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185 results on '"DUBRAC, Alexandre"'

7. Mild Hypoxia Accelerates Cerebral Cavernous Malformation Disease Through CX3CR1-CX3CL1 Signaling

Author

Frias-Anaya, Eduardo, Gallego-Gutierrez, Helios, Gongol, Brendan, Weinsheimer, Shantel, Lai, Catherine Chinhchu, Orecchioni, Marco, Sriram, Aditya, Bui, Cassandra M., Nelsen, Bliss, Hale, Preston, Pham, Angela, Shenkar, Robert, DeBiasse, Dorothy, Lightle, Rhonda, Girard, Romuald, Li, Ying, Srinath, Abhinav, Daneman, Richard, Nudleman, Eric, Sun, Hao, Guma, Monica, Dubrac, Alexandre, Mesarwi, Omar A., Ley, Klaus, Kim, Helen, Awad, Issam A., Ginsberg, Mark H., and Lopez-Ramirez, Miguel Alejandro

Published
2024
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10. Pathological angiogenesis in retinopathy engages cellular senescence and is amenable to therapeutic elimination via BCL-xL inhibition

Author

Crespo-Garcia, Sergio, Tsuruda, Pamela R., Dejda, Agnieszka, Ryan, Rathi D., Fournier, Frederik, Chaney, Shawnta Y., Pilon, Frederique, Dogan, Taner, Cagnone, Gael, Patel, Priyanka, Buscarlet, Manuel, Dasgupta, Sonali, Girouard, Gabrielle, Rao, Surabhi R., Wilson, Ariel M., O’Brien, Robert, Juneau, Rachel, Guber, Vera, Dubrac, Alexandre, Beausejour, Christian, Armstrong, Scott, Mallette, Frederick A., Yohn, Christopher B., Joyal, Jean-Sebastien, Marquess, Dan, Beltran, Pedro J., and Sapieha, Przemyslaw

Published
2021
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12. Exploring the Impact of Saccharin on Neovascular Age-Related Macular Degeneration: A Comprehensive Study in Patients and Mice

Author

Künzel, Steffen E., primary, Pompös, Inga-Marie, additional, Flesch, Leonie T. M., additional, Frentzel, Dominik P., additional, Knecht, Vitus A., additional, Winkler, Silvia, additional, Skosyrski, Sergej, additional, Rübsam, Anne, additional, Dreher, Felix, additional, Kociok, Norbert, additional, Schütte, Moritz, additional, Dubrac, Alexandre, additional, Lange, Bodo, additional, Yaspo, Marie-Laure, additional, Lehrach, Hans, additional, Strauß, Olaf, additional, Joussen, Antonia M., additional, and Zeitz, Oliver, additional

Published
2024
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14. Metabolic Reprogramming of the Neovascular Niche Promotes Regenerative Angiogenesis in Proliferative Retinopathy

Author

Joyal, Jean-Sebastien, primary, Cagnone, Gael, additional, Pundir, Sheetal, additional, Kim, Jin Sung, additional, Rivera, Jose, additional, Agnihotri, Tapan, additional, Harvey, Noemie-Rose, additional, Heckel, Emilie, additional, Betus, Charlotte, additional, Chen, Mei, additional, Situ, Anu, additional, Gaub, Perrine, additional, Kim, Nicholas, additional, Das, Ashim, additional, Leclerc, Severine, additional, Wünnemann, Florian, additional, Andelfinger, Gregor, additional, Crespo-Garcia, Sergio, additional, Dubrac, Alexandre, additional, Rezende, Flavio, additional, Clish, Clary, additional, Maranda, Bruno, additional, Smith, Lois, additional, and Sapieha, Przemyslaw, additional

Published
2024
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16. Metabolic Reprogramming of the Neovascular Niche Promotes Regenerative Angiogenesis in Proliferative Retinopathy

