Kaposi's sarcoma-associated herpes virus disrupts adherens junctions and increases endothelial permeability by inducing degradation of VE-cadherin
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
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1750-9378
- Extent
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Online-Ressource
- Language
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Englisch
- Notes
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online resource.
- Bibliographic citation
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Kaposi's sarcoma-associated herpes virus disrupts adherens junctions and increases endothelial permeability by inducing degradation of VE-cadherin ; volume:4 ; number:2 ; day:17 ; month:6 ; year:2009 ; pages:1 ; date:6.2009
Infectious agents and cancer ; 4, Heft 2 (17.6.2009), 1, 6.2009
- Creator
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Qian, LW
- Contributor
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Greene, W.
Ye, FC
Gao, SJ
SpringerLink (Online service)
- DOI
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10.1186/1750-9378-4-S2-P18
- URN
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urn:nbn:de:1111-2016072623007
- Rights
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Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
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14.08.2025, 10:50 AM CEST
Data provider
This object is provided by:
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Qian, LW
- Greene, W.
- Ye, FC
- Gao, SJ
- SpringerLink (Online service)
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Upregulation of angiopoietin-like 4 by viral G protein-coupled receptor promotes angiogenesis and vascular permeability in Kaposi’s sarcoma
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ESAM controls opening of endothelial junctions via phosphorylation of VE-cadherin at Y685 residue
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Mbt/PAK4 together with SRC modulates N-Cadherin adherens junctions in the developing Drosophila eye
Protein Ser/Thr phosphatase-6 is required for maintenance of E-cadherin at adherens junctions
Heterocellular N-cadherin junctions enable nontransformed cells to inhibit the growth of adjacent transformed cells
CMTM4 regulates angiogenesis by promoting cell surface recycling of VE-cadherin to endothelial adherens junctions
Ubiquitin ligase CHFR mediated degradation of VE-cadherin through ubiquitylation disrupts endothelial adherens junctions
Clathrin inhibitor Pitstop-2 disrupts the nuclear pore complex permeability barrier
Conditional deletion of Cadherin 13 perturbs Golgi cells and disrupts social and cognitive behaviors
Upregulation of angiopoietin-like 4 by viral G protein-coupled receptor promotes angiogenesis and vascular permeability in Kaposi’s sarcoma
Diagnostic dilemma in Kaposi’s sarcoma
ESAM controls opening of endothelial junctions via phosphorylation of VE-cadherin at Y685 residue
Case report of ocular Kaposi’s sarcoma
Aging disrupts blood–brain and blood-spinal cord barrier homeostasis, but does not increase paracellular permeability
Mbt/PAK4 together with SRC modulates N-Cadherin adherens junctions in the developing Drosophila eye
Protein Ser/Thr phosphatase-6 is required for maintenance of E-cadherin at adherens junctions
Heterocellular N-cadherin junctions enable nontransformed cells to inhibit the growth of adjacent transformed cells
CMTM4 regulates angiogenesis by promoting cell surface recycling of VE-cadherin to endothelial adherens junctions
Ubiquitin ligase CHFR mediated degradation of VE-cadherin through ubiquitylation disrupts endothelial adherens junctions
Clathrin inhibitor Pitstop-2 disrupts the nuclear pore complex permeability barrier
Conditional deletion of Cadherin 13 perturbs Golgi cells and disrupts social and cognitive behaviors
Upregulation of angiopoietin-like 4 by viral G protein-coupled receptor promotes angiogenesis and vascular permeability in Kaposi’s sarcoma
Diagnostic dilemma in Kaposi’s sarcoma
ESAM controls opening of endothelial junctions via phosphorylation of VE-cadherin at Y685 residue
Case report of ocular Kaposi’s sarcoma
Aging disrupts blood–brain and blood-spinal cord barrier homeostasis, but does not increase paracellular permeability
Mbt/PAK4 together with SRC modulates N-Cadherin adherens junctions in the developing Drosophila eye
Protein Ser/Thr phosphatase-6 is required for maintenance of E-cadherin at adherens junctions
Heterocellular N-cadherin junctions enable nontransformed cells to inhibit the growth of adjacent transformed cells