CMTM4 regulates angiogenesis by promoting cell surface recycling of VE-cadherin to endothelial adherens junctions
- Standort
-
Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
-
1573-7209
- Umfang
-
Online-Ressource
- Sprache
-
Englisch
- Anmerkungen
-
online resource.
- Erschienen in
-
CMTM4 regulates angiogenesis by promoting cell surface recycling of VE-cadherin to endothelial adherens junctions ; day:10 ; month:8 ; year:2018 ; pages:1-19
Angiogenesis ; (10.8.2018), 1-19
- Urheber
-
Chrifi, Ihsan
- Beteiligte Personen und Organisationen
-
Louzao-Martinez, Laura
Brandt, Maarten M.
Dijk, Christian G. M. van
Bürgisser, Petra E.
Zhu, Changbin
Kros, Johan M.
Verhaar, Marianne C.
Duncker, Dirk J.
Cheng, Caroline
SpringerLink (Online service)
- DOI
-
10.1007/s10456-018-9638-1
- URN
-
urn:nbn:de:101:1-2018101000080172372673
- Rechteinformation
-
Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
-
15.08.2025, 07:22 MESZ
Datenpartner
Dieses Objekt wird bereitgestellt von:
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Beteiligte
- Chrifi, Ihsan
- Louzao-Martinez, Laura
- Brandt, Maarten M.
- Dijk, Christian G. M. van
- Bürgisser, Petra E.
- Zhu, Changbin
- Kros, Johan M.
- Verhaar, Marianne C.
- Duncker, Dirk J.
- Cheng, Caroline
- SpringerLink (Online service)
Ähnliche Objekte (12)
PLK1 and its substrate MISP facilitate intrahepatic cholangiocarcinoma progression by promoting lymphatic invasion and impairing E-cadherin adherens junctions
Soluble E-cadherin promotes tumor angiogenesis and localizes to exosome surface
Promoting residential recycling: An alternative policy based on a recycling reward system
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
Changes in expression of VE-cadherin and MMPs in endothelial cells: Implications for angiogenesis
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
Molecular Electronics: Creating and Bridging Molecular Junctions and Promoting Its Commercialization
Tumor endothelial cell-derived cadherin-2 promotes angiogenesis and has prognostic significance for lung adenocarcinoma
Polarized actin and VE-cadherin dynamics regulate junctional remodelling and cell migration during sprouting angiogenesis
PLK1 and its substrate MISP facilitate intrahepatic cholangiocarcinoma progression by promoting lymphatic invasion and impairing E-cadherin adherens junctions
Soluble E-cadherin promotes tumor angiogenesis and localizes to exosome surface
Promoting residential recycling: An alternative policy based on a recycling reward system
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
Changes in expression of VE-cadherin and MMPs in endothelial cells: Implications for angiogenesis
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
Molecular Electronics: Creating and Bridging Molecular Junctions and Promoting Its Commercialization
Tumor endothelial cell-derived cadherin-2 promotes angiogenesis and has prognostic significance for lung adenocarcinoma
Polarized actin and VE-cadherin dynamics regulate junctional remodelling and cell migration during sprouting angiogenesis
PLK1 and its substrate MISP facilitate intrahepatic cholangiocarcinoma progression by promoting lymphatic invasion and impairing E-cadherin adherens junctions
Soluble E-cadherin promotes tumor angiogenesis and localizes to exosome surface
Promoting residential recycling: An alternative policy based on a recycling reward system
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
Changes in expression of VE-cadherin and MMPs in endothelial cells: Implications for angiogenesis
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
Molecular Electronics: Creating and Bridging Molecular Junctions and Promoting Its Commercialization
Tumor endothelial cell-derived cadherin-2 promotes angiogenesis and has prognostic significance for lung adenocarcinoma