Jean‐Pierre Couty

ORCID: 0000-0003-3492-9136
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About
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Research Areas
  • Cytomegalovirus and herpesvirus research
  • Viral-associated cancers and disorders
  • Hepatocellular Carcinoma Treatment and Prognosis
  • Liver Disease Diagnosis and Treatment
  • Liver physiology and pathology
  • Immune Cell Function and Interaction
  • Parvovirus B19 Infection Studies
  • Immunotherapy and Immune Responses
  • Herpesvirus Infections and Treatments
  • Cancer Immunotherapy and Biomarkers
  • Drug-Induced Hepatotoxicity and Protection
  • Fibroblast Growth Factor Research
  • Hepatitis B Virus Studies
  • Liver Disease and Transplantation
  • Wnt/β-catenin signaling in development and cancer
  • Immune cells in cancer
  • Histiocytic Disorders and Treatments
  • Metabolism, Diabetes, and Cancer
  • Microtubule and mitosis dynamics
  • Medicinal Plant Pharmacodynamics Research
  • Phagocytosis and Immune Regulation
  • Autophagy in Disease and Therapy
  • Chemokine receptors and signaling
  • Erythropoietin and Anemia Treatment
  • Galectins and Cancer Biology

Inserm
2008-2023

Université Paris Cité
2008-2023

Centre de Recherche des Cordeliers
2019-2023

Sorbonne Université
2019-2023

Immunité et Cancer
2023

Institut Cochin
2007-2022

Sorbonne Paris Cité
2012-2019

Génomique Fonctionnelle des Tumeurs Solides
2019

Centre National de la Recherche Scientifique
1999-2018

Délégation Paris 7
2008-2018

Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide. Its pathogenesis frequently linked to liver inflammation. Gain-of-function mutations in gene encoding β-catenin are frequent genetic modifications found human HCCs. Thus, we investigated whether inflammation was a component β-catenin–induced tumorigenesis using genetically modified mouse models that recapitulated stages initiation and progression this tumoral process. Oncogenic signaling induce an...

10.1172/jci43937 article EN Journal of Clinical Investigation 2012-01-17

During hepatogenesis, after the liver has budded out of endoderm, hepatoblasts quickly expand and differentiate into either hepatocytes or biliary cells, latter which arise only within ductal plate surrounding portal vein. Because Wnt/β-catenin pathway is involved in homeostasis regeneration carcinogenesis, we investigated here a role for signaling embryonic liver. A cyclization recombination (Cre)/locus X-over P1 (loxP) strategy was chosen to perform adenomatous polyposis coli ( Apc )...

10.1002/hep.21952 article EN Hepatology 2007-11-25

Objectives Polyploidy is a fascinating characteristic of liver parenchyma. Hepatocyte polyploidy depends on the DNA content each nucleus (nuclear ploidy) and number nuclei per cell (cellular ploidy). Which role can be assigned to during human hepatocellular carcinoma (HCC) development still an open question. Here, we investigated whether specific ploidy spectrum associated with clinical molecular features HCC. Design Ploidy spectra were determined surgically resected tissues from patients...

10.1136/gutjnl-2018-318021 article EN cc-by-nc Gut 2019-04-12

Kaposi's sarcoma-associated herpesvirus (KSHV; human 8) encodes a chemokine-like G protein-coupled receptor (KSHV-GPCR) that is implicated in the pathogenesis of sarcoma (KS). Since endothelial cells appear to be targets for virus, we developed an <i>in vitro</i> mouse lung cell model which KSHV-GPCR stably expressed and signaling was studied. In cells: 1) does not exhibit basal through phosphoinositide-specific phospholipase C pathway but inositol phosphate production stimulated by...

10.1074/jbc.m104631200 article EN cc-by Journal of Biological Chemistry 2001-09-01

Leukocyte cell‐derived chemotaxin‐2 (LECT2) was originally identified as a hepatocyte‐secreted chemokine‐like factor and positive target of β‐catenin signaling. Here, we dissected out the mechanisms by which LECT2 modulates hepatocellular carcinoma (HCC) development using both HCC mouse models human samples. We have demonstrated that exhibits dual abilities it has profound repercussions on tumor phenotype itself immune microenvironment. Its absence confers Ctnnb‐1‐mutated hepatocytes...

