Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2004-3-19
pubmed:abstractText
K562 cells contain a Bcr-Abl chimeric gene and differentiate into various lineages in response to different inducers. We studied the role of the mitogen-activated protein kinase (MAPK) kinase 1 (MEK1)/extracellular signal-regulated kinase (ERK) pathway during the erythroid differentiation of K562 cells induced by tyrosine kinase inhibitors (herbimycin A or STI571), using genetically modified cells (constitutively MEK1-activated K562: K562/MEK1, and inducible ERK-inactivated K562: K562/CL100). Basal expression of glycophorin A was markedly reduced in K562/MEK1 cells compared with that in parental cells, while it was augmented in K562/CL100 cells. Herbimycin A and STI571 differentiated K562 cells accompanying with the transient down-regulated ERK. Moreover, the erythroid differentiation was markedly suppressed in K562/MEK1 cells, and early down-regulation of ERK activity was not observed in these cells. In contrast, the induction of ERK-specific phosphatase in K562/CL100 cells potentiated erythroid differentiation. Once the phosphatase was induced, the initial ERK activity became repressed and its early down-regulation by the inhibition of Bcr-Abl was marked and prolonged. These results demonstrate that the erythroid differentiation of K562 cells induced by herbimycin A or STI571 requires the down-regulation of MEK1/ ERK pathway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/B59 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Benzoquinones, http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors, http://linkedlifedata.com/resource/pubmed/chemical/Extracellular Signal-Regulated MAP..., http://linkedlifedata.com/resource/pubmed/chemical/Fusion Proteins, bcr-abl, http://linkedlifedata.com/resource/pubmed/chemical/Glycophorin, http://linkedlifedata.com/resource/pubmed/chemical/Lactams, Macrocyclic, http://linkedlifedata.com/resource/pubmed/chemical/MAP Kinase Kinase 1, http://linkedlifedata.com/resource/pubmed/chemical/MAP2K1 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Piperazines, http://linkedlifedata.com/resource/pubmed/chemical/Protein Tyrosine Phosphatases, http://linkedlifedata.com/resource/pubmed/chemical/Pyrimidines, http://linkedlifedata.com/resource/pubmed/chemical/Quinones, http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins, http://linkedlifedata.com/resource/pubmed/chemical/herbimycin, http://linkedlifedata.com/resource/pubmed/chemical/imatinib
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0300-8177
pubmed:author
pubmed:issnType
Print
pubmed:volume
258
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
25-33
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:15030167-Benzoquinones, pubmed-meshheading:15030167-Cell Differentiation, pubmed-meshheading:15030167-Enzyme Activation, pubmed-meshheading:15030167-Enzyme Inhibitors, pubmed-meshheading:15030167-Erythroblasts, pubmed-meshheading:15030167-Extracellular Signal-Regulated MAP Kinases, pubmed-meshheading:15030167-Fusion Proteins, bcr-abl, pubmed-meshheading:15030167-Glycophorin, pubmed-meshheading:15030167-Humans, pubmed-meshheading:15030167-K562 Cells, pubmed-meshheading:15030167-Lactams, Macrocyclic, pubmed-meshheading:15030167-MAP Kinase Kinase 1, pubmed-meshheading:15030167-Piperazines, pubmed-meshheading:15030167-Protein Tyrosine Phosphatases, pubmed-meshheading:15030167-Pyrimidines, pubmed-meshheading:15030167-Quinones, pubmed-meshheading:15030167-Recombinant Proteins, pubmed-meshheading:15030167-Signal Transduction, pubmed-meshheading:15030167-Transfection
pubmed:year
2004
pubmed:articleTitle
Inactivation of ERK accelerates erythroid differentiation of K562 cells induced by herbimycin A and STI571 while activation of MEK1 interferes with it.
pubmed:affiliation
Department of Molecular Genetics, Institute of DNA Medicine, Jikei University School of Medicine, Minato-ku, Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't