pubmed-article:9949177 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9949177 | lifeskim:mentions | umls-concept:C0029016 | lld:lifeskim |
pubmed-article:9949177 | lifeskim:mentions | umls-concept:C0033640 | lld:lifeskim |
pubmed-article:9949177 | lifeskim:mentions | umls-concept:C1415015 | lld:lifeskim |
pubmed-article:9949177 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
pubmed-article:9949177 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
pubmed-article:9949177 | lifeskim:mentions | umls-concept:C1704666 | lld:lifeskim |
pubmed-article:9949177 | lifeskim:mentions | umls-concept:C1517892 | lld:lifeskim |
pubmed-article:9949177 | lifeskim:mentions | umls-concept:C0208973 | lld:lifeskim |
pubmed-article:9949177 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:9949177 | pubmed:dateCreated | 1999-3-11 | lld:pubmed |
pubmed-article:9949177 | pubmed:abstractText | The Bcr-Abl oncogene, found in Philadelphia chromosome-positive myelogenous leukemia (CML), activates Ras and triggers the stress-activated protein kinase (SAPK or Jun NH2-terminal kinase [JNK]) pathway. Interruption of Ras or SAPK activation dramatically reduces Bcr-Abl-mediated transformation. Here, we report that Bcr-Abl through a Ras-dependent pathway signals the serine/threonine protein kinase GCKR (Germinal Center Kinase Related) leading to SAPK activation. Either an oncogenic form of Ras or Bcr-Abl enhances GCKR catalytic activity and its activation of SAPK, whereas inhibition of GCKR impairs Bcr-Abl-induced SAPK activation. Bcr-Abl mutants that are impaired for GCKR activation are also unable to activate SAPK. Consistent with GCKR being a functional target in CML, GCKR is constitutively active in CML cell lines and found in association with Bcr-Abl. Our results indicate that GCKR is a downstream target of Bcr-Abl and strongly implicate GCKR as a mediator of Bcr-Abl in its transformation of cells. | lld:pubmed |
pubmed-article:9949177 | pubmed:language | eng | lld:pubmed |
pubmed-article:9949177 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9949177 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:9949177 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9949177 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9949177 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9949177 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9949177 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9949177 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9949177 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9949177 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9949177 | pubmed:month | Feb | lld:pubmed |
pubmed-article:9949177 | pubmed:issn | 0006-4971 | lld:pubmed |
pubmed-article:9949177 | pubmed:author | pubmed-author:WitteO NON | lld:pubmed |
pubmed-article:9949177 | pubmed:author | pubmed-author:KehrlJ HJH | lld:pubmed |
pubmed-article:9949177 | pubmed:author | pubmed-author:ShiC SCS | lld:pubmed |
pubmed-article:9949177 | pubmed:author | pubmed-author:TuscanoJ MJM | lld:pubmed |
pubmed-article:9949177 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9949177 | pubmed:day | 15 | lld:pubmed |
pubmed-article:9949177 | pubmed:volume | 93 | lld:pubmed |
pubmed-article:9949177 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9949177 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9949177 | pubmed:pagination | 1338-45 | lld:pubmed |
pubmed-article:9949177 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
pubmed-article:9949177 | pubmed:meshHeading | pubmed-meshheading:9949177-... | lld:pubmed |
pubmed-article:9949177 | pubmed:meshHeading | pubmed-meshheading:9949177-... | lld:pubmed |
pubmed-article:9949177 | pubmed:meshHeading | pubmed-meshheading:9949177-... | lld:pubmed |
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pubmed-article:9949177 | pubmed:meshHeading | pubmed-meshheading:9949177-... | lld:pubmed |
pubmed-article:9949177 | pubmed:meshHeading | pubmed-meshheading:9949177-... | lld:pubmed |
pubmed-article:9949177 | pubmed:meshHeading | pubmed-meshheading:9949177-... | lld:pubmed |
pubmed-article:9949177 | pubmed:meshHeading | pubmed-meshheading:9949177-... | lld:pubmed |
pubmed-article:9949177 | pubmed:meshHeading | pubmed-meshheading:9949177-... | lld:pubmed |
pubmed-article:9949177 | pubmed:year | 1999 | lld:pubmed |
pubmed-article:9949177 | pubmed:articleTitle | GCKR links the Bcr-Abl oncogene and Ras to the stress-activated protein kinase pathway. | lld:pubmed |
pubmed-article:9949177 | pubmed:affiliation | B-Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institutes of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892-1876, USA. | lld:pubmed |
pubmed-article:9949177 | pubmed:publicationType | Journal Article | lld:pubmed |
entrez-gene:25 | entrezgene:pubmed | pubmed-article:9949177 | lld:entrezgene |
entrez-gene:613 | entrezgene:pubmed | pubmed-article:9949177 | lld:entrezgene |
entrez-gene:11183 | entrezgene:pubmed | pubmed-article:9949177 | lld:entrezgene |
http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:9949177 | lld:entrezgene |
http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:9949177 | lld:entrezgene |