A5024464643- Immunotherapy and Immune Responses
- Immune Cell Function and Interaction
- Immune Response and Inflammation
- Cell Adhesion Molecules Research
- Fibroblast Growth Factor Research
- Angiogenesis and VEGF in Cancer
- Intracerebral and Subarachnoid Hemorrhage Research
- Vascular Malformations Diagnosis and Treatment
- T-cell and B-cell Immunology
- Intracranial Aneurysms: Treatment and Complications
- Kruppel-like factors research
- Moyamoya disease diagnosis and treatment
- Hippo pathway signaling and YAP/TAZ
- Neonatal Respiratory Health Research
- Proteoglycans and glycosaminoglycans research
- Wnt/β-catenin signaling in development and cancer
- RNA Interference and Gene Delivery
- Eosinophilic Disorders and Syndromes
- Pituitary Gland Disorders and Treatments
- Pluripotent Stem Cells Research
- Cerebrovascular and Carotid Artery Diseases
- Platelet Disorders and Treatments
- Cardiovascular Health and Disease Prevention
- Luminescence and Fluorescent Materials
- Connective tissue disorders research
ETH Zurich
2015-2021
IFOM
2009-2016
University of Milan
2010
European Institute of Oncology
2010
Endothelial adherens junctions maintain vascular integrity. Arteries and veins differ in their permeability but whether organization strength of vary has not been demonstrated vivo. Here we report that endothelial cadherin, an specific adhesion protein located at junctions, is phosphorylated Y658 Y685 vivo arteries under resting conditions. This difference due to shear stress-induced junctional Src activation veins. Phosphorylated endothelial-cadherin internalized ubiquitinated response...
Little is known about the molecular mechanisms that regulate organization of vascular lumen. In this paper we show lumen formation correlates with endothelial polarization. Adherens junctions (AJs) and VE-cadherin (VEC, encoded by CDH5) are required for apicobasal polarity in vitro during embryonic development. Silencing CDH5 gene expression leads to abrogation accompanied strong alterations lumenal structure. VEC co-distributes members Par complex (Par3 PKCzeta) needed activation PKCzeta....
Research Article26 November 2015Open Access Source Data KLF4 is a key determinant in the development and progression of cerebral cavernous malformations Roberto Cuttano IFOM, FIRC Institute Molecular Oncology, Milan, Italy Search for more papers by this author Noemi Rudini Luca Bravi Monica Corada Costanza Giampietro Department Biosciences, University Eleanna Papa on leave absence at Neurology, Laboratory Neuro-Oncology, Hospital Zurich, Switzerland Marco Francesco Morini Biomedicine, Basel,...
Cerebral cavernous malformations (CCM) are vascular of the central nervous system (CNS) that lead to cerebral hemorrhages. Familial CCM occurs as an autosomal dominant condition caused by loss-of-function mutations in one three genes. Constitutive or tissue-specific ablation any Ccm genes mice previously established crucial role gene expression endothelial cells for proper angiogenesis. However, embryonic lethality precluded development relevant mouse models. Here, we show...
Reproducing the characteristics and functional responses of blood–brain barrier (BBB) in vitro represents an important task for research community, would be a critical biotechnological breakthrough. Pharmaceutical biotechnology industries provide strong demand inexpensive easy-to-handle BBB models to screen novel drug candidates. Recently, it was shown that canonical Wnt signaling is responsible induction properties neonatal brain microvasculature vivo. In present study, following on from...
Significance Cerebral cavernous malformation (CCM) disease can lead to brain hemorrhages, seizures, and paralysis. No pharmacological therapy is currently available. Here we define, our knowledge for the first time in vivo, sequence of molecular events that CCM vascular cavernomas. We found β-catenin activation trigger followed by TGF-β signaling, which, turn, mediates progression disease. also show signaling cell-autonomous independent Wnt-receptor activation. Most importantly, these...
The adhesion molecule L1, which is extensively characterized in the nervous system, also expressed dendritic cells (DCs), but its function there has remained elusive. To address this issue, we ablated L1 expression DCs of conditional knockout mice. L1-deficient were impaired to and transmigration through monolayers either lymphatic or blood vessel endothelial cells, implicating transendothelial migration DCs. In agreement with these findings, was cutaneous that migrated draining lymph nodes,...
