"By maintaining a low level of PIP3, PTEN suppresses motility [XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR], cell multiplication [XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR], adhesion [XREF_BIBR], aggregation [XREF_BIBR, XREF_BIBR], and resistance to apoptosis [XREF_BIBR, XREF_BIBR, XREF_BIBR]."
"PTEN dephosphorylates phosphatidylinositol-3,4,5-triphosphate (PIP3) at the D3 position generating phosphatidylinositol 4,5-biphosphate (PIP2), decreasing cellular PIP3 levels."
"PTEN negatively regulates the intracellular levels of PIP3 in cells and functions as a tumor suppressor by regulating Akt signaling pathway XREF_BIBR."
"PIP3 levels are antagonized by the regulatory phosphatases PTEN that converts PI (3,4,5) P 3 back to PI (4,5) P 2, and SH2 domain containing inositol 5 '-phosphatase 1 (SHIP) that converts PI (3,4,5) P 3 to PI (3,4) 2."
"The balance of cellular PIP3 is regulated primarily by a phosphatase called PTEN that reduces PIP3 levels thereby lowering Akt activity."
"PTEN must be inactivated to increase cellular levels of PIP3 for recruiting downstream signaling molecules, such as Akt, and inhibiting GSK-3beta, whose inactivation plays a vital role in the development of cardiac hypertrophy [XREF_BIBR, XREF_BIBR, XREF_BIBR]."
"In the present study we have examined this widely accepted theory using a new class I PI3K inhibitor (GDC-0941), as well as Akt inhibitors, and PTEN phosphatase constructs to reduce PIP3 levels."
"For example, seen frequently in prostate cancer is loss of function of phosphatase and tension homologue (PTEN), a phosphatase that negatively regulates intracellular levels of PIP3 and functions as a tumor suppressor by negatively regulating the PKB and Akt signaling pathway, one of the two major signaling pathways downstream of IGF-1R discussed previously in this review [XREF_BIBR]."
"PTEN prevents elevated levels of PIP3 by dephosphorylating its 3 ' position."
"PTEN activity to prevent elevated levels of PIP3 and tumorigenesis depends on its interaction with the lipid bilayer."