(Q28201688)

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c-Cbl associates directly with the C-terminal tail of the receptor for the macrophage colony-stimulating factor, c-Fms, and down-modulates this receptor but not the viral oncogene v-Fms

scientific article (publication date: 26 April 2002)

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c-Cbl associates directly with the C-terminal tail of the receptor for the macrophage colony-stimulating factor, c-Fms, and down-modulates this receptor but not the viral oncogene v-Fms (English)

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author name string

Annalisa Mancini

1

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Alexandra Koch

2

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Regina Wilms

3

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Teruko Tamura

4

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language of work or name

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publication date

26 April 2002

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Journal of Biological Chemistry

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277

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17

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14635-40

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Molecular themes in oncogenesis

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M109214200

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Identification of a second Grb2 binding site in the v-Fms tyrosine kinase

1 reference

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Sequential activation of phoshatidylinositol 3-kinase and phospholipase C-gamma2 by the M-CSF receptor is necessary for differentiation signaling

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FMIP, a novel Fms-interacting protein, affects granulocyte/macrophage differentiation

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Tyrosine phosphorylation of the juxtamembrane domain of the v-Fms oncogene product is required for its association with a 55-kDa protein

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Activation of the feline c-fms proto-oncogene: multiple alterations are required to generate a fully transformed phenotype

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A point mutation in the extracellular domain of the human CSF-1 receptor (c-fms proto-oncogene product) activates its transforming potential

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A point mutation at tyrosine-809 in the human colony-stimulating factor 1 receptor impairs mitogenesis without abrogating tyrosine kinase activity, association with phosphatidylinositol 3-kinase, or induction of c-fos and junB genes

1 reference

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Biological consequences of a point mutation at codon 969 of the FMS gene

1 reference

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FMS mutations in myelodysplastic, leukemic, and normal subjects

1 reference

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Association of Cbl with Fms and p85 in response to macrophage colony-stimulating factor.

1 reference

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CSF-1 stimulation induces the formation of a multiprotein complex including CSF-1 receptor, c-Cbl, PI 3-kinase, Crk-II and Grb2

1 reference

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The proto-oncogene product c-Cbl becomes tyrosine phosphorylated by stimulation with GM-CSF or Epo and constitutively binds to the SH3 domain of Grb2/Ash in human hematopoietic cells

1 reference

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The Cbl protooncoprotein stimulates CSF-1 receptor multiubiquitination and endocytosis, and attenuates macrophage proliferation

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The tyrosine kinase negative regulator c-Cbl as a RING-type, E2-dependent ubiquitin-protein ligase

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Ubiquitin ligase activity and tyrosine phosphorylation underlie suppression of growth factor signaling by c-Cbl/Sli-1

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The tyrosine kinase regulator Cbl enhances the ubiquitination and degradation of the platelet-derived growth factor receptor alpha

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Cbl-mediated negative regulation of platelet-derived growth factor receptor-dependent cell proliferation. A critical role for Cbl tyrosine kinase-binding domain

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Involvement of Shc and Cbl-PI 3-kinase in Lyn-dependent proliferative signaling pathways for G-CSF.

1 reference

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21 January 2018

c-Cbl is a suppressor of the neu oncogene

1 reference

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21 January 2018

Mammalian tumor susceptibility gene 101 (TSG101) and the yeast homologue, Vps23p, both function in late endosomal trafficking.

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The Notch intracellular domain is ubiquitinated and negatively regulated by the mammalian Sel-10 homolog

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21 January 2018

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10.1074/JBC.M109214200

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