Author

Cagnone, Gael, primary, Pundir, Sheetal, additional, Sung-Kim, Jin, additional, Rivera, Jose Carlos, additional, Agnihotri, Tapan, additional, Harvey, Noemie-Rose, additional, Heckel, Emilie, additional, Betus, Charlotte, additional, Chen, Mei Xi, additional, Situ, Anu, additional, Gaub, Perrine, additional, Kim, Nicholas, additional, Das, Ashim, additional, Leclerc, Severine, additional, Wunnemann, Florian, additional, Andelfinger, Gregor, additional, Crespo-Garcia, Sergio, additional, Dubrac, Alexandre, additional, Rezende, Flavio, additional, Clish, Clary B, additional, Maranda, Bruno, additional, Smith, Lois E.H., additional, Sapieha, Przemyslaw, additional, and Joyal, Jean-Sebastien, additional

Published
2023
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17. Lacteal junction zippering protects against diet-induced obesity

Author

Zhang, Feng, Zarkada, Georgia, Han, Jinah, Li, Jinyu, Dubrac, Alexandre, Ola, Roxana, Genet, Gael, Boyé, Kevin, Michon, Pauline, Künzel, Steffen E., Camporez, Joao Paulo, Singh, Abhishek K., Fong, Guo-Hua, Simons, Michael, Tso, Patrick, Fernández-Hernando, Carlos, Shulman, Gerald I., Sessa, William C., and Eichmann, Anne

Published
2018

19. Systemic Blood Proteome Patterns Reflect Disease Phenotypes in Neovascular Age-Related Macular Degeneration

Author

Künzel, Steffen E., primary, Flesch, Leonie T. M., additional, Frentzel, Dominik P., additional, Knecht, Vitus A., additional, Rübsam, Anne, additional, Dreher, Felix, additional, Schütte, Moritz, additional, Dubrac, Alexandre, additional, Lange, Bodo, additional, Yaspo, Marie-Laure, additional, Lehrach, Hans, additional, Joussen, Antonia M., additional, and Zeitz, Oliver, additional

Published
2023
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22. Fig.S4 from Dual Roles for CXCL4 Chemokines and CXCR3 in Angiogenesis and Invasion of Pancreatic Cancer

Author

Quemener, Cathy, primary, Baud, Jessica, primary, Boyé, Kevin, primary, Dubrac, Alexandre, primary, Billottet, Clotilde, primary, Soulet, Fabienne, primary, Darlot, Florence, primary, Dumartin, Laurent, primary, Sire, Marie, primary, Grepin, Renaud, primary, Daubon, Thomas, primary, Rayne, Fabienne, primary, Wodrich, Harald, primary, Couvelard, Anne, primary, Pineau, Raphael, primary, Schilling, Martin, primary, Castronovo, Vincent, primary, Sue, Shih-Che, primary, Clarke, Kim, primary, Lomri, Abderrahim, primary, Khatib, Abdel-Majid, primary, Hagedorn, Martin, primary, Prats, Hervé, primary, and Bikfalvi, Andreas, primary

Published
2023
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23. Supplemental Material and Methods from Dual Roles for CXCL4 Chemokines and CXCR3 in Angiogenesis and Invasion of Pancreatic Cancer

Author

Quemener, Cathy, primary, Baud, Jessica, primary, Boyé, Kevin, primary, Dubrac, Alexandre, primary, Billottet, Clotilde, primary, Soulet, Fabienne, primary, Darlot, Florence, primary, Dumartin, Laurent, primary, Sire, Marie, primary, Grepin, Renaud, primary, Daubon, Thomas, primary, Rayne, Fabienne, primary, Wodrich, Harald, primary, Couvelard, Anne, primary, Pineau, Raphael, primary, Schilling, Martin, primary, Castronovo, Vincent, primary, Sue, Shih-Che, primary, Clarke, Kim, primary, Lomri, Abderrahim, primary, Khatib, Abdel-Majid, primary, Hagedorn, Martin, primary, Prats, Hervé, primary, and Bikfalvi, Andreas, primary

Published
2023
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24. Data from Dual Roles for CXCL4 Chemokines and CXCR3 in Angiogenesis and Invasion of Pancreatic Cancer

Author

Quemener, Cathy, primary, Baud, Jessica, primary, Boyé, Kevin, primary, Dubrac, Alexandre, primary, Billottet, Clotilde, primary, Soulet, Fabienne, primary, Darlot, Florence, primary, Dumartin, Laurent, primary, Sire, Marie, primary, Grepin, Renaud, primary, Daubon, Thomas, primary, Rayne, Fabienne, primary, Wodrich, Harald, primary, Couvelard, Anne, primary, Pineau, Raphael, primary, Schilling, Martin, primary, Castronovo, Vincent, primary, Sue, Shih-Che, primary, Clarke, Kim, primary, Lomri, Abderrahim, primary, Khatib, Abdel-Majid, primary, Hagedorn, Martin, primary, Prats, Hervé, primary, and Bikfalvi, Andreas, primary

