Zobrazeno 1 - 4
of 4
pro vyhledávání: '"Natalia Colás-Algora"'
Autor:
Cristina Cacho-Navas, Carmen López-Pujante, Natalia Reglero-Real, Natalia Colás-Algora, Ana Cuervo, Jose Javier Conesa, Susana Barroso, Gema de Rivas, Sergio Ciordia, Alberto Paradela, Gianluca D'Agostino, Carlo Manzo, Jorge Feito, Germán Andrés, Francisca Molina-Jiménez, Pedro Majano, Isabel Correas, José-Maria Carazo, Sussan Nourshargh, Meritxell Huch, Jaime Millán
Publikováno v:
eLife, Vol 12 (2024)
Epithelial intercellular adhesion molecule (ICAM)-1 is apically polarized, interacts with, and guides leukocytes across epithelial barriers. Polarized hepatic epithelia organize their apical membrane domain into bile canaliculi and ducts, which are n
Externí odkaz:
https://doaj.org/article/773515c15a6d4f4ebbf37f60f7041ad5
Autor:
Jaime Millán, Natalia Colás-Algora
Publikováno v:
Cellular and Molecular Life Sciences. 76:1299-1317
The vasculature is the paradigm of a compartment generated by parallel cellular barriers that aims to transport oxygen, nutrients and immune cells in complex organisms. Vascular barrier dysfunction leads to fatal acute and chronic inflammatory diseas
Autor:
Cristina Cacho-Navas, Natalia Reglero-Real, Natalia Colás-Algora, Susana Barroso, Gema de Rivas, Kostantinos Stamatakis, Jorge Feito, Germán Andrés, Manuel Fresno, Leonor Kremer, Isabel Correas, Miguel A. Alonso, Jaime Millán
Publikováno v:
Cellular and Molecular Life Sciences
Biblos-e Archivo. Repositorio Institucional de la UAM
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Biblos-e Archivo. Repositorio Institucional de la UAM
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Apical localization of Intercellular Adhesion Receptor (ICAM)-1 regulates the adhesion and guidance of leukocytes across polarized epithelial barriers. Here, we investigate the molecular mechanisms that determine ICAM-1 localization into apical membr
Autor:
Jaime Millán, Diego García-Weber, Álvaro Caballero, Catalina Ribas, Natalia Colás-Algora, Isabel Correas, Cristina Cacho-Navas, Susana Barroso
Publikováno v:
Digital.CSIC. Repositorio Institucional del CSIC
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VE-cadherin plays a central role in controlling endothelial barrier function, which is transiently disrupted by proinflammatory cytokines such as tumor necrosis factor (TNFα). Here we show that human endothelial cells compensate VE-cadherin degradat