Afficher la notice abrégée

hal.structure.identifierBiothérapies des maladies génétiques et cancers
dc.contributor.authorESPADINHA, Anne-Sophie
hal.structure.identifierBiothérapies des maladies génétiques et cancers
dc.contributor.authorPROUZET-MAULEON, Valerie
hal.structure.identifierPlateforme Protéome [Bordeaux]
dc.contributor.authorCLAVEROL, Stephane
hal.structure.identifierBiothérapies des maladies génétiques et cancers
dc.contributor.authorLAGARDE, Valerie
hal.structure.identifierPlateforme Protéome [Bordeaux]
dc.contributor.authorBONNEU, Marc
hal.structure.identifierBiothérapies des maladies génétiques et cancers
dc.contributor.authorMAHON, Francois-Xavier
hal.structure.identifierBiothérapies des maladies génétiques et cancers
dc.contributor.authorCARDINAUD, Bruno
dc.date.accessioned2020-07-09T14:16:57Z
dc.date.available2020-07-09T14:16:57Z
dc.date.issued2017-09-29
dc.identifier.issn1949-2553
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/10328
dc.description.abstractEnMicroRNAs (miRNAs) are regulators of several key patho-physiological processes, including cell cycle and apoptosis. Using microarray-based miRNA profiling in K562 cells, a model of chronic myeloid leukemia (CML), we found that the oncoprotein BCR-ABL1 regulates the expression of miR-21, an "onco-microRNA", found to be overexpressed in several cancers. This effect relies on the presence of two STAT binding sites on the promoter of miR-21, and on the phosphorylation status of STAT5, a transcription factor activated by the kinase activity of BCR-ABL1. Mir-21 regulates the expression of PDCD4 (programmed cell death protein 4), a tumor suppressor identified through a proteomics approach. The phosphoSTAT5 - miR-21 - PDCD4 pathway was active in CML primary CD34(+) cells, but also in acute myeloid leukemia (AML) models like MV4.11 and MOLM13, where the constitutively active tyrosine kinase FLT3-ITD plays a similar role to BCR-ABL1 in the K562 cell line.
dc.title.enA tyrosine kinase-STAT5-miR21-PDCD4 regulatory axis in chronic and acute myeloid leukemia cells
dc.typeArticle de revue
dc.identifier.doi10.18632/oncotarget.19192
dc.subject.halChimie/Matériaux
bordeaux.journalOncotarget
bordeaux.page76174-76188
bordeaux.volume8
bordeaux.hal.laboratoriesInstitut de Chimie & de Biologie des Membranes & des Nano-objets (CBMN) - UMR 5248*
bordeaux.hal.laboratoriesInstitut de Chimie & de Biologie des Membranes & des Nano-objets (CBMN, UMR 5248)
bordeaux.issue44
bordeaux.institutionUniversité de Bordeaux
bordeaux.institutionBordeaux INP
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Oncotarget&rft.date=2017-09-29&rft.volume=8&rft.issue=44&rft.spage=76174-76188&rft.epage=76174-76188&rft.eissn=1949-2553&rft.issn=1949-2553&rft.au=ESPADINHA,%20Anne-Sophie&PROUZET-MAULEON,%20Valerie&CLAVEROL,%20Stephane&LAGARDE,%20Valerie&BONNEU,%20Marc&rft.genre=article


Fichier(s) constituant ce document

FichiersTailleFormatVue

Il n'y a pas de fichiers associés à ce document.

Ce document figure dans la(les) collection(s) suivante(s)

Afficher la notice abrégée