ArticleMolecular and cellular biology1998
Definition of the role of tyrosine residues of the common beta subunit regulating multiple signaling pathways of granulocyte-macrophage colony-stimulating factor receptor.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 78 citations in OpenAlex.
- Selective activation of STAT3 and STAT5 dictates the fate of myeloid progenitor cells.Cell death discovery · 2023Article
- Siglec-F is induced by granulocyte-macrophage colony-stimulating factor and enhances interleukin-4-induced expression of arginase-1 in mouse macrophages.Immunology · 2019Article
- A Frameshift in CSF2RB Predominant Among Ashkenazi Jews Increases Risk for Crohn's Disease and Reduces Monocyte Signaling via GM-CSF.Gastroenterology · 2016Article
- CBL linker region and RING finger mutations lead to enhanced granulocyte-macrophage colony-stimulating factor (GM-CSF) signaling via elevated levels of JAK2 and LYN.The Journal of biological chemistry · 2013Article
- Genetic disruption of the PI3K regulatory subunits, p85α, p55α, and p50α, normalizes mutant PTPN11-induced hypersensitivity to GM-CSF.Haematologica · 2012Article
- The role of interchain heterodisulfide formation in activation of the human common beta and mouse betaIL-3 receptors.The Journal of biological chemistry · 2010Article
- Crossing paths: interactions between the cell death machinery and growth factor survival signals.Cellular and molecular life sciences : CMLS · 2010Review
- CREB in the pathophysiology of cancer: implications for targeting transcription factors for cancer therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009Article
- Article
- Growth factor pleiotropy is controlled by a receptor Tyr/Ser motif that acts as a binary switch.The EMBO journal · 2006Article
- Immunostimulatory properties of human dendritic cells generated using IFN-beta associated either with IL-3 or GM-CSF.Cancer immunology, immunotherapy : CII · 2005Article
- Signal transduction activator of transcription 5 (STAT5) dysfunction in autoimmune monocytes and macrophages.Journal of autoimmunity · 2005Article
- Article
- JAK/STAT, Raf/MEK/ERK, PI3K/Akt and BCR-ABL in cell cycle progression and leukemogenesis.Leukemia · 2004Review
- Catalytic-dependent and -independent roles of SHP-2 tyrosine phosphatase in interleukin-3 signaling.Oncogene · 2003Article
- Cooperation of cytokine signaling with chimeric transcription factors in leukemogenesis: PML-retinoic acid receptor alpha blocks growth factor-mediated differentiation.Molecular and cellular biology · 2003Article
- Structural and functional hot spots in cytokine receptors.International journal of hematology · 2001Review
- New role for Shc in activation of the phosphatidylinositol 3-kinase/Akt pathway.Molecular and cellular biology · 2000Article
- The role of STAT proteins in growth hormone signaling.Oncogene · 2000Review
- Cooperation between STAT5 and phosphatidylinositol 3-kinase in the IL-3-dependent survival of a bone marrow derived cell line.Oncogene · 2000Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Granulocyte-macrophage colony-stimulating factor (GM-CSF) induces various functions, including the proliferation and differentiation of a broad range of hematopoietic cells. We previously reported that at least two distinct pathways are involved in human GM-CSF receptor signaling; both require the box 1 region of the common beta subunit (beta c). This region is essential for the activation of JAK2, which is necessary for all the biological functions of GM-CSF. The activation of JAK2 by GM-CSF leads to rapid tyrosine phosphorylation of cellular proteins, including the beta c. However, the significance of beta c phosphorylation with regard to the regulation of signaling molecules and the expression of GM-CSF functions is less well understood. Here we investigated the role of the cytoplasmic tyrosine residues of the beta c by using a series of beta c mutants expressed in murine BA/F3 cells. A mutant beta c with all eight cytoplasmic tyrosines converted to phenylalanine (Fall) activated JAK2 but not SHP-2, MAPK cascades, STAT5, or the c-fos promoter in BA/F3 cells, and it did not effectively induce proliferation. Adding back each tyrosine to Fall revealed that Tyr577, Tyr612, and Tyr695 are involved in the activation of SHP-2, MAPK cascades, and c-fos transcription, while every tyrosine, particularly Tyr612, Tyr695, Tyr750, and Tyr806, facilitated STAT5 activation. Impaired growth was also restored, at least partly, by any of the tyrosines. These results provide evidence that beta c tyrosines possess distinct yet overlapping functions in activating multiple signaling pathways induced by GM-CSF.
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