Published
2023
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29. Slit2 signaling through Robo1 and Robo2 is required for retinal neovascularization

Author

Rama, Nicolas, Dubrac, Alexandre, Mathivet, Thomas, Charthaigh, Roisin-Ana Ni, Genet, Gael, Cristofaro, Brunella, Pibouin-Fragner, Laurence, Ma, Le, Eichmann, Anne, and Chedotal, Alain

Subjects
Eye diseases -- Genetic aspects -- Development and progression, Neovascularization -- Genetic aspects, Cellular signal transduction -- Health aspects, Biological sciences, Health
Abstract

Ocular neovascular diseases are a leading cause of blindness. Vascular endothelial growth factor (VEGF) blockade improves vision, but not all individuals respond to anti-VEGF treatment, making additional means to prevent neovascularization necessary. Slit-family proteins (Slits) are ligands of Roundabout (Robo) receptors that repel developing axons in the nervous system. Robo1 expression is altered in ocular neovascular diseases, and previous in vitro studies have reported both pro- and anti-angiogenic effects of Slits. However, genetic evidence supporting a role for Slits in ocular neovascularization is lacking. Here we generated conditional knockout mice deficient in various Slit and Robo proteins and found that Slit2 potently and selectively promoted angiogenesis via Robo1 and Robo2 in mouse postnatal retina and in a model of ocular neovascular disease. Mechanistically, Slit2 acting through Robo1 and Robo2 promoted the migration of endothelial cells. These receptors are required for both Slit2- and VEGF-induced Rac1 activation and lamellipodia formation. Thus, Slit2 blockade could potentially be used therapeutically to inhibit angiogenesis in individuals with ocular neovascular disease., Ocular neovascular diseases are the most common cause of vision loss, affecting millions of people in the industrialized world. Such diseases include the wet form of age-related macular degeneration (AMD), [...]

Published
2015
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31. Transmembrane protein ESDN promotes endothelial VEGF signaling and regulates angiogenesis: values) or 2-way ANOVA with Bonferroni post hoc test (for >2 groups). A P value less than 0.05 was considered significant

Author

Nie, Lei, Guo, Xiaojia, Esmailzadeh, Leila, Zhang, Jiasheng, Asadi, Abolfazl, Collinge, Mark, Li, Xuan, Kim, Jun-Dae, Woolls, Melissa, Jin, Suk-Won, Dubrac, Alexandre, Eichmann, Anne, Simons, Michael, Bender, Jeffrey R., and Sadeghi, Mehran M.

Subjects
Neovascularization -- Health aspects -- Research, Endothelium -- Health aspects -- Physiological aspects, Vascular endothelial growth factor -- Health aspects -- Physiological aspects, Membrane proteins -- Physiological aspects, Health care industry
Abstract

Aberrant blood vessel formation contributes to a wide variety of pathologies, and factors that regulate angiogenesis are attractive therapeutic targets. Endothelial and smooth muscle cell-derived neuropilin-like protein (ESDN) is a neuropilin-related transmembrane protein expressed in ECs; however, its potential effect on VEGF responses remains undefined. Here, we generated global and EC-specific Esdn knockout mice and demonstrated that ESDN promotes VEGF-induced human and murine EC proliferation and migration. Deletion of Esdn in the mouse interfered with adult and developmental angiogenesis, and knockdown of the Esdn homolog (dcbld2) in zebrafish impaired normal vascular development. Loss of ESDN in ECs blunted VEGF responses in vivo and attenuated VEGF-induced VEGFR-2 signaling without altering VEGF receptor or neuropilin expression. Finally, we found that ESDN associates with VEGFR-2 and regulates its complex formation with negative regulators of VEGF signaling, protein tyrosine phosphatases PTP1B and TC-PTP, and VE-cadherin. These findings establish ESDN as a regulator of VEGF responses in ECs that acts through a mechanism distinct from neuropilins. As such, ESDN may serve as a therapeutic target for angiogenesis regulation., Introduction Angiogenesis is a tightly regulated process during development and growth, and wound healing in adult organisms. Dysregulated angiogenesis, whether inadequate or exaggerated, con-tributes to a wide variety of pathologies, [...]

