How moderate changes in Akt T-loop phosphorylation impact on tumorigenesis and insulin resistance. - Wikidata - awgldk - TriplyDB

How moderate changes in Akt T-loop phosphorylation impact on tumorigenesis and insulin resistance.

How moderate changes in Akt T-loop phosphorylation impact on tumorigenesis and insulin resistance.

http://www.wikidata.org/entity/Q41441919

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Investigation of LKB1 Ser431 phosphorylation and Cys433 farnesylation using mouse knockin analysis reveals an unexpected role of prenylation in regulating AMPK activity Molecular cues on obesity signals, tumor markers and endometrial cancer.Role of TAPP1 and TAPP2 adaptor binding to PtdIns(3,4)P2 in regulating insulin sensitivity defined by knock-in analysis.Quantitative MRI establishes the efficacy of PI3K inhibitor (GDC-0941) multi-treatments in PTEN-deficient mice lymphoma Interaction of PDK1 with phosphoinositides is essential for neuronal differentiation but dispensable for neuronal survival PTEN protein phosphatase activity correlates with control of gene expression and invasion, a tumor-suppressing phenotype, but not with AKT activity.Effect of PI3K- and mTOR-specific inhibitors on spontaneous B-cell follicular lymphomas in PTEN/LKB1-deficient mice Constitutive Akt1 signals attenuate B-cell receptor signaling and proliferation, but enhance B-cell migration and effector function.Reducing the Levels of Akt Activation by PDK1 Knock-in Mutation Protects Neuronal Cultures against Synthetic Amyloid-Beta Peptides.

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How moderate changes in Akt T-loop phosphorylation impact on tumorigenesis and insulin resistance.

http://www.wikidata.org/entity/Q41441919

description

2010 nî lūn-bûn

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2010年の論文

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2010年論文

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2010年论文

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2010年论文

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2010年论文

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name

How moderate changes in Akt T- ...... enesis and insulin resistance.

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How moderate changes in Akt T- ...... enesis and insulin resistance.

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How moderate changes in Akt T- ...... enesis and insulin resistance.

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Disease Models & Mechanisms

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How moderate changes in Akt T- ...... enesis and insulin resistance.

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Kei Sakamoto

http://www.w3.org/2001/XMLSchema#string

Lana Johnstone

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Stephan Wullschleger

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Stewart Fleming

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Suzanne Duce

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The lipid phosphatase activity of PTEN is critical for its tumor supressor function

The tumor suppressor, PTEN/MMAC1, dephosphorylates the lipid second messenger, phosphatidylinositol 3,4,5-trisphosphate

mTOR complex 2 (mTORC2) controls hydrophobic motif phosphorylation and activation of serum- and glucocorticoid-induced protein kinase 1 (SGK1)

AKT/PKB signaling: navigating downstream

mTOR complex 2 is required for the development of prostate cancer induced by Pten loss in mice

Mutation of the PDK1 PH Domain Inhibits Protein Kinase B/Akt, Leading to Small Size and Insulin Resistance

TOR signaling in growth and metabolism

Pten is essential for embryonic development and tumour suppression

Negative regulation of PKB/Akt-dependent cell survival by the tumor suppressor PTEN

Mutation of Pten/Mmac1 in mice causes neoplasia in multiple organ systems

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95-103

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10.1242/DMM.005603

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1

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