Research Article8 July 2011Open Access The adhesion molecule NCAM promotes ovarian cancer progression via FGFR signalling Silvia Zecchini IFOM – FIRC Institute of Molecular Oncology, Milano, Italy These authors contributed equally to this work. Search for more papers by author Lorenzo Bombardelli Alessandra Decio Department Mario Negri Pharmacological Research, Marco Bianchi Giovanni Mazzarol European Fabio Sanguineti Aletti Luigi Maddaluno Vladimir Berezin Protein Laboratory, Neuroscience...
While tumor blood vessels share many characteristics with normal vasculature, they also exhibit morphological and functional aberrancies. For example, the neural adhesion molecule L1, which mediates neurite outgrowth, fasciculation, pathfinding, is expressed on vasculature. Here, using an orthotopic mouse model of pancreatic carcinoma, we evaluated L1 functionality in cancer vessels. Tumor-bearing mice specifically lacking endothelial cells or treated anti-L1 antibodies exhibited decreased...
Abstract Junctional adhesion molecule-A (JAM-A)–null dendritic cells (DCs) are more motile and effective than their wild-type counterpart in promoting contact hypersensitivity reaction. Here, we show that the growth aggressiveness of pancreatic islet cell carcinoma induced by SV40 T antigen expression β (Rip1Tag2 mice) significantly reduced JAM-A–null mice. Because these tumor do not express JAM-A, focused on changes stroma reactivity. In absence tumors showed a small but significant...
Article27 July 2020Open Access Source DataTransparent process Antagonism of interferon signaling by fibroblast growth factors promotes viral replication Luigi Maddaluno Corresponding Author [email protected] orcid.org/0000-0002-4325-6220 Department Biology, Institute Molecular Health Sciences, ETH Zurich, Switzerland Search for more papers this author Corinne Urwyler Theresa Rauschendorfer Michael Meyer Debora Stefanova Roman Spörri Microbiology, Mateusz Wietecha Luca Ferrarese Diana...
Chronic skin inflammation resulting from a defective epidermal barrier is hallmark of atopic dermatitis (AD). We previously demonstrated that mice lacking FGF receptors 1 and 2 in keratinocytes (K5-R1/R2 mice) develop an AD-like chronic as result impaired barrier. Here, we show γδ T cells, which rapidly respond to various insults, accumulate the epidermis K5-R1/R2 before development histological abnormalities. Their number activation further increase phenotype progresses, most likely...
FGFs and their high-affinity receptors (FGFRs) play key roles in development, tissue repair, disease. Because FGFRs bind overlapping sets of ligands, individual functions cannot be determined using ligand stimulation. Here, we generated a light-activated FGFR2 variant (OptoR2) to selectively activate signaling by the major FGFR keratinocytes. Illumination OptoR2-expressing HEK 293T cells activated with remarkable temporal precision promoted cell migration proliferation. In murine human...
Primary myelofibrosis (PMF) is a Philadelphia-negative (Ph−) myeloproliferative disorder, showing abnormal CD34+ progenitor cell trafficking, splenomegaly, marrow fibrosis leading to extensive extramedullary haematopoiesis, and neoangiogenesis in either the bone or spleen. Monocytes expressing angiopoietin-2 receptor (Tie2) have been shown support angiogenic processes solid tumors through paracrine action that takes place proximity vessels. In this study we investigated frequency of Tie2...
The article "Loss of nuclear pro-IL-16 facilitates cell cycle progression in human cutaneous T lymphoma" is being retracted, with the agreement corresponding author.Several duplicated bands were recently identified immunoblot images Figures 1 and3, and authors are unable to retrieve original source files that used generate these data.
The adhesion molecule L1, which is extensively characterized in the nervous system, also expressed dendritic cells (DCs), but its function there has remained elusive. To address this issue, we ablated L1 expression DCs of conditional knockout mice. L1-deficient were impaired to and transmigration through monolayers either lymphatic or blood vessel endothelial cells, implicating transendothelial migration DCs. In agreement with these findings, was cutaneous that migrated draining lymph nodes,...
Supplementary Methods, Figure Legends 1-5 from Inactivation of Junctional Adhesion Molecule-A Enhances Antitumoral Immune Response by Promoting Dendritic Cell and T Lymphocyte Infiltration
Supplementary Figure 2 from Inactivation of Junctional Adhesion Molecule-A Enhances Antitumoral Immune Response by Promoting Dendritic Cell and T Lymphocyte Infiltration