ArticleMolecular and cellular biology1997
A deletion mutation in the SH2-N domain of Shp-2 severely suppresses hematopoietic cell development.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 165 citations in OpenAlex.
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- RNA-Seq Analysis Reveals Altered Expression of Cell Adhesion-Related Genes Following PZR Knockout in Lung Cancer Cells.Applied biochemistry and biotechnology · 2024Article
- A comprehensive review of SHP2 and its role in cancer.Cellular oncology (Dordrecht, Netherlands) · 2022Review
- Molecular, clinical, and prognostic implications of PTPN11 mutations in acute myeloid leukemia.Blood advances · 2022Article
- miR-514a-3p: a novel SHP-2 regulatory miRNA that modulates human cytotrophoblast proliferation.Journal of molecular endocrinology · 2022Article
- Rapid detection by hydrops panel of Noonan syndrome with PTPN11 mutation (p.Thr73Ile) and persistent thrombocytopenia.Molecular genetics & genomic medicine · 2020Article
- Tumor immunology and immunotherapy: a journey I started from Hangzhou.Journal of Zhejiang University. Science. B · 2019Article
- Feedback regulation of RTK signaling in development.Developmental biology · 2019Review
- Shp2-Mitogen-Activated Protein Kinase Signaling Drives Proliferation during Zebrafish Embryo Caudal Fin Fold Regeneration.Molecular and cellular biology · 2018Article
- SHP2 is required for BCR-ABL1-induced hematologic neoplasia.Leukemia · 2018Article
- SHP2-Mediated Signal Networks in Stem Cell Homeostasis and Dysfunction.Stem cells international · 2018Review
- Tyrosine phosphatase SHP2 negatively regulates NLRP3 inflammasome activation via ANT1-dependent mitochondrial homeostasis.Nature communications · 2017Article
- SHP2 regulates proliferation and tumorigenicity of glioma stem cells.Journal of neuro-oncology · 2017Article
- Article
- New and Unexpected Biological Functions for the Src-Homology 2 Domain-Containing Phosphatase SHP-2 in the Gastrointestinal Tract.Cellular and molecular gastroenterology and hepatology · 2016Review
- Protein-tyrosine phosphatase Shp2 positively regulates macrophage oxidative burst.The Journal of biological chemistry · 2015Article
- T cell activation is reduced by the catalytically inactive form of protein tyrosine phosphatase SHP-2.International journal of clinical and experimental medicine · 2015Article
- Article
- Hematopoietic colony formation from human growth factor-dependent TF1 cells and human cord blood myeloid progenitor cells depends on SHP2 phosphatase function.Stem cells and development · 2013Article
- S-nitrosylated SHP-2 contributes to NMDA receptor-mediated excitotoxicity in acute ischemic stroke.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
9 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Shp-1 and Shp-2 are cytoplasmic protein tyrosine phosphatases that contain two Src homology 2 (SH2) domains. A negative regulatory role of Shp-1 in hematopoiesis has been strongly implicated by the phenotype of motheaten mice with a mutation in the Shp-1 locus, which is characterized by leukocyte hypersensitivity, deregulated mast cell function, and excessive erythropoiesis. A targeted deletion of 65 amino acids in the N-terminal SH2 (SH2-N) domain of Shp-2 leads to an embryonic lethality at midgestation in homozygous mutant mice. To further dissect the Shp-2 function in hematopoietic development, we have isolated homozygous Shp-2 mutant embryonic stem (ES) cells. Significantly reduced hematopoietic activity was observed when the mutant ES cells were allowed to differentiate into embryoid bodies (EBs), compared to the wild-type and heterozygous ES cells. Further analysis of ES cell differentiation in vitro showed that mutation in the Shp-2 locus severely suppressed the development of primitive and definitive erythroid progenitors and completely blocked the production of progenitor cells for granulocytes-macrophages and mast cells. Reverse transcriptase PCR analysis of the mutant EBs revealed reduced expression of several specific marker genes that are induced during blood cell differentiation. Stem cell factor induction of mitogen-activated protein kinase activity was also blocked in Shp-2 mutant cells. Taken together, these results indicate that Shp-2 is an essential component and primarily plays a positive role in signaling pathways that mediate hematopoiesis in mammals. Furthermore, stimulation of its catalytic activity is not sufficient, while interaction via the SH2 domains with the targets or regulators is necessary for its biological functions in cells. The in vitro ES cell differentiation assay can be used as a biological tool in dissecting cytoplasmic signaling pathways.
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