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<identifier>oai:HAL:inserm-00821109v1</identifier>
<datestamp>2017-12-21</datestamp>
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<setSpec>subject:sdv</setSpec>
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<publisher>HAL CCSD</publisher>
<title lang=en>JAK2V617F activates Lu/BCAM-mediated red cell adhesion in polycythemia vera through an EpoR-independent Rap1/Akt pathway.</title>
<title lang=en>JAK2V617F activates Lu/BCAM-mediated red cell adhesion in polycythemia vera through an EpoR-independent Rap1/Akt pathway. : JAK2V617F activates Lu/BCAM through Rap1/Akt</title>
<creator>De Grandis, Maria</creator>
<creator>Cambot, Marie</creator>
<creator>Wautier, Marie-Paule</creator>
<creator>Cassinat, Bruno</creator>
<creator>Chomienne, Christine</creator>
<creator>Colin, Yves</creator>
<creator>Wautier, Jean-Luc</creator>
<creator>Le Van Kim, Caroline</creator>
<creator>El Nemer, Wassim</creator>
<contributor>Protéines de la membrane érythrocytaire et homologues non-érythroides ; Université des Antilles et de la Guyane (UAG) - Institut National de la Transfusion Sanguine [Paris] (INTS) - Université Paris Diderot - Paris 7 (UPD7) - Université de la Réunion (UR) - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor>
<contributor>GR-Ex ; Laboratoire d'Excellence</contributor>
<contributor>Institut National de la Transfusion Sanguine [Paris] (INTS)</contributor>
<contributor>Unite de Biologie Cellulaire ; Assistance publique - Hôpitaux de Paris (AP-HP) - Groupe Hospitalier Saint-Louis-Lariboisière- Fernand-Widal</contributor>
<contributor>Hématologie -Immunologie -Cibles thérapeutiques ; Université Paris Diderot - Paris 7 (UPD7) - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor>
<contributor>The work was funded by the Institut National de la Santé et de la Recherche Médicale (Inserm), the Institut National de la Transfusion Sanguine (INTS), and a grant from Région Île-de-France (SESAME 2007 no. F-08-1104/R). The PhD student, Maria De Grandis, was funded by the Ministère de l'Enseignement Supérieur et de la Recherche at the Ecole Doctorale B3MI.</contributor>
<description>International audience</description>
<source>ISSN: 0006-4971</source>
<source>EISSN: 1528-0020</source>
<source>Blood</source>
<publisher>American Society of Hematology</publisher>
<identifier>inserm-00821109</identifier>
<identifier>http://www.hal.inserm.fr/inserm-00821109</identifier>
<identifier>http://www.hal.inserm.fr/inserm-00821109/document</identifier>
<identifier>http://www.hal.inserm.fr/inserm-00821109/file/De_Grandis_Blood_2013.pdf</identifier>
<source>http://www.hal.inserm.fr/inserm-00821109</source>
<source>Blood, American Society of Hematology, 2013, 121 (4), pp.658-65. 〈10.1182/blood-2012-07-440487〉</source>
<identifier>DOI : 10.1182/blood-2012-07-440487</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1182/blood-2012-07-440487</relation>
<identifier>PUBMED : 23160466</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/23160466</relation>
<language>en</language>
<subject>[SDV.BC] Life Sciences [q-bio]/Cellular Biology</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Polycythemia vera (PV) is characterized by an increased RBC mass, spontaneous erythroid colony formation, and the JAK2V617F mutation. PV is associated with a high risk of mesenteric and cerebral thrombosis. PV RBC adhesion to endothelial laminin is increased and mediated by phosphorylated erythroid Lu/BCAM. In the present work, we investigated the mechanism responsible for Lu/BCAM phosphorylation in the presence of JAK2V617F using HEL and BaF3 cell lines as well as RBCs from patients with PV. High levels of Rap1-GTP were found in HEL and BaF3 cells expressing JAK2V617F compared with BaF3 cells with wild-type JAK2. This finding was associated with increased Akt activity, Lu/BCAM phosphorylation, and cell adhesion to laminin that were inhibited by the dominant-negative Rap1S17N or by the specific Rap1 inhibitor GGTI-298. Surprisingly, knocking-down EpoR in HEL cells did not alter Akt activity or cell adhesion to laminin. Our findings reveal a novel EpoR-independent Rap1/Akt signaling pathway that is activated by JAK2V617F in circulating PV RBCs and responsible for Lu/BCAM activation. This new characteristic of JAK2V617F could play a critical role in initiating abnormal interactions among circulating and endothelial cells in patients with PV.</description>
<date>2013-01-24</date>
</dc>
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