Published
2013

34. FGF-dependent metabolic control of vascular development

Author

Yu, Pengchun, Wilhelm, Kerstin, Dubrac, Alexandre, Tung, Joe K., Alves, Tiago C., Fang, Jennifer S., Xie, Yi, Zhu, Jie, Chen, Zehua, De Smet, Frederik, Zhang, Jiasheng, Jin, Suk-Won, Sun, Lele, Sun, Hongye, Kibbey, Richard G., Hirschi, Karen K., Hay, Nissim, Carmeliet, Peter, Chittenden, Thomas W., Eichmann, Anne, Potente, Michael, and Simons, Michael

Subjects
Fibroblast growth factors -- Health aspects, Metabolism -- Observations, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): Pengchun Yu [1]; Kerstin Wilhelm [2]; Alexandre Dubrac [1]; Joe K. Tung [1]; Tiago C. Alves [3]; Jennifer S. Fang [1]; Yi Xie [1]; Jie Zhu [4]; Zehua Chen [...]

Published
2017
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35. Noncanonical TGFβ Signaling Promotes Specialized Neuroretina Tip-Cell Sprouting and Blood-Retina Barrier Formation

Author

Zarkada, Georgia, primary, Howard, Joel P., additional, Xiao, Xue, additional, Park, Hyojin, additional, Bizou, Mathilde, additional, Leclerc, Severine, additional, Künzel, Steffen E., additional, Cagnone, Gael, additional, Joyal, Jean Sebastien, additional, Andelfinger, Gregor, additional, Eichmann, Anne, additional, and Dubrac, Alexandre, additional

Published
2021
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36. The Robo4 cytoplasmic domain is dispensable for vascular permeability and neovascularization

Author

Zhang, Feng, Prahst, Claudia, Mathivet, Thomas, Pibouin-Fragner, Laurence, Zhang, Jiasheng, Genet, Gael, Tong, Raymond, Dubrac, Alexandre, and Eichmann, Anne

Subjects
Mice, Knockout, Wound Healing, Diabetic Retinopathy, Neovascularization, Pathologic, Science, Oxygen Inhalation Therapy, Nerve Tissue Proteins, Receptors, Cell Surface, Vascular Endothelial Growth Factor Receptor-2, Article, Capillary Permeability, Mice, Retinal Diseases, cardiovascular system, Animals, Intercellular Signaling Peptides and Proteins, Retinopathy of Prematurity, Phosphorylation, Receptors, Immunologic, Netrin Receptors, Signal Transduction
Abstract

Vascular permeability and neovascularization are implicated in many diseases including retinopathies and diabetic wound healing. Robo4 is an endothelial-specific transmembrane receptor that stabilizes the vasculature, as shown in Robo4−/− mice that develop hyperpermeability, but how Robo4 signals remained unclear. Here we show that Robo4 deletion enhances permeability and revascularization in oxygen-induced retinopathy (OIR) and accelerates cutaneous wound healing. To determine Robo4 signalling pathways, we generated transgenic mice expressing a truncated Robo4 lacking the cytoplasmic domain (Robo4ΔCD). Robo4ΔCD expression is sufficient to prevent permeability, and inhibits OIR revascularization and wound healing in Robo4−/− mice. Mechanistically, Robo4 does not affect Slit2 signalling, but Robo4 and Robo4ΔCD counteract Vegfr2-Y949 (Y951 in human VEGFR2) phosphorylation by signalling through the endothelial UNC5B receptor. We conclude that Robo4 inhibits angiogenesis and vessel permeability independently of its cytoplasmic domain, while activating VEGFR2-Y951 via ROBO4 inhibition might accelerate tissue revascularization in retinopathy of prematurity and in diabetic patients., Robo4 is a transmembrane protein that regulates vascular permeability. Zhang et al. now reveal the mechanism of Robo4 action and show that Robo4 and UncB are required for VEGF-mediated regulation of vascular barrier by suppressing VEGF-induced phosphorylation of its receptor Vegfr2 on Y949.

