth and metabolism

2. SH2 domains recognize specific phosphopeptide sequences

3. Regulation of the p85/p110 Phosphatidylinositol 3′-Kinase: Stabilization and Inhibition of the p110α Catalytic Subunit by the p85 Regulatory Subunit

4. The PTEN–PI3K pathway: of feedbacks and cross-talks

5. The role of PTEN signaling perturbations in cancer and in targeted therapy

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