Hot-spot mutations in p110alpha of phosphatidylinositol 3-kinase (pI3K): differential interactions with the regulatory subunit p85 and with RAS. - Wikidata - wikimedia - TriplyDB

Hot-spot mutations in p110alpha of phosphatidylinositol 3-kinase (pI3K): differential interactions with the regulatory subunit p85 and with RAS.

Hot-spot mutations in p110alpha of phosphatidylinositol 3-kinase (pI3K): differential interactions with the regulatory subunit p85 and with RAS.

http://www.wikidata.org/entity/Q33716552

about

RAS signalling through PI3-Kinase controls cell migration via modulation of Reelin expression The therapeutic potential of targeting the PI3K pathway in pediatric brain tumors Modeling of tumor progression in NSCLC and intrinsic resistance to TKI in loss of PTEN expression RAS Interaction with PI3K: More Than Just Another Effector Pathway The PTEN/PI3K/AKT Pathway in vivo, Cancer Mouse Models.Genetically engineered mouse models of PI3K signaling in breast cancer.Multiple oncogenic mutations and clonal relationship in spatially distinct benign human epidermal tumors mTOR inhibition elicits a dramatic response in PI3K-dependent colon cancers.PIK3CA activating mutation in colorectal carcinoma: associations with molecular features and survival.Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging.Activating mutations of TOR (target of rapamycin).A drug targeting only p110α can block phosphoinositide 3-kinase signalling and tumour growth in certain cell types PI3K in cancer: divergent roles of isoforms, modes of activation and therapeutic targeting.Involvement of Akt and mTOR in chemotherapeutic- and hormonal-based drug resistance and response to radiation in breast cancer cells.Involvement of Akt-1 and mTOR in sensitivity of breast cancer to targeted therapy Cooperative effects of Akt-1 and Raf-1 on the induction of cellular senescence in doxorubicin or tamoxifen treated breast cancer cells.Hormesis does not make sense except in the light of TOR-driven aging.Molecular damage in cancer: an argument for mTOR-driven aging Colon Cancer Tumorigenesis Initiated by the H1047R Mutant PI3K.Tumor suppression by p53 without apoptosis and senescence: conundrum or rapalog-like gerosuppression?PIK3CA mutations can initiate pancreatic tumorigenesis and are targetable with PI3K inhibitors Genome Analysis of Latin American Cervical Cancer: Frequent Activation of the PIK3CA Pathway Mechanistic or mammalian target of rapamycin (mTOR) may determine robustness in young male mice at the cost of accelerated aging.Mice expressing activated PI3K rapidly develop advanced colon cancer.Mutations and deregulation of Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades which alter therapy response.Conditional loss of ErbB3 delays mammary gland hyperplasia induced by mutant PIK3CA without affecting mammary tumor latency, gene expression, or signaling.p87 and p101 subunits are distinct regulators determining class IB phosphoinositide 3-kinase (PI3K) specificity PIK3CA and APC mutations are synergistic in the development of intestinal cancers.Therapeutic resistance resulting from mutations in Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR signaling pathways.Implementing prognostic and predictive biomarkers in CRC clinical trials.Protein-protein interactions: principles, techniques, and their potential role in new drug development.Modeling tumor progression by the sequential introduction of genetic alterations into the genome of human normal cells.Role of aberrant PI3K pathway activation in gallbladder tumorigenesis.Yeast-like chronological senescence in mammalian cells: phenomenon, mechanism and pharmacological suppression Addition of N-terminal peptide sequences activates the oncogenic and signaling potentials of the catalytic subunit p110α of phosphoinositide-3-kinase PI3K/AKT Signaling in Cancer Constitutive Signaling by Aberrant PI3K in Cancer Dynamic modeling of folliculogenesis signaling pathways in the presence of miRNAs expression.Dual PI3K/mTOR Inhibition in Colorectal Cancers with APC and PIK3CA Mutations.PIK3CA C2 Domain Deletions Hyperactivate Phosphoinositide 3-kinase (PI3K), Generate Oncogene Dependence, and Are Exquisitely Sensitive to PI3Kα Inhibitors.

P2860

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P2860

Hot-spot mutations in p110alpha of phosphatidylinositol 3-kinase (pI3K): differential interactions with the regulatory subunit p85 and with RAS.

http://www.wikidata.org/entity/Q33716552

description

2010 nî lūn-bûn

@nan

2010 թուականի Փետրուարին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի փետրվարին հրատարակված գիտական հոդված

@hy

2010年の論文

@ja

2010年論文

@yue

2010年論文

@zh-hant

2010年論文

@zh-hk

2010年論文

@zh-mo

2010年論文

@zh-tw

2010年论文

@wuu

name

Hot-spot mutations in p110alph ...... tory subunit p85 and with RAS.

@ast

Hot-spot mutations in p110alph ...... tory subunit p85 and with RAS.

@en

type

label

Hot-spot mutations in p110alph ...... tory subunit p85 and with RAS.

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Hot-spot mutations in p110alph ...... tory subunit p85 and with RAS.

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prefLabel

Hot-spot mutations in p110alph ...... tory subunit p85 and with RAS.

@ast

Hot-spot mutations in p110alph ...... tory subunit p85 and with RAS.

@en

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Hot-spot mutations in p110alph ...... tory subunit p85 and with RAS.

@en

P2860

Binding of ras to phosphoinositide 3-kinase p110alpha is required for ras-driven tumorigenesis in mice

Activation of phosphoinositide 3-kinase by interaction with Ras and by point mutation

Cloning of a novel, ubiquitously expressed human phosphatidylinositol 3-kinase and identification of its binding site on p85

Crystal structure and functional analysis of Ras binding to its effector phosphoinositide 3-kinase gamma

Mechanism of two classes of cancer mutations in the phosphoinositide 3-kinase catalytic subunit

The structure of a human p110alpha/p85alpha complex elucidates the effects of oncogenic PI3Kalpha mutations

A frequent kinase domain mutation that changes the interaction between PI3K and the membrane

Phosphatidylinositol 3-kinase mutations identified in human cancer are oncogenic

High frequency of mutations of the PIK3CA gene in human cancers

Phosphatidylinositol 3-kinase: structure and expression of the 110 kd catalytic subunit

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596-600

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scholarly article

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10.4161/CC.9.3.10599

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3

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9

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20009532

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