IndraLab

Statements


PTEN inhibits PDPK1. 10 / 10
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"PTEN and SHIP prevent activation of PDK, upstream of p-Akt308."

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"Loss of PTEN leads to increased PDK1 and AKT due to PIP3 accumulation resulting in activation of mTORC1 and its downstream effectors [XREF_BIBR]."

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"Therefore , PTEN deficiency activates the PDK1 / mTORC2 ( Sin1 ) - AKT axis , subsequently phosphorylating SNAP23 and enhancing alpha-granule secretion of platelets ."

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"On the other hand, the lipid phosphatase PTEN deactivates PDK1 by transforming PIP 3 to PIP 2."

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"In PTEN disrupted cells, PDK1, AKT, and PKCzeta exhibited elevated basal activities, which prevented EGF induced further activation of these molecules."

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"PTEN deletion thus induces the growth and proliferation of T cell progenitors independently of PDK1."

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"Therefore, PTEN deficiency activates the PDK1/mTORC2(Sin1)-AKT axis, subsequently phosphorylating SNAP23 and enhancing α-granule secretion of platelets.We next sought to ask whether Pten-deficient platelets regulate Tfh cell differentiation."

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"PTEN functions as a lipid and protein phosphatase, inhibiting the ability of PDK1 to activate AKT."

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"PI3K promotes while PTEN (phosphatase and tensin homology) inhibits the activities of downstream PDK1 (3-phosphoinositide-dependent protein kinase-1) and AKT (or PKB, protein kinase B)."

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"A surprising result is that PTEN deletion results in strong activation of PDK1 and PKB, but bypasses the normal PDK1 requirement for cell growth and proliferation of T cells."