ArticleMolecular and cellular biology1996
Involvement of the protein tyrosine phosphatase SHP-1 in Ras-mediated activation of the mitogen-activated protein kinase pathway.
Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 45 citations in OpenAlex.
- Review
- Alveolar macrophage metabolic programming via a C-type lectin receptor protects against lipo-toxicity and cell death.Nature communications · 2022Article
- Identification of a c-Jun N-terminal kinase-2-dependent signal amplification cascade that regulates c-Myc levels in ras transformation.Oncogene · 2012Article
- The SHP-1 protein tyrosine phosphatase negatively modulates Akt signaling in the ghrelin/GHSR1a system.Molecular biology of the cell · 2011Article
- S-glutathionylation: from molecular mechanisms to health outcomes.Antioxidants & redox signaling · 2011Review
- SHP-1 deficient mast cells are hyperresponsive to stimulation and critical in initiating allergic inflammation in the lung.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Survival of monocytes and macrophages and their role in health and disease.Frontiers in bioscience (Landmark edition) · 2009Review
- SHP-1 inhibition by 4-hydroxynonenal activates Jun N-terminal kinase and glutamate cysteine ligase.American journal of respiratory cell and molecular biology · 2008Article
- TGF-beta 1 inhibition of IFN-gamma-induced signaling and Th1 gene expression in CD4+ T cells is Smad3 independent but MAP kinase dependent.Molecular immunology · 2007Article
- Article
- Antagonism or synergism. Role of tyrosine phosphatases SHP-1 and SHP-2 in growth factor signaling.The Journal of biological chemistry · 2006Article
- Subversion mechanisms by which Leishmania parasites can escape the host immune response: a signaling point of view.Clinical microbiology reviews · 2005Review
- SHP-1 negatively regulates neuronal survival by functioning as a TrkA phosphatase.The Journal of cell biology · 2003Article
- Protective role of Raf-1 in Salmonella-induced macrophage apoptosis.The Journal of experimental medicine · 2001Article
- ets-2 is a target for an akt (Protein kinase B)/jun N-terminal kinase signaling pathway in macrophages of motheaten-viable mutant mice.Molecular and cellular biology · 2000Article
- A role for the SHP-2 tyrosine phosphatase in nerve growth-induced PC12 cell differentiation.Molecular biology of the cell · 1997Article
- Mutant N-RAS induces erythroid lineage dysplasia in human CD34+ cells.The Journal of experimental medicine · 1997Article
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
Ubiquitously expressed SH2-containing tyrosine phosphatases interact physically with tyrosine kinase receptors or their substrates and relay positive mitogenic signals via the activation of the Ras-mitogen-activated protein kinase (MAPK) pathway. Conversely, the structurally related phosphatase SHP-1 is predominantly expressed in hemopoietic cells and becomes tyrosine phosphorylated upon colony-stimulating factor 1 treatment of macrophages without associating with the colony-stimulating factor 1 receptor tyrosine kinase. Mice lacking functional SHP-1 (me/me and me(v)/me(v)) develop systemic autoimmune disease with accumulation of macrophages, suggesting that SHP-1 may be a negative regulator of hemopoietic cell growth. By using macrophages expressing dominant negative Ras and the me(v)/me(v) mouse mutant, we show that SHP-1 is activated in the course of mitogenic signal transduction in a Ras-dependent manner and that its activity is necessary for the Ras-dependent activation of the MAPK pathway but not of the Raf-1 kinase. Consistent with a role for SHP-1 as an intermediate between Ras and the MEK-MAPK pathway, Ras-independent activation of the latter kinases by bacterial lipopolysaccharide occurred normally in me(v)/me(v) cells. Our results sharply accentuate the diversity of signal transduction in mammalian cells, in which the same signaling intermediates can be rearranged to form different pathways.
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