ArticleJournal of cellular physiology2014
Involvement of IRS-1 interaction with ADAM10 in the regulation of neurite extension.
Article in Journal of cellular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Article
- Fetal Brain Injury Models of Fetal Alcohol Syndrome: Examination of Neuronal Morphologic Condition Using Sholl Assay.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Insulin-Like Growth Factor-1 Alleviates Expression of AβJournal of molecular neuroscience : MN · 2018Article
- Metalloprotease Adam10 suppresses epilepsy through repression of hippocampal neuroinflammation.Journal of neuroinflammation · 2018Article
- Fractalkine shedding is mediated by p38 and the ADAM10 protease under pro-inflammatory conditions in human astrocytes.Journal of neuroinflammation · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The insulin-like growth factor-1 (IGF-1) signaling pathway plays an important role in neuronal cell differentiation. Recent studies have shown that IGF-1 has the capacity to counteract the retraction of neuronal processes in response to inflammatory cytokines such as TNF-α, which is a known factor for neuronal injury in the central nervous system. This event is thought to be mediated via interference of TNF-α-induced interaction of β1-integrin with insulin receptor substrate-1 (IRS-1). Here, we demonstrate the interaction of IRS-1 with disintegrin and metalloproteinase ADAM10 through the N-terminal domain of IRS-1 and that this is involved in the regulation of neurite extension and retraction by IGF-1 and TNF-α, respectively. PC12 cells expressing the N-terminal domain show enhanced neurite extension after IGF-1 treatment and reduced neurite depletion relative to control cells after TNF-α treatment. The level of ADAM10 was found to be increased in immunohistochemical studies of HIV encephalitis clinical samples and is present with TNF-α and TNFR1 in both astrocytes and neurons. Altogether, these observations suggest a role for ADAM10 in the mechanism for IGF1/IRS-1 signaling pathway in sustaining the stability of neuronal processes.
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Registered trials
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