Negative regulation of urokinase-type plasminogen activator production through FGF-2-mediated activation of phosphoinositide 3-kinase (Q44172494)

30 November 2017

Negative regulation of urokinase-type plasminogen activator production through FGF-2-mediated activation of phosphoinositide 3-kinase (English)

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30 November 2017

Yasushi Mochizuki

1

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30 November 2017

Satoshi Tsuda

series ordinal

2

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30 November 2017

Hiroshi Kanetake

series ordinal

3

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30 November 2017

Shigeru Kanda

series ordinal

4

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30 November 2017

language of work or name

English

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publication date

1 October 2002

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30 November 2017

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30 November 2017

21

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30 November 2017

46

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30 November 2017

7027-7033

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https://scigraph.springernature.com/pub.10.1038/sj.onc.1205736

30 November 2017

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Absence of host plasminogen activator inhibitor 1 prevents cancer invasion and vascularization.

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The plasminogen activator inhibitor PAI-1 controls in vivo tumor vascularization by interaction with proteases, not vitronectin. Implications for antiangiogenic strategies

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Urokinase and urokinase receptor: a paracrine/autocrine system regulating cell migration and invasiveness

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FGF signals for cell proliferation and migration through different pathways

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AKT/PKB and other D3 phosphoinositide-regulated kinases: kinase activation by phosphoinositide-dependent phosphorylation

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Downstream signalling events regulated by phosphatidylinositol 3-kinase activity.

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Phosphoinositide kinases

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Stimulation of urokinase-type plasminogen activator receptor expression by PMA requires JNK1-dependent and -independent signaling modules.

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Phosphatidylinositol 3-kinase activation is mediated by high-affinity interactions between distinct domains within the p110 and p85 subunits

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Phosphatidylinositol 3-kinase signaling mediates angiogenesis and expression of vascular endothelial growth factor in endothelial cells

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Phosphatidylinositol 3'-kinase-independent p70 S6 kinase activation by fibroblast growth factor receptor-1 is important for proliferation but not differentiation of endothelial cells.

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Shc and a novel 89-kDa component couple to the Grb2-Sos complex in fibroblast growth factor-2-stimulated cells

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The C-terminal SH2 domain of p85 accounts for the high affinity and specificity of the binding of phosphatidylinositol 3-kinase to phosphorylated platelet-derived growth factor beta receptor

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Membrane localization of phosphatidylinositol 3-kinase is sufficient to activate multiple signal-transducing kinase pathways

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Dominant negative forms of Akt (protein kinase B) and atypical protein kinase Clambda do not prevent insulin inhibition of phosphoenolpyruvate carboxykinase gene transcription

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Pocket protein-independent repression of urokinase-type plasminogen activator and plasminogen activator inhibitor 1 gene expression by E2F1

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Identification of six novel autophosphorylation sites on fibroblast growth factor receptor 1 and elucidation of their importance in receptor activation and signal transduction

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Phosphatidylinositol-3-OH kinase as a direct target of Ras

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Differentiation stage-specific inhibition of the Raf-MEK-ERK pathway by Akt.

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Phosphatidylinositol 3-kinases in tumor progression

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SH2 domains recognize specific phosphopeptide sequences

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PI3-kinase inhibition: a target for drug development?

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A phosphatidylinositol 3-kinase-dependent pathway that differentially regulates c-Raf and A-Raf

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Amiloride selectively inhibits the urokinase-type plasminogen activator

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Overexpression of urokinase-type plasminogen activator in pancreatic adenocarcinoma is regulated by constitutively activated RelA

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Phosphorylation and regulation of Raf by Akt (protein kinase B)

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Induction of urokinase-type plasminogen activator by fibroblast growth factor (FGF)-2 is dependent on expression of FGF receptors and does not require activation of phospholipase Cgamma1

21 January 2018

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inferred from DOI database lookup

7 January 2021

based on heuristic

Protein kinase B activation and lamellipodium formation are independent phosphoinositide 3-kinase-mediated events differentially regulated by endogenous Ras.

1 reference

https://api.crossref.org/works/10.1038%2FSJ.ONC.1205736

inferred from DOI database lookup

7 January 2021

based on heuristic

Identifiers

DOI

10.1038/SJ.ONC.1205736

1 reference

30 November 2017

1 reference