Hypoxia-inducible factor-1alpha expression requires PI 3-kinase activity and correlates with Akt1 phosphorylation in invasive breast carcinomas (Q83305663)

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scientific article published on 08 May 2006

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English	Hypoxia-inducible factor-1alpha expression requires PI 3-kinase activity and correlates with Akt1 phosphorylation in invasive breast carcinomas	scientific article published on 08 May 2006

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20 January 2020

Hypoxia-inducible factor-1alpha expression requires PI 3-kinase activity and correlates with Akt1 phosphorylation in invasive breast carcinomas (English)

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20 January 2020

Paul J van Diest

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van Diest PJ

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20 January 2020

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Gort EH

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20 January 2020

Groot AJ

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20 January 2020

Derks van de Ven TL

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20 January 2020

van der Groep P

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20 January 2020

Verlaan I

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20 January 2020

van Laar T

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20 January 2020

van der Wall E

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20 January 2020

Shvarts A

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20 January 2020

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8 May 2006

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20 January 2020

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20 January 2020

25

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20 January 2020

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20 January 2020

6123-6127

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20 January 2020

Mechanism of activation of protein kinase B by insulin and IGF-1

1 reference

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Lack of evidence for the involvement of the phosphoinositide 3-kinase/Akt pathway in the activation of hypoxia-inducible factors by low oxygen tension.

1 reference

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Phosphatidylinositol 3-kinase/Akt signaling is neither required for hypoxic stabilization of HIF-1 alpha nor sufficient for HIF-1-dependent target gene transcription

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Growth factor-mediated induction of HDM2 positively regulates hypoxia-inducible factor 1alpha expression

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Levels of hypoxia-inducible factor-1alpha independently predict prognosis in patients with lymph node negative breast carcinoma

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Levels of hypoxia-inducible factor-1 alpha during breast carcinogenesis

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A conserved family of prolyl-4-hydroxylases that modify HIF

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Protein kinase B (c-Akt) in phosphatidylinositol-3-OH kinase signal transduction

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Overexpression of hypoxia-inducible factor HIF-1alpha predicts early relapse in breast cancer: retrospective study in a series of 745 patients

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C. elegans EGL-9 and mammalian homologs define a family of dioxygenases that regulate HIF by prolyl hydroxylation

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Activation of vascular endothelial growth factor gene transcription by hypoxia-inducible factor 1

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Insulin-like growth factor 1 induces hypoxia-inducible factor 1-mediated vascular endothelial growth factor expression, which is dependent on MAP kinase and phosphatidylinositol 3-kinase signaling in colon cancer cells

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Upstream and downstream of mTOR

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Regulation of hypoxia-inducible factor 1alpha expression and function by the mammalian target of rapamycin.

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HIFalpha targeted for VHL-mediated destruction by proline hydroxylation: implications for O2 sensing

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Targeting of HIF-alpha to the von Hippel-Lindau ubiquitylation complex by O2-regulated prolyl hydroxylation

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Dimerization, DNA binding, and transactivation properties of hypoxia-inducible factor 1

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AKT activation predicts outcome in breast cancer patients treated with tamoxifen

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Phosphorylation of Akt (Ser473) is an excellent predictor of poor clinical outcome in prostate cancer.

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Cleavage of Structural Proteins during the Assembly of the Head of Bacteriophage T4

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Transcriptional regulation of the rat vascular endothelial growth factor gene by hypoxia

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The tumour suppressor protein VHL targets hypoxia-inducible factors for oxygen-dependent proteolysis

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Regulation of hypoxia-inducible factor-1alpha protein level during hypoxic conditions by the phosphatidylinositol 3-kinase/Akt/glycogen synthase kinase 3beta pathway in HepG2 cells

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Prognostic relevance of activated Akt kinase in node-negative breast cancer: a clinicopathological study of 99 cases

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Hydroxylation of HIF-1: oxygen sensing at the molecular level

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Enhancement of gene expression under hypoxic conditions using fragments of the human vascular endothelial growth factor and the erythropoietin genes

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Vascular endothelial growth factor transcriptional activation is mediated by hypoxia-inducible factor 1alpha, HDM2, and p70S6K1 in response to phosphatidylinositol 3-kinase/AKT signaling

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The forkhead transcription factor FOXO4 induces the down-regulation of hypoxia-inducible factor 1 alpha by a von Hippel-Lindau protein-independent mechanism

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Insulin stimulates hypoxia-inducible factor 1 through a phosphatidylinositol 3-kinase/target of rapamycin-dependent signaling pathway

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No consent should be needed for using leftover body material for scientific purposes. For.

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Hypoxia-inducible factor 1 is a basic-helix-loop-helix-PAS heterodimer regulated by cellular O2 tension

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PI3K/Akt is required for heat shock proteins to protect hypoxia-inducible factor 1alpha from pVHL-independent degradation.

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