10.1002/hep.30140 article EN Hepatology 2018-08-07

The beta-turn is a well-studied motif in both proteins and peptides. Four residues, making almost complete 180 degree-turn the direction of peptide chain, define beta-turn. Several types are defined according to Phi Psi torsional angles backbone for residues i + 1 2. One special type beta-turn, VI-turn, usually contains proline with cis-amide bond at residue In an aza-amino acid, alpha-carbon amino acid changed nitrogen. Peptides containing azaproline (azPro) have been shown prefer VI...

10.1021/ja020994o article EN Journal of the American Chemical Society 2003-01-09

Abstract Interactions between leukocytes and vascular endothelial cells are mediated by a complex set of membrane adhesion molecules which transduce bi‐directional signals in both cell types. Endothelium the cerebral blood vessels, constitute blood–brain barrier, strictly controls trafficking into brain. Investigating signaling pathways triggered engagement expressed on brain cells, we previously documented role ICAM‐1 activation tyrosine phosphorylation several actin‐binding proteins...

10.1111/j.1471-4159.2007.04782.x article EN other-oa Journal of Neurochemistry 2007-06-28

Liver kinase B1 (LKB1) is involved in several biological processes and a key regulator of hepatic metabolism polarity. Here, we demonstrate that the master LKB1 plays dual role liver regeneration, independently its major target, AMP-activated protein (AMPK). We found loss Lkb1 expression promoted hepatocyte proliferation acceleration metabolic/energetic balance. regulates G0/G1 progression, specifically by controlling epidermal growth factor receptor (EGFR) signaling. Furthermore, later...

10.1016/j.celrep.2018.01.086 article EN cc-by-nc-nd Cell Reports 2018-02-01

AMP‐activated protein kinase (AMPK) plays a pivotal role in regulating cellular energy metabolism. We previously showed that AMPKα1−/− mice develop moderate anemia associated with splenomegaly and high reticulocytosis. Here, we report splenectomy of worsened supporting evidence developed compensatory response through extramedullary erythropoiesis the spleen. Transplantation bone marrow from into wild‐type recipients recapitulated hematologic phenotype. Further, red blood cells (RBC) less...

10.1016/j.febslet.2010.07.041 article EN FEBS Letters 2010-07-27

Abstract Mammalian p38α MAPK (Mitogen-Activated Protein Kinase) transduces a variety of extracellular signals that regulate cellular processes, such as inflammation, differentiation, proliferation or apoptosis. In the liver, depending physiopathological context, acts negative regulator hepatocyte well promotor inflammatory processes. However, its function during an acute injury, in adult remains uncharacterized. this study, using mice are deficient specifically mature hepatocytes, we...

10.1038/s41598-019-51175-z article EN cc-by Scientific Reports 2019-10-10

A constitutively active G protein-coupled receptor (GPCR) encoded by Kaposi9s sarcoma-associated herpesvirus (human herpesvirus-8) (KSHV) is expressed in endothelial (spindle) cells of sarcoma lesions. In this study, we report novel effects basal signaling and inverse agonist chemokines on migration KSHV-GPCR-expressing mouse lung cells. We show that KSHV-GPCR inhibits two systems, movement through porous filters vitro wound closure. Naturally occurring chemokines, interferon γ-inducible...

10.1124/jpet.108.147686 article EN Journal of Pharmacology and Experimental Therapeutics 2009-03-03

Summry— HHV‐8‐GPCR is a chemokine‐like receptor encoded by KSHV, the etiologic agent of KS. constitutively active. Although it homologous to mammalian CXCR2, binds CXC and CC chemokines. Structure‐function analysis showed that chemokines bind primarily amino terminus whereas signaling occurs in absence of: terminus, which is, therefore, not tethered agonist. In vitro systems, signals via multiple transduction pathways including, activation phospholipase C PKC, inhibition adenylyl cyclase,...

10.1111/j.1768-322x.2004.tb01425.x article EN Biology of the Cell 2004-06-01

avec Mathias Heikenwalder, l'équipe de Tim Greten

10.1051/medsci/20163211021 article FR médecine/sciences 2016-11-01
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