Hochschulschrift
The roles of VE-cadherin-serine 665 and -tyrosine 685 for endocytosis in the control of endothelial junctions
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- Dimensions
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30 cm
- Extent
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VI, 248 Seiten
- Language
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Englisch
- Notes
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Illustrationen, Diagramme
Westfälische Wilhelms-Universität Münster, Dissertation, 2016
- Keyword
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Membrantransport
Biomembran
Endothel
- Table of contents
- Rights
-
Bei diesem Objekt liegt nur das Inhaltsverzeichnis digital vor. Der Zugriff darauf ist unbeschränkt möglich.
- Last update
-
11.06.2025, 1:38 PM CEST
Data provider
This object is provided by:
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Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Object type
- Hochschulschrift
Associated
Time of origin
- 2016
Other Objects (12)
Tyrosine-protein kinase Yes controls endothelial junctional plasticity and barrier integrity by regulating VE-cadherin phosphorylation and endocytosis
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Pcdh18a regulates endocytosis of E-cadherin during axial mesoderm development in zebrafish
Correction to: Disruption of endothelial adherens junctions by high glucose is mediated by protein kinase C-β–dependent vascular endothelial cadherin tyrosine phosphorylation
Downregulation of praja2 restrains endocytosis and boosts tyrosine kinase receptors in kidney cancer
Functional role of the Synaptic Adhesion Molecule N-cadherin in Synaptic Vesicle Exo- and Endocytosis
Regulation of VE-cadherin tyrosine 731 phosphorylation under basal and inflammatory conditions
A delay in vesicle endocytosis by a C-terminal fragment of N-cadherin enhances Aβ synaptotoxicity
Serine threonine tyrosine kinase 1 is a potential prognostic marker in colorectal cancer
ESAM controls opening of endothelial junctions via phosphorylation of VE-cadherin at Y685 residue
Ubiquitin ligase CHFR mediated degradation of VE-cadherin through ubiquitylation disrupts endothelial adherens junctions
ZNPs reduce epidermal mechanical strain resistance by promoting desmosomal cadherin endocytosis via mTORC1-TFEB-BLOC1S3 axis
Tyrosine-protein kinase Yes controls endothelial junctional plasticity and barrier integrity by regulating VE-cadherin phosphorylation and endocytosis
Endocytosis and the Src family of non-receptor tyrosine kinases
Pcdh18a regulates endocytosis of E-cadherin during axial mesoderm development in zebrafish
Correction to: Disruption of endothelial adherens junctions by high glucose is mediated by protein kinase C-β–dependent vascular endothelial cadherin tyrosine phosphorylation
Downregulation of praja2 restrains endocytosis and boosts tyrosine kinase receptors in kidney cancer
Functional role of the Synaptic Adhesion Molecule N-cadherin in Synaptic Vesicle Exo- and Endocytosis
Regulation of VE-cadherin tyrosine 731 phosphorylation under basal and inflammatory conditions
A delay in vesicle endocytosis by a C-terminal fragment of N-cadherin enhances Aβ synaptotoxicity
Serine threonine tyrosine kinase 1 is a potential prognostic marker in colorectal cancer
ESAM controls opening of endothelial junctions via phosphorylation of VE-cadherin at Y685 residue
Ubiquitin ligase CHFR mediated degradation of VE-cadherin through ubiquitylation disrupts endothelial adherens junctions
ZNPs reduce epidermal mechanical strain resistance by promoting desmosomal cadherin endocytosis via mTORC1-TFEB-BLOC1S3 axis
Tyrosine-protein kinase Yes controls endothelial junctional plasticity and barrier integrity by regulating VE-cadherin phosphorylation and endocytosis
Endocytosis and the Src family of non-receptor tyrosine kinases
Pcdh18a regulates endocytosis of E-cadherin during axial mesoderm development in zebrafish
Correction to: Disruption of endothelial adherens junctions by high glucose is mediated by protein kinase C-β–dependent vascular endothelial cadherin tyrosine phosphorylation
Downregulation of praja2 restrains endocytosis and boosts tyrosine kinase receptors in kidney cancer
Functional role of the Synaptic Adhesion Molecule N-cadherin in Synaptic Vesicle Exo- and Endocytosis
Regulation of VE-cadherin tyrosine 731 phosphorylation under basal and inflammatory conditions
A delay in vesicle endocytosis by a C-terminal fragment of N-cadherin enhances Aβ synaptotoxicity
Serine threonine tyrosine kinase 1 is a potential prognostic marker in colorectal cancer
ESAM controls opening of endothelial junctions via phosphorylation of VE-cadherin at Y685 residue
Ubiquitin ligase CHFR mediated degradation of VE-cadherin through ubiquitylation disrupts endothelial adherens junctions