File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Activation of the Jak3 pathway is associated with granulocytic differentiation of myeloid precursor cells

TitleActivation of the Jak3 pathway is associated with granulocytic differentiation of myeloid precursor cells
Authors
Issue Date2002
PublisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/
Citation
Blood, 2002, v. 100 n. 8, p. 2753-2762 How to Cite?
AbstractJak3, a member of the Janus kinase family of cytoplasmic tyrosine kinases, is expressed at low levels in immature hematopoietic cells and its expression is dramatically up-regulated during the terminal differentiation of these cells. To better understand the role of Jak3 in myeloid cell development, we have investigated the role of Jak3 in myeloid cell differentiation using the 32Dcl3 cell system. Our studies show that Jak3 is a primary response gene for granulocyte colony-stimulating factor (G-CSF) and the accumulation of tyrosine phosphorylated Jak3 correlated with cell growth inhibition and terminal granulocytic differentiation in response to G-CSF. Ectopic overexpression of Jak3 in 32Dcl3 cells resulted in an acceleration of the G-CSF-induced differentiation program that was preceded by G1 cell cycle arrest, which was associated with the up-regulation of the cyclin-dependent kinase inhibitor p27Kip1 and down-regulation of Cdk2, Cdk4, Cdk6, and Cyclin E. In addition, ectopic over-expression of Jak3 appears to result in the inactivation of PKB/Akt and Stat3- mediated proliferative pathways in the presence of G-CSF. Similarly, overexpression of Jak3 in primary bone marrow cells resulted in an acceleration of granulocytic differentiation in the presence of granulocyte-macrophage colony-stimulating factor, which was associated with their growth arrest in the G1 phase of the cell cycle. Taken together, these results indicate that Jak3-mediated signals play an important role in myeloid cell differentiation. © 2002 by The American Society of Hematology.
Persistent Identifierhttp://hdl.handle.net/10722/68013
ISSN
2015 Impact Factor: 11.841
2015 SCImago Journal Rankings: 6.395
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorRane, SGen_HK
dc.contributor.authorMangan, JKen_HK
dc.contributor.authorAmanullah, Aen_HK
dc.contributor.authorWong, BCen_HK
dc.contributor.authorVora, RKen_HK
dc.contributor.authorLiebermann, DAen_HK
dc.contributor.authorHoffman, Ben_HK
dc.contributor.authorGraña, Xen_HK
dc.contributor.authorPremkumar Reddy, Een_HK
dc.date.accessioned2010-09-06T06:00:30Z-
dc.date.available2010-09-06T06:00:30Z-
dc.date.issued2002en_HK
dc.identifier.citationBlood, 2002, v. 100 n. 8, p. 2753-2762en_HK
dc.identifier.issn0006-4971en_HK
dc.identifier.urihttp://hdl.handle.net/10722/68013-
dc.description.abstractJak3, a member of the Janus kinase family of cytoplasmic tyrosine kinases, is expressed at low levels in immature hematopoietic cells and its expression is dramatically up-regulated during the terminal differentiation of these cells. To better understand the role of Jak3 in myeloid cell development, we have investigated the role of Jak3 in myeloid cell differentiation using the 32Dcl3 cell system. Our studies show that Jak3 is a primary response gene for granulocyte colony-stimulating factor (G-CSF) and the accumulation of tyrosine phosphorylated Jak3 correlated with cell growth inhibition and terminal granulocytic differentiation in response to G-CSF. Ectopic overexpression of Jak3 in 32Dcl3 cells resulted in an acceleration of the G-CSF-induced differentiation program that was preceded by G1 cell cycle arrest, which was associated with the up-regulation of the cyclin-dependent kinase inhibitor p27Kip1 and down-regulation of Cdk2, Cdk4, Cdk6, and Cyclin E. In addition, ectopic over-expression of Jak3 appears to result in the inactivation of PKB/Akt and Stat3- mediated proliferative pathways in the presence of G-CSF. Similarly, overexpression of Jak3 in primary bone marrow cells resulted in an acceleration of granulocytic differentiation in the presence of granulocyte-macrophage colony-stimulating factor, which was associated with their growth arrest in the G1 phase of the cell cycle. Taken together, these results indicate that Jak3-mediated signals play an important role in myeloid cell differentiation. © 2002 by The American Society of Hematology.en_HK
dc.languageengen_HK
dc.publisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/en_HK
dc.relation.ispartofBlooden_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCell Differentiationen_HK
dc.subject.meshCell Divisionen_HK
dc.subject.meshCycloheximide - pharmacologyen_HK
dc.subject.meshFlow Cytometryen_HK
dc.subject.meshGene Deletionen_HK
dc.subject.meshGene Expression Regulation, Enzymologic - physiologyen_HK
dc.subject.meshGranulocyte Colony-Stimulating Factor - pharmacologyen_HK
dc.subject.meshGranulocytes - cytology - enzymologyen_HK
dc.subject.meshHematopoietic Stem Cells - cytology - drug effects - enzymologyen_HK
dc.subject.meshJanus Kinase 3en_HK
dc.subject.meshKineticsen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred C57BLen_HK
dc.subject.meshModels, Animalen_HK
dc.subject.meshProtein-Tyrosine Kinases - genetics - metabolismen_HK
dc.subject.meshTime Factorsen_HK
dc.titleActivation of the Jak3 pathway is associated with granulocytic differentiation of myeloid precursor cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0006-4971&volume=100&issue=8&spage=2753&epage=2762&date=2002&atitle=Activation+of+the+Jak3+pathway+is+associated+with+granulocytic+differentiation+of+myeloid+precursor+cells.en_HK
dc.identifier.emailWong, BC:bcwwong@hkucc.hku.hken_HK
dc.identifier.authorityWong, BC=rp00369en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1182/blood.V100.8.2753en_HK
dc.identifier.pmid12351382-
dc.identifier.scopuseid_2-s2.0-0037108112en_HK
dc.identifier.hkuros115761en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037108112&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume100en_HK
dc.identifier.issue8en_HK
dc.identifier.spage2753en_HK
dc.identifier.epage2762en_HK
dc.identifier.isiWOS:000178519100015-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridRane, SG=7005884921en_HK
dc.identifier.scopusauthoridMangan, JK=7005389031en_HK
dc.identifier.scopusauthoridAmanullah, A=7005005869en_HK
dc.identifier.scopusauthoridWong, BC=35733052400en_HK
dc.identifier.scopusauthoridVora, RK=7004952118en_HK
dc.identifier.scopusauthoridLiebermann, DA=7006163062en_HK
dc.identifier.scopusauthoridHoffman, B=7402351898en_HK
dc.identifier.scopusauthoridGraña, X=7003557292en_HK
dc.identifier.scopusauthoridPremkumar Reddy, E=6602906983en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats