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http://purl.uniprot.org/citations/16705167http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16705167http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16705167http://www.w3.org/2000/01/rdf-schema#comment"Mice null for the T-cell protein tyrosine phosphatase (Tcptp-/-) die shortly after birth due to complications arising from the development of a systemic inflammatory disease. It was originally reported that Tcptp-/-mice have increased numbers of macrophages in the spleen; however, the mechanism underlying the aberrant growth and differentiation of macrophages in Tcptp-/-mice is not known. We have identified Tcptp as an important regulator of colony-stimulating factor 1 (CSF-1) signaling and mononuclear phagocyte development. The number of CSF-1-dependent CFU is increased in Tcptp-/- bone marrow. Tcptp-/-mice also have increased numbers of granulocyte-macrophage precursors (GMP), and these Tcptp-/-GMP yield more macrophage colonies in response to CSF-1 relative to wild-type cells. Furthermore, we have identified the CSF-1 receptor (CSF-1R) as a physiological target of Tcptp through substrate-trapping experiments and its hyperphosphorylation in Tcptp-/- macrophages. Tcptp-/-macrophages also have increased tyrosine phosphorylation and recruitment of a Grb2/Gab2/Shp2 complex to the CSF-1R and enhanced activation of Erk after CSF-1 stimulation, which are important molecular events in CSF-1-induced differentiation. These data implicate Tcptp as a critical regulator of CSF-1 signaling and mononuclear phagocyte development in hematopoiesis."xsd:string
http://purl.uniprot.org/citations/16705167http://purl.org/dc/terms/identifier"doi:10.1128/mcb.01932-05"xsd:string
http://purl.uniprot.org/citations/16705167http://purl.org/dc/terms/identifier"doi:10.1128/mcb.01932-05"xsd:string
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/author"Tremblay M.L."xsd:string
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/author"Tremblay M.L."xsd:string
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/author"McGlade C.J."xsd:string
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/author"McGlade C.J."xsd:string
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/author"Stanley E.R."xsd:string
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/author"Stanley E.R."xsd:string
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/author"Bourdeau A."xsd:string
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/author"Bourdeau A."xsd:string
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/author"Lee-Loy A."xsd:string
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/author"Lee-Loy A."xsd:string
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/author"Rohrschneider L.R."xsd:string
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/author"Rohrschneider L.R."xsd:string
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/author"Simoncic P.D."xsd:string
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/author"Simoncic P.D."xsd:string
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/name"Mol. Cell. Biol."xsd:string
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/name"Mol. Cell. Biol."xsd:string
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/pages"4149-4160"xsd:string
http://purl.uniprot.org/citations/16705167http://purl.uniprot.org/core/pages"4149-4160"xsd:string