ArticleThe Journal of cell biology2003
SHP-1 negatively regulates neuronal survival by functioning as a TrkA phosphatase.
Article in The Journal of cell biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 91 citations in OpenAlex.
- Proteomic Investigation of Neurotrophic trans-Banglene Reveals Potential Link to Iron Homeostasis.Molecular neurobiology · 2025Article
- Interaction of Erdosteine with TrkA Signaling Pathways: Implications for Analgesia.International journal of molecular sciences · 2025Article
- PTPN23-dependent ESCRT machinery functions as a cell death checkpoint.Nature communications · 2024Article
- Article
- SHP-1 tyrosine phosphatase binding to c-Src kinase phosphor-dependent conformations: A comparative structural framework.PloS one · 2023Article
- Retrograde nerve growth factor signaling abnormalities and the pathogenesis of familial dysautonomia.Neural regeneration research · 2021Article
- Protein Tyrosine Phosphatases in Neuroblastoma: Emerging Roles as Biomarkers and Therapeutic Targets.Frontiers in cell and developmental biology · 2021Review
- Retrograde nerve growth factor signaling abnormalities in familial dysautonomia.The Journal of clinical investigation · 2020Article
- (H)Elping nerve growth factor: Elp1 inhibits TrkA's phosphatase to maintain retrograde signaling.The Journal of clinical investigation · 2020Article
- Phospho-Regulation of Soma-to-Axon Transcytosis of Neurotrophin Receptors.Developmental cell · 2017Article
- NEAP/DUSP26 suppresses receptor tyrosine kinases and regulates neuronal development in zebrafish.Scientific reports · 2017Article
- Article
- Microarray Analysis Reveals Increased Transcriptional Repression and Reduced Metabolic Activity but Not Major Changes in the Core Apoptotic Machinery during Maturation of Sympathetic Neurons.Frontiers in cellular neuroscience · 2016Article
- Imbalance of the Nerve Growth Factor and Its Precursor: Implication in Diabetic Retinopathy.Journal of clinical & experimental ophthalmology · 2015Article
- Neuroblastoma tyrosine kinase signaling networks involve FYN and LYN in endosomes and lipid rafts.PLoS computational biology · 2015Article
- Nerve growth factor (NGF) regulates activity of nuclear factor of activated T-cells (NFAT) in neurons via the phosphatidylinositol 3-kinase (PI3K)-Akt-glycogen synthase kinase 3β (GSK3β) pathway.The Journal of biological chemistry · 2014Article
- Nerve growth factor in diabetic retinopathy: beyond neurons.Expert review of ophthalmology · 2014Article
- Regulation of neurotrophin receptor (Trk) signaling: suppressor of cytokine signaling 2 (SOCS2) is a new player.Frontiers in molecular neuroscience · 2014Review
- Proteomic analysis of novel targets associated with TrkA-mediated tyrosine phosphorylation signaling pathways in SK-N-MC neuroblastoma cells.Proteomics · 2013Article
- Novel sorafenib analogues induce apoptosis through SHP-1 dependent STAT3 inactivation in human breast cancer cells.Breast cancer research : BCR · 2013Article
Corrections and comments
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Authors and funding
14 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nerve growth factor (NGF) mediates the survival and differentiation of neurons by stimulating the tyrosine kinase activity of the TrkA/NGF receptor. Here, we identify SHP-1 as a phosphotyrosine phosphatase that negatively regulates TrkA. SHP-1 formed complexes with TrkA at Y490, and dephosphorylated it at Y674/675. Expression of SHP-1 in sympathetic neurons induced apoptosis and TrkA dephosphorylation. Conversely, inhibition of endogenous SHP-1 with a dominant-inhibitory mutant stimulated basal tyrosine phosphorylation of TrkA, thereby promoting NGF-independent survival and causing sustained and elevated TrkA activation in the presence of NGF. Mice lacking SHP-1 had increased numbers of sympathetic neurons during the period of naturally occurring neuronal cell death, and when cultured, these neurons survived better than wild-type neurons in the absence of NGF. These data indicate that SHP-1 can function as a TrkA phosphatase, controlling both the basal and NGF-regulated level of TrkA activity in neurons, and suggest that SHP-1 regulates neuron number during the developmental cell death period by directly regulating TrkA activity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.