Published
2016

37. Glioblastoma invasion and cooption depend on IRE1α endoribonuclease activity

Author

Jabouille, Arnaud, Delugin, Maylis, Pineau, Raphäel, Dubrac, Alexandre, Soulet, Fabienne, Lhomond, Stéphanie, Pallares-Lupon, Nestor, Prats, Hervé, Bikfalvi, Andreas, Chevet, Eric, Touriol, Christian, Moenner, Michel, Laboratoire Angiogenèse et Micro-environnement des Cancers (LAMC), Université Sciences et Technologies - Bordeaux 1-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Composantes innées de la réponse immunitaire et différenciation (CIRID), Université Bordeaux Segalen - Bordeaux 2-Centre National de la Recherche Scientifique (CNRS), Institut de médecine moléculaire de Rangueil (I2MR), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Physiopathologie du cancer du foie, Université Bordeaux Segalen - Bordeaux 2-Institut National de la Santé et de la Recherche Médicale (INSERM), Oncogenesis Stress Signaling (OSS), Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-CRLCC Eugène Marquis (CRLCC), Centre de Recherches en Cancérologie de Toulouse (CRCT), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Sciences et Technologies - Bordeaux 1 (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Toulouse (UT)-Université de Toulouse (UT)- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Rennes (UR)-CRLCC Eugène Marquis (CRLCC), and Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
[SDV]Life Sciences [q-bio], Immunoblotting, perivascular growth, Kaplan-Meier Estimate, Protein Serine-Threonine Kinases, Mice, angiogenesis, Cell Movement, Cell Line, Tumor, Endoribonucleases, Pathology Section, Animals, Humans, Neoplasm Invasiveness, Cell Proliferation, Microscopy, Confocal, Neovascularization, Pathologic, Brain Neoplasms, glioblastoma, invasion, Xenograft Model Antitumor Assays, Tumor Burden, Doxycycline, Mutation, mesenchymal differentiation, Research Paper
Abstract

International audience; IRE1α is an endoplasmic reticulum (ER)-resident transmembrane signaling protein and a cellular stress sensor. The protein harbors a cytosolic dual kinase/endoribonuclease activity required for adaptive responses to micro-environmental changes. In an orthotopic xenograft model of human glioma, invalidation of IRE1α RNase or/and kinase activities generated tumors with remarkably distinct phenotypes. Contrasting with the extensive angiogenesis observed in tumors derived from control cells, the double kinase/RNase invalidation reprogrammed mesenchymal differentiation of cancer cells and produced avascular and infiltrative glioblastomas with blood vessel co-option. In comparison, selective invalidation of IRE1α RNase did not compromise tumor angiogenesis but still elicited invasive features and vessel co-option. In vitro, IRE1α RNase deficient cells were also endowed with a higher ability to migrate. Constitutive activation of both enzymes led to wild-type-like lesions. The presence of IRE1α, but not its RNase activity, is therefore required for glioblastoma neovascularization, whereas invasion results only from RNase inhibition. In this model, two key mechanisms of tumor progression and cancer cell survival are functionally linked to IRE1α

Published
2015
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38. Alk1 and Alk5 inhibition by Nrp1 controls vascular sprouting downstream of Notch

Author

Aspalter, Irene Maria, Gordon, Emma, Dubrac, Alexandre, Ragab, Anan, Narloch, Jarek, Vizán, Pedro, Geudens, Ilse, Collins, Russell Thomas, Franco, Claudio Areias, Abrahams, Cristina Luna, Thurston, Gavin, Fruttiger, Marcus, Rosewell, Ian, Eichmann, Anne, and Gerhardt, Holger

Subjects
Receptors, Notch, Activin Receptors, Type II, Intracellular Signaling Peptides and Proteins, Receptor, Transforming Growth Factor-beta Type I, Membrane Proteins, Endoteli vascular, Smad2 Protein, Protein Serine-Threonine Kinases, Endoteli, Article, Neuropilin-1, Mice, Phenotype, Cardiovascular and Metabolic Diseases, Growth Differentiation Factor 2, Human Umbilical Vein Endothelial Cells, cardiovascular system, Animals, Humans, Endothelium, Vascular, Smad3 Protein, Activin Receptors, Type I, Receptors, Transforming Growth Factor beta, Vasos sanguinis, Sistema cardiovascular
Abstract

