ArticleOncogene2001
The role of the insulin receptor substrate-1 in the differentiation of rat hippocampal neuronal cells.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 30 citations in OpenAlex.
- Functional characterization of FAM120A as a novel effector in the progranulin/EphA2 oncogenic axis in bladder cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- Complexity of progranulin mechanisms of action in mesothelioma.Journal of experimental & clinical cancer research : CR · 2022Article
- Discoidin Domain Receptor 1 functionally interacts with the IGF-I system in bladder cancer.Matrix biology plus · 2020Article
- IGF1 regulates RUNX1 expression via IRS1/2: Implications for antler chondrocyte differentiation.Cell cycle (Georgetown, Tex.) · 2017Article
- Insulin Receptor Substrate-1 Activation Mediated p53 Downregulation Protects Against Hypoxic-Ischemia in the Neonatal Brain.Molecular neurobiology · 2016Article
- Suppression of progranulin expression inhibits bladder cancer growth and sensitizes cancer cells to cisplatin.Oncotarget · 2016Article
- Effects of APP 5-mer peptide analogue P165 on the synaptic proteins and insulin signal transduction proteins.International journal of clinical and experimental medicine · 2014Article
- Proline-rich tyrosine kinase 2 (Pyk2) regulates IGF-I-induced cell motility and invasion of urothelial carcinoma cells.PloS one · 2012Article
- Proepithelin is an autocrine growth factor for bladder cancer.Carcinogenesis · 2009Article
- Transformation by the simian virus 40 T antigen is regulated by IGF-I receptor and IRS-1 signaling.Oncogene · 2006Article
- Role of pescadillo and upstream binding factor in the proliferation and differentiation of murine myeloid cells.Molecular and cellular biology · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
H19-7/IGF-IR cells are rat hippocampal cells expressing a human IGF-I receptor, which differentiate to a neuronal phenotype when stimulated by IGF-I at 39 degrees C. H19-7/IGF-IR cells have low levels of expression of insulin receptor substrate-l (IRS-1), a major substrate of the IGF-IR. IGF-I induces serine-phosphorylation and down-regulation of the endogenous IRS-1 upon differentiation of H19-7/IGF-IR cells. The profound influence of IRS-1 on differentiation of H19-7/IGF-IR cells was confirmed by transfecting these cells with a plasmid expressing mouse IRS-1. Over-expression of wild type IRS-1 in H19-7/IGF-IR cells abolishes IGF-I-induced differentiation at 39 degrees C. A mutant of IRS-1 lacking the PTB domain loses the ability to inhibit the differentiation program. H19-7/IGF-IR/IRS-1 cells at 39 degrees C show a stronger and prolonged activation of Akt, when compared to H19-7/IGF-IR cells. The role of Akt in the inhibition of the differentiation program was confirmed by using the inhibitor of Class I PI3 kinases LY29400, which restores IGF-I-induced differentiation of H19-7/IGF-IR/IRS-1 cells. H19-7/IGF-IR/IRS-1 cells show a strong reduction in MAP kinases signaling, which is related to the superactivation of Akt. This was confirmed by expressing in H19-7/IGF-IR cells a constitutively active Akt, which inhibited MAP kinases activation in these cells. These experiments confirm the importance of MAPK in the mechanism of IGF-I-mediated differentiation of H19-7/IGF-IR cells
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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.