The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice. - Wikidata - awgldk - TriplyDB

The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice.

The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice.

http://www.wikidata.org/entity/Q34693888

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Prdx1 inhibits tumorigenesis via regulating PTEN/AKT activity mTOR complex 2 is required for the development of prostate cancer induced by Pten loss in mice The PI3K/Akt Pathway in Tumors of Endocrine Tissues Genetically engineered mouse models of prostate cancer Therapeutic targeting of cancers with loss of PTEN function.A novel androgen receptor splice variant is up-regulated during prostate cancer progression and promotes androgen depletion-resistant growth Role of PI3K, mTOR and Akt2 signalling in hepatic tumorigenesis via the control of PKM2 expression Poly(ester amine)-mediated, aerosol-delivered Akt1 small interfering RNA suppresses lung tumorigenesis Id4 deficiency attenuates prostate development and promotes PIN-like lesions by regulating androgen receptor activity and expression of NKX3.1 and PTEN Regulation of PI3K effector signalling in cancer by the phosphoinositide phosphatases Targeting the phosphoinositide 3-kinase pathway in cancer Molecular cues on obesity signals, tumor markers and endometrial cancer.Activation of Akt signaling in prostate induces a TGFβ-mediated restraint on cancer progression and metastasis.Akt-dependent regulation of NF-{kappa}B is controlled by mTOR and Raptor in association with IKK.Genetic profiling to determine risk of relapse-free survival in high-risk localized prostate cancer.RFP-mediated ubiquitination of PTEN modulates its effect on AKT activation PTEN is a tumor suppressor in CML stem cells and BCR-ABL-induced leukemias in mice Conditional loss of uterine Pten unfailingly and rapidly induces endometrial cancer in mice Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways The PI3K-Akt-mTOR pathway in initiation and progression of thyroid tumors.Progesterone: the ultimate endometrial tumor suppressor.Subcellular localization of activated AKT in estrogen receptor- and progesterone receptor-expressing breast cancers: potential clinical implications Loss of CDH1 and Pten accelerates cellular invasiveness and angiogenesis in the mouse uterus.Novel inhibitors of AKT: assessment of a different approach targeting the pleckstrin homology domain.A novel three-dimensional culture system of polarized epithelial cells to study endometrial carcinogenesis.Inhibition of Akt with small molecules and biologics: historical perspective and current status of the patent landscape.PTEN-deficient tumors depend on AKT2 for maintenance and survival.Artemin Reduces Sensitivity to Doxorubicin and Paclitaxel in Endometrial Carcinoma Cells through Specific Regulation of CD24.Inhibition of phosphatidylinositol 3-kinase/Akt signaling suppresses tumor cell proliferation and neuroendocrine marker expression in GI carcinoid tumors Akt1 deletion prevents lung tumorigenesis by mutant K-ras.The impact of microRNA-mediated PI3K/AKT signaling on epithelial-mesenchymal transition and cancer stemness in endometrial cancer.Molecular genetics of prostate cancer: new prospects for old challenges Mouse models of endocrine tumours.MicroRNAs/TP53 feedback circuitry in glioblastoma multiforme mTOR pathway is activated by PKA in adrenocortical cells and participates in vivo to apoptosis resistance in primary pigmented nodular adrenocortical disease (PPNAD).An allosteric Akt inhibitor effectively blocks Akt signaling and tumor growth with only transient effects on glucose and insulin levels in vivo.Reduction of Pten dose leads to neoplastic development in multiple organs of Pten (shRNA) mice Interrogating two schedules of the AKT inhibitor MK-2206 in patients with advanced solid tumors incorporating novel pharmacodynamic and functional imaging biomarkers.Receptor-recognized α₂-macroglobulin binds to cell surface-associated GRP78 and activates mTORC1 and mTORC2 signaling in prostate cancer cells.Requirement for ribosomal protein S6 kinase 1 to mediate glycolysis and apoptosis resistance induced by Pten deficiency.

P2860

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P2860

The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice.

http://www.wikidata.org/entity/Q34693888

description

2006 nî lūn-bûn

@nan

2006 թուականի Յունիսին հրատարակուած գիտական յօդուած

@hyw

2006 թվականի հունիսին հրատարակված գիտական հոդված

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2006年の論文

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2006年論文

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2006年論文

@zh-hant

2006年論文

@zh-hk

2006年論文

@zh-mo

2006年論文

@zh-tw

2006年论文

@wuu

name

The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice.

@ast

The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice.

@en

The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice.

@nl

type

label

The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice.

@ast

The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice.

@en

The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice.

@nl

prefLabel

The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice.

@ast

The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice.

@en

The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice.

@nl

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Genes & Development

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The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice.

@en

P2093

Antonio Di Cristofano

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

Grace Guzman

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

Mei-Ling Chen

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

Nissim Hay

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Pei-Zhang Xu

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

William S Chen

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Xiao-ding Peng

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Ximing Yang

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P2860

The phosphoinositide 3-kinase pathway

Molecular determinants of resistance to antiandrogen therapy

The biology and clinical relevance of the PTEN tumor suppressor pathway

Growth retardation and increased apoptosis in mice with homozygous disruption of the Akt1 gene

Pten is essential for embryonic development and tumour suppression

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

Allosteric Akt (PKB) inhibitors: discovery and SAR of isozyme selective inhibitors.

The regulation and activities of the multifunctional serine/threonine kinase Akt/PKB.

Ten years of protein kinase B signalling: a hard Akt to follow.

Prostate pathology of genetically engineered mice: definitions and classification. The consensus report from the Bar Harbor meeting of the Mouse Models of Human Cancer Consortium Prostate Pathology Committee.

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1569-1574

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10.1101/GAD.1395006

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12

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20

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Pier Paolo Pandolfi

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2006-06-01T00:00:00Z

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7005811

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16778075

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1482477

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