Sprouting angiogenesis drives blood vessel growth in healthy and diseased tissues. Vegf and Dll4/Notch signalling cooperate in a negative feedback loop that specifies endothelial tip and stalk cells to ensure adequate vessel branching and function. Current concepts posit that endothelial cells default to the tip-cell phenotype when Notch is inactive. Here we identify instead that the stalk-cell phenotype needs to be actively repressed to allow tip-cell formation. We show this is a key endothelial function of neuropilin-1 (Nrp1), which suppresses the stalk-cell phenotype by limiting Smad2/3 activation through Alk1 and Alk5. Notch downregulates Nrp1, thus relieving the inhibition of Alk1 and Alk5, thereby driving stalk-cell behaviour. Conceptually, our work shows that the heterogeneity between neighbouring endothelial cells established by the lateral feedback loop of Dll4/Notch utilizes Nrp1 levels as the pivot, which in turn establishes differential responsiveness to TGF-β/BMP signalling., Notch signals are crucial for organization of angiogenic sprouting cells into the leading ‘tip' and trailing ‘stalk' cells. Here the authors show that endothelial neuropilin-1 quantitatively inhibits TGF-β/BMP signalling, explaining how Notch-mediated regulation of neuropilin-1 specifies endothelial tip and stalk cells.

Published
2015

39. Defective fluid shear stress mechanotransduction mediates hereditary hemorrhagic telangiectasia.

Author

Baeyens, Nicolas, Larrivée, Bruno, Ola, Roxana, Hayward-Piatkowskyi, Brielle, Dubrac, Alexandre, Huang, Billy, Ross, Tyler D, Coon, Brian BG, Min, Elizabeth, Tsarfati, Maya, Tong, Haibin, Eichmann, Anne, Schwartz, Martin A, Baeyens, Nicolas, Larrivée, Bruno, Ola, Roxana, Hayward-Piatkowskyi, Brielle, Dubrac, Alexandre, Huang, Billy, Ross, Tyler D, Coon, Brian BG, Min, Elizabeth, Tsarfati, Maya, Tong, Haibin, Eichmann, Anne, and Schwartz, Martin A

Abstract

Morphogenesis of the vascular system is strongly modulated by mechanical forces from blood flow. Hereditary hemorrhagic telangiectasia (HHT) is an inherited autosomal-dominant disease in which arteriovenous malformations and telangiectasias accumulate with age. Most cases are linked to heterozygous mutations in Alk1 or Endoglin, receptors for bone morphogenetic proteins (BMPs) 9 and 10. Evidence suggests that a second hit results in clonal expansion of endothelial cells to form lesions with poor mural cell coverage that spontaneously rupture and bleed. We now report that fluid shear stress potentiates BMPs to activate Alk1 signaling, which correlates with enhanced association of Alk1 and endoglin. Alk1 is required for BMP9 and flow responses, whereas endoglin is only required for enhancement by flow. This pathway mediates both inhibition of endothelial proliferation and recruitment of mural cells; thus, its loss blocks flow-induced vascular stabilization. Identification of Alk1 signaling as a convergence point for flow and soluble ligands provides a molecular mechanism for development of HHT lesions., info:eu-repo/semantics/published

Published
2016

40. PI3 kinase inhibition improves vascular malformations in mouse models of hereditary haemorrhagic telangiectasia

Author

Ola, Roxana, primary, Dubrac, Alexandre, additional, Han, Jinah, additional, Zhang, Feng, additional, Fang, Jennifer S., additional, Larrivée, Bruno, additional, Lee, Monica, additional, Urarte, Ana A., additional, Kraehling, Jan R., additional, Genet, Gael, additional, Hirschi, Karen K., additional, Sessa, William C., additional, Canals, Francesc V., additional, Graupera, Mariona, additional, Yan, Minhong, additional, Young, Lawrence H., additional, Oh, Paul S., additional, and Eichmann, Anne, additional

Published
2016
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41. Dual Roles for CXCL4 Chemokines and CXCR3 in Angiogenesis and Invasion of Pancreatic Cancer

