Endothelial barrier disruption by VEGF-mediated Src activity potentiates tumor cell extravasation and metastasis - Wikidata - wikimedia - TriplyDB

Endothelial barrier disruption by VEGF-mediated Src activity potentiates tumor cell extravasation and metastasis

Endothelial barrier disruption by VEGF-mediated Src activity potentiates tumor cell extravasation and metastasis

http://www.wikidata.org/entity/Q36322698

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The neurotransmitter dopamine modulates vascular permeability in the endothelium Histone deacetylase inhibition reduces myocardial ischemia-reperfusion injury in mice Traversing the basement membrane in vivo: a diversity of strategies The role of sphingosine-1-phosphate in endothelial barrier function Physical biology in cancer. 4. Physical cues guide tumor cell adhesion and migration VE-cadherin-independent cancer cell incorporation into the vascular endothelium precedes transmigration Metastatic colonization by circulating tumour cells Vascular permeability--the essentials Diminution of signal transducer and activator of transcription 3 signaling inhibits vascular permeability and anaphylaxis Ethanol disrupts vascular endothelial barrier: implication in cancer metastasis Predilection of contralateral upper lung metastasis in upper lobe lung adenocarcinoma patients Molecular resistance fingerprint of pemetrexed and platinum in a long-term survivor of mesothelioma Endothelium-Derived 5-Methoxytryptophan Protects Endothelial Barrier Function by Blocking p38 MAPK Activation A role for a CXCR2/phosphatidylinositol 3-kinase gamma signaling axis in acute and chronic vascular permeability.Specific oncogenic activity of the Src-family tyrosine kinase c-Yes in colon carcinoma cells.Src tyrosine kinase regulates the stem cell factor-induced breakdown of the blood-retinal barrier Tumor metastasis: molecular insights and evolving paradigms YES oncogenic activity is specified by its SH4 domain and regulates RAS/MAPK signaling in colon carcinoma cells VEGFR2 induces c-Src signaling and vascular permeability in vivo via the adaptor protein TSAd.The lysyl oxidase inhibitor, beta-aminopropionitrile, diminishes the metastatic colonization potential of circulating breast cancer cells Paxillin-Y118 phosphorylation contributes to the control of Src-induced anchorage-independent growth by FAK and adhesion.High-resolution imaging of the dynamic tumor cell vascular interface in transparent zebrafish Mechanisms of integrin-vascular endothelial growth factor receptor cross-activation in angiogenesis.Visualizing extravasation dynamics of metastatic tumor cells CCL2 disrupts the adherens junction: implications for neuroinflammation Three-dimensional microfluidic model for tumor cell intravasation and endothelial barrier function.Dynamic analysis of lung metastasis by mouse osteosarcoma LM8: VEGF is a candidate for anti-metastasis therapy Mechanisms of tumor cell extravasation in an in vitro microvascular network platform Invadosomes in their natural habitat.Dual suppression of hemangiogenesis and lymphangiogenesis by splice-shifting morpholinos targeting vascular endothelial growth factor receptor 2 (KDR)Data-Driven Discovery of Extravasation Pathway in Circulating Tumor Cells.Retinal vascular permeability suppression by topical application of a novel VEGFR2/Src kinase inhibitor in mice and rabbits.Chemoattractant signaling between tumor cells and macrophages regulates cancer cell migration, metastasis and neovascularization.Vascular endothelial-cadherin tyrosine phosphorylation in angiogenic and quiescent adult tissues Vascular endothelial-cadherin stabilizes at cell-cell junctions by anchoring to circumferential actin bundles through alpha- and beta-catenins in cyclic AMP-Epac-Rap1 signal-activated endothelial cells.Methylnaltrexone potentiates the anti-angiogenic effects of mTOR inhibitors Endothelial permeability and VE-cadherin: a wacky comradeship.Cholecystokinin mediates progression and metastasis of pancreatic cancer associated with dietary fat.Survival advantages conferred to colon cancer cells by E-selectin-induced activation of the PI3K-NFκB survival axis downstream of Death receptor-3.C-Src and c-Yes are two unlikely partners of spermatogenesis and their roles in blood-testis barrier dynamics.

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P2860

Endothelial barrier disruption by VEGF-mediated Src activity potentiates tumor cell extravasation and metastasis

http://www.wikidata.org/entity/Q36322698

description

2004 nî lūn-bûn

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2004年の論文

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2004年学术文章

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2004年学术文章

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2004年学术文章

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2004年学术文章

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2004年学术文章

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2004年學術文章

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2004年學術文章

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2004年學術文章

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Endothelial barrier disruption ...... l extravasation and metastasis

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Endothelial barrier disruption ...... l extravasation and metastasis

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Endothelial barrier disruption ...... l extravasation and metastasis

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Endothelial barrier disruption ...... l extravasation and metastasis

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Endothelial barrier disruption ...... l extravasation and metastasis

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Endothelial barrier disruption ...... l extravasation and metastasis

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P2093

David Cheresh

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Jianhua Cui

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Leo Barnes

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Sara Weis

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P2860

The biology of VEGF and its receptors

Generation of a syngeneic mouse model to study the effects of vascular endothelial growth factor in ovarian carcinoma.

Src blockade stabilizes a Flk/cadherin complex, reducing edema and tissue injury following myocardial infarction.

Optimization of 4-phenylamino-3-quinolinecarbonitriles as potent inhibitors of Src kinase activity.

Vascular permeability factor (VPF, VEGF) in tumor biology.

Selective requirement for Src kinases during VEGF-induced angiogenesis and vascular permeability.

Selective targeting of angiogenic tumor vasculature by vascular endothelial-cadherin antibody inhibits tumor growth without affecting vascular permeability.

Tumor regression by targeted gene delivery to the neovasculature.

Effect of the vascular endothelial growth factor receptor-2 antibody DC101 plus gemcitabine on growth, metastasis and angiogenesis of human pancreatic cancer growing orthotopically in nude mice.

SKI-606, a 4-anilino-3-quinolinecarbonitrile dual inhibitor of Src and Abl kinases, is a potent antiproliferative agent against chronic myelogenous leukemia cells in culture and causes regression of K562 xenografts in nude mice.

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10.1083/JCB.200408130

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2

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15504909

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2172541

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