The c-fgr proto-oncogene, which is a member of the c-src gene family, encodes the cytoplasmic tyrosine kinase p55c-fgr. Expression of the c-fgr gene is activated in human B lymphocytes following infection with Epstein-Barr virus, and the viral protein EBNA-2 is involved in mediating this effect. The only normal cells in which the c-fgr gene is known to be expressed are peripheral-blood granulocytes and monocytes, and tissue macrophages. In accordance with this, levels of c-fgr mRNA increase when the human promonocytic cell line U937 and the human myelomonocytic cell line HL60 are induced to differentiate. The enzyme activity and the expression pattern of p55c-fgr suggest that it is involved in regulating the responses of terminally differentiated granulocytes and monocytes to external stimuli, perhaps by controlling changes in cytoskeletal structure.
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http://dx.doi.org/10.1159/000163665 | DOI Listing |
Sci Rep
January 2025
Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Suite 523, Bridgeside Point II, 450 Technology Drive, Pittsburgh, PA, 15219, USA.
Overexpression of the myeloid Src-family kinases Fgr and Hck has been linked to the development of acute myeloid leukemia (AML). Here we characterized the contribution of active forms of these kinases to AML cell cytokine dependence, inhibitor sensitivity, and AML cell engraftment in vivo. The human TF-1 erythroleukemia cell line was used as a model system as it does not express endogenous Hck or Fgr.
View Article and Find Full Text PDFNature
January 2022
Area of Cell and Developmental Biology, Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain.
Transcriptional and proteomic profiling of individual cells have revolutionized interpretation of biological phenomena by providing cellular landscapes of healthy and diseased tissues. These approaches, however, do not describe dynamic scenarios in which cells continuously change their biochemical properties and downstream 'behavioural' outputs. Here we used 4D live imaging to record tens to hundreds of morpho-kinetic parameters describing the dynamics of individual leukocytes at sites of active inflammation.
View Article and Find Full Text PDFJ Mol Biol
January 2022
Department of Biochemistry, Vanderbilt University, Nashville, TN 37232-0146, USA; Department of Pharmacology, Vanderbilt University, Nashville, TN 37232-0146, USA; Center for Structural Biology, Nashville, TN 37232-0146, USA; Vanderbilt Institute of Chemical Biology, Nashville, TN 37232-0146, USA. Electronic address:
Arrestins regulate a wide range of signaling events, most notably when bound to active G protein-coupled receptors (GPCRs). Among the known effectors recruited by GPCR-bound arrestins are Src family kinases, which regulate cellular growth and proliferation. Here, we focus on arrestin-3 interactions with Fgr kinase, a member of the Src family.
View Article and Find Full Text PDFCell Biochem Funct
June 2021
Department of Molecular Life Science, Tokai University School of Medicine, Isehara, Japan.
Chronic recurrent multifocal osteomyelitis (CRMO) is an autoinflammatory bone disease that presents with bone destruction and pain. Although genetic studies have identified signalling pathways involving CRMO, molecularly targeted drugs remain unavailable. We used an animal model of CRMO as an in vivo screening system for candidate therapeutic agents.
View Article and Find Full Text PDFJCI Insight
October 2020
Department of Anesthesiology.
Thalamic pain, a type of central poststroke pain, frequently occurs following ischemia/hemorrhage in the thalamus. Current treatment of this disorder is often ineffective, at least in part due to largely unknown mechanisms that underlie thalamic pain genesis. Here, we report that hemorrhage caused by microinjection of type IV collagenase or autologous whole blood into unilateral ventral posterior lateral nucleus and ventral posterior medial nucleus of the thalamus increased the expression of Fgr, a member of the Src family nonreceptor tyrosine kinases, at both mRNA and protein levels in thalamic microglia.
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