Author

Quemener, Cathy, primary, Baud, Jessica, additional, Boyé, Kevin, additional, Dubrac, Alexandre, additional, Billottet, Clotilde, additional, Soulet, Fabienne, additional, Darlot, Florence, additional, Dumartin, Laurent, additional, Sire, Marie, additional, Grepin, Renaud, additional, Daubon, Thomas, additional, Rayne, Fabienne, additional, Wodrich, Harald, additional, Couvelard, Anne, additional, Pineau, Raphael, additional, Schilling, Martin, additional, Castronovo, Vincent, additional, Sue, Shih-Che, additional, Clarke, Kim, additional, Lomri, Abderrahim, additional, Khatib, Abdel-Majid, additional, Hagedorn, Martin, additional, Prats, Hervé, additional, and Bikfalvi, Andreas, additional

Published
2016
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42. Defective fluid shear stress mechanotransduction mediates hereditary hemorrhagic telangiectasia

Author

Baeyens, Nicolas, primary, Larrivée, Bruno, additional, Ola, Roxana, additional, Hayward-Piatkowskyi, Brielle, additional, Dubrac, Alexandre, additional, Huang, Billy, additional, Ross, Tyler D., additional, Coon, Brian G., additional, Min, Elizabeth, additional, Tsarfati, Maya, additional, Tong, Haibin, additional, Eichmann, Anne, additional, and Schwartz, Martin A., additional

Published
2016
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44. PERK mediates the IRES-dependent translational activation of mRNAs encoding angiogenic growth factors after ischemic stress

Author

Philippe, Céline, primary, Dubrac, Alexandre, additional, Quelen, Cathy, additional, Desquesnes, Aurore, additional, Van Den Berghe, Loic, additional, Ségura, Christèle, additional, Filleron, Thomas, additional, Pyronnet, Stéphane, additional, Prats, Hervé, additional, Brousset, Pierre, additional, and Touriol, Christian, additional

Published
2016
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46. Alk1 and Alk5 inhibition by Nrp1 controls vascular sprouting downstream of Notch

Author

Aspalter, Irene Maria, primary, Gordon, Emma, additional, Dubrac, Alexandre, additional, Ragab, Anan, additional, Narloch, Jarek, additional, Vizán, Pedro, additional, Geudens, Ilse, additional, Collins, Russell Thomas, additional, Franco, Claudio Areias, additional, Abrahams, Cristina Luna, additional, Thurston, Gavin, additional, Fruttiger, Marcus, additional, Rosewell, Ian, additional, Eichmann, Anne, additional, and Gerhardt, Holger, additional

Published
2015
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49. The nonlysosomal β‐glucosidase GBA2 promotes endoplasmic reticulum stress and impairs tumorigenicity of human melanoma cells

Author

Sorli, Sonia‐Caroline, primary, Colié, Sandra, additional, Albinet, Virginie, additional, Dubrac, Alexandre, additional, Touriol, Christian, additional, Guilbaud, Nicolas, additional, Bedia, Carmen, additional, Fabriàs, Gemma, additional, Casas, Josefina, additional, Ségui, Bruno, additional, Levade, Thierry, additional, and Andrieu‐Abadie, Nathalie, additional

Published
2012
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50. Ephrin-B1 Is a Novel Specific Component of the Lateral Membrane of the Cardiomyocyte and Is Essential for the Stability of Cardiac Tissue Architecture Cohesion

Author

Genet, Gaël, primary, Guilbeau-Frugier, Céline, additional, Honton, Benjamin, additional, Dague, Etienne, additional, Schneider, Michael D., additional, Coatrieux, Christelle, additional, Calise, Denis, additional, Cardin, Christelle, additional, Nieto, Cécile, additional, Payré, Bruno, additional, Dubroca, Caroline, additional, Marck, Pauline, additional, Heymes, Christophe, additional, Dubrac, Alexandre, additional, Arvanitis, Dina, additional, Despas, Fabien, additional, Altié, Marie-Françoise, additional, Seguelas, Marie-Hélène, additional, Delisle, Marie-Bernadette, additional, Davy, Alice, additional, Sénard, Jean-Michel, additional, Pathak, Atul, additional, and Galés, Céline, additional

Published
2012
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