ORMDL deregulation increases stress responses and modulates repair pathways in Drosophila airways - 13/05/15
Doi : 10.1016/j.jaci.2015.04.009
Kimberley Kallsen, PhD a, b, Nicole Zehethofer, PhD c, Ahmed Abdelsadik, PhD a, Buko Lindner, PhD c, Michael Kabesch, MD d, e, Holger Heine, PhD b, f, Thomas Roeder, PhD a, f 
a Department of Molecular Physiology, Institute of Zoology, Christian-Albrechts University Kiel, Kiel, Germany
b Division of Innate Immunity, Priority Area Asthma & Allergies, Research Center Borstel, Borstel, Germany
c Division of Immunochemistry, Priority Area Infections, Research Center Borstel, Borstel, Germany
d Department of Pediatric Pneumology and Allergy, KUNO University Children's Hospital, Regensburg, Germany
e Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), German Center for Lung Research (DZL), Germany
f Airway Research Center North, German Center for Lung Research (DZL), Germany
Sous presse. Épreuves corrigées par l'auteur.
Disponible en ligne depuis le Wednesday 13 May 2015
Cet article a été publié dans un numéro de la revue, cliquez ici pour y accéder
Cet article a été publié dans un numéro de la revue, cliquez ici pour y accéder
| This work was supported by the German Research Foundation, DFG, SFB/Transregio 22, project A07. |
|
| Disclosure of potential conflict of interest: K. Kallsen has received research support from the German Research Foundation (SFB/Transregio 22 [SFB/TR22]—funding of PhD position and material costs), has received travel scholarships from the German Society for Immunology (DGfI) and Verein zur Erforschung infektiologischer und allergischer Prozesse e.V. (VEIAP), and is employed by Boehringer Ingelheim Pharma GmbH & Co. KG. B. Lindner has received research support and travel support from the German Research Foundation (SFB/TR22). M. Kabesch has received research support from the European Union, the German Ministry of Education and Research, and the German Research Foundation and has received lecture fees from the European Respiratory Society, the European Academy of Allergy and Clinical Immunology, the American Thoracic Society, Novartis, and Glaxo. H. Heine has received research support and travel support from the German Research Foundation (SFB/TR22). T. Roeder has received research support from the German Research Foundation (SFB/TR22, TPA7). The rest of the authors declare that they have no relevant conflicts of interest. |
© 2015
American Academy of Allergy, Asthma & Immunology. Publié par Elsevier Masson SAS. Tous droits réservés.
Bienvenue sur EM-consulte, la référence des professionnels de santé.
L’accès au texte intégral de cet article nécessite un abonnement.
Déjà abonné à cette revue ?