ArticleThe Journal of biological chemistry2013
Interaction of constitutive photomorphogenesis 1 protein with protein-tyrosine phosphatase 1B suppresses protein-tyrosine phosphatase 1B activity and enhances insulin signaling.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 6 citations in OpenAlex.
- RING-finger E3 ligases regulatory network in PI3K/AKT-mediated glucose metabolism.Cell death discovery · 2022Review
- DHHC7 Palmitoylates Glucose Transporter 4 (Glut4) and Regulates Glut4 Membrane Translocation.The Journal of biological chemistry · 2017Article
- IGF-1R modulation of acute GH-induced STAT5 signaling: role of protein tyrosine phosphatase activity.Molecular endocrinology