RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/15655368http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15655368http://www.w3.org/2000/01/rdf-schema#comment"The v-Abl tyrosine kinase activates several signaling pathways during transformation of bone marrow cells in mice. Because the SH2-containing inositol 5'-phosphatase (SHIP) and Downstream of tyrosine kinase 1 (Dok1) have been shown to interact with Abl, the effect of SHIP and Dok1 deficiency on v-Abl transformation was investigated. Bone marrow cells from either Dok1- or SHIP-deficient mice are more susceptible to transformation by v-Abl. v-Abl-transformed preB cells from these knockout mice show Abl kinase-dependent hyperproliferation and moderate resistance to apoptosis. Elevated activation of Ras, Raf-1, and Erk, but not of Akt, was observed in either SHIP(-/-) or Dok1(-/-) v-Abl-transformed cells. This activation is sensitive to treatment with STI571. Furthermore, treatment of these cells with either a farnesyltransferase inhibitor or a MEK1/2 inhibitor abrogates the increased proliferation of SHIP(-/-) or Dok1(-/-) cells in a dose-dependent manner. Complementation of SHIP(-/-) or Dok1(-/-) cells abrogates their hyperproliferation and intracellular Erk activation. These data indicate that both SHIP and Dok1 functionally regulate the activation of Ras-Erk pathway by v-Abl and affect the mitogenic activity of v-Abl transformed bone marrow cells."xsd:string
http://purl.uniprot.org/citations/15655368http://purl.uniprot.org/core/author"Pandolfi P.P."xsd:string
http://purl.uniprot.org/citations/15655368http://purl.uniprot.org/core/author"Niki M."xsd:string
http://purl.uniprot.org/citations/15655368http://purl.uniprot.org/core/author"Yao P.M."xsd:string
http://purl.uniprot.org/citations/15655368http://purl.uniprot.org/core/author"Rothman P.B."xsd:string
http://purl.uniprot.org/citations/15655368http://purl.uniprot.org/core/author"Limnander A."xsd:string
http://purl.uniprot.org/citations/15655368http://purl.uniprot.org/core/author"Oki S."xsd:string
http://purl.uniprot.org/citations/15655368http://purl.uniprot.org/core/date"2005"xsd:gYear
http://purl.uniprot.org/citations/15655368http://purl.uniprot.org/core/name"Cell Cycle"xsd:string
http://purl.uniprot.org/citations/15655368http://purl.uniprot.org/core/pages"310-314"xsd:string
http://purl.uniprot.org/citations/15655368http://purl.uniprot.org/core/title"Dok1 and SHIP act as negative regulators of v-Abl-induced pre-B cell transformation, proliferation and Ras/Erk activation."xsd:string
http://purl.uniprot.org/citations/15655368http://purl.uniprot.org/core/volume"4"xsd:string
http://purl.uniprot.org/citations/15655368http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/15655368
http://purl.uniprot.org/citations/15655368http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/15655368
http://purl.uniprot.org/uniprot/#_P97465-mappedCitation-15655368http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15655368
http://purl.uniprot.org/uniprot/#_Q9QZC9-mappedCitation-15655368http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15655368
http://purl.uniprot.org/uniprot/#_Q9QZD0-mappedCitation-15655368http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15655368
http://purl.uniprot.org/uniprot/#_Q3UWF9-mappedCitation-15655368http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15655368
http://purl.uniprot.org/uniprot/#_Q3UEU0-mappedCitation-15655368http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15655368
http://purl.uniprot.org/uniprot/#_Q9ESD5-mappedCitation-15655368http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15655368
http://purl.uniprot.org/uniprot/#_Q9ES52-mappedCitation-15655368http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15655368
http://purl.uniprot.org/uniprot/P97465http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/15655368
http://purl.uniprot.org/uniprot/Q9ES52http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/15655368
http://purl.uniprot.org/uniprot/Q3UEU0http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/15655368