Jean‐Luc Villeval

ORCID: 0000-0002-0562-925X
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About
Contact & Profiles
Research Areas
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Platelet Disorders and Treatments
  • Chronic Myeloid Leukemia Treatments
  • Acute Myeloid Leukemia Research
  • Eosinophilic Disorders and Syndromes
  • Kruppel-like factors research
  • Erythrocyte Function and Pathophysiology
  • Hemoglobinopathies and Related Disorders
  • Blood groups and transfusion
  • Blood properties and coagulation
  • Mast cells and histamine
  • Cytokine Signaling Pathways and Interactions
  • Multiple Myeloma Research and Treatments
  • Enzyme function and inhibition
  • Blood disorders and treatments
  • Virus-based gene therapy research
  • CRISPR and Genetic Engineering
  • PARP inhibition in cancer therapy
  • Hematopoietic Stem Cell Transplantation
  • Erythropoietin and Anemia Treatment
  • RNA Interference and Gene Delivery
  • Cell Adhesion Molecules Research
  • Glycosylation and Glycoproteins Research
  • Immune Cell Function and Interaction
  • Renal Diseases and Glomerulopathies

Inserm
2013-2024

Institut Gustave Roussy
2014-2024

Université Paris-Saclay
2011-2024

Centre National de la Recherche Scientifique
2022

Institut Curie
2022

Université Paris Sciences et Lettres
2022

Laboratory of Excellence GR-Ex
2013-2020

La Ligue Contre le Cancer
2014-2020

Laboratoire d'études sur les monothéismes
2017-2018

Université Paris-Sud
2007-2014

Recent reports have challenged the notion that retroviruses and retroviral vectors integrate randomly into host genome. These pointed to a strong bias toward integration in near gene coding regions and, for gammaretroviral vectors, around transcription start sites. Here, we report results obtained from large-scale mapping of 572 sites (RISs) isolated cells 9 patients with X-linked SCID (SCID-X1) treated retrovirus-based therapy protocol. Our data showed two-thirds insertions occurred or very...

10.1172/jci31659 article EN Journal of Clinical Investigation 2007-08-01

Thrombosis is the main cause of morbidity and mortality in patients with JAK2V617F myeloproliferative neoplasms. Recent studies have reported presence endothelial cells some We investigated role that express thrombus formation using an vitro model human overexpressing vivo mice endothelial-specific expression. Interestingly, these displayed a higher propensity for thrombus. When deciphering mechanisms by which JAK2V617F-expressing promote thrombosis, we observed they pro-adhesive phenotype...

10.3324/haematol.2018.195321 article EN cc-by-nc Haematologica 2018-08-31

Abstract Aberrant JAK 2 signalling plays a central role in myeloproliferative neoplasms ( MPN ). inhibitors have proven to be clinically efficacious, however, they are not mutation‐specific and competent enough suppress neoplastic clonal haematopoiesis. We hypothesized that, by simultaneously targeting multiple activated pathways, could more effectively treated. To this end we investigated the efficacy of BEZ 235, dual PI3K/ mTOR inhibitor, alone combination with 1/ inhibitor ruxolitinib,...

10.1111/jcmm.12162 article EN Journal of Cellular and Molecular Medicine 2013-11-01

Arterial cardiovascular events are the leading cause of death in patients with JAK2V617F myeloproliferative neoplasms (MPNs). However, their mechanisms poorly understood. The high prevalence myocardial infarction without significant coronary stenosis or atherosclerosis MPNs suggests that vascular function is altered. consequences mutation on reactivity unknown. We observe here increased responses to vasoconstrictors arteries from Jak2V617F mice resulting a disturbed endothelial NO pathway...

10.1172/jci124566 article EN cc-by Journal of Clinical Investigation 2020-02-11

Blood-sucking arthropods have evolved a number of inhibitors platelet aggregation and blood coagulation. In this study we molecularly functionally characterized aegyptin, member the family 30-kDa salivary allergens from Aedes aegypti, whose function remained elusive thus far. Aegyptin displays unique sequence by glycine, glutamic acid, aspartic acid repeats was shown to specifically block collagen-induced human granule secretion. Plasmon resonance experiments demonstrate that aegyptin binds...

10.1074/jbc.m705669200 article EN cc-by Journal of Biological Chemistry 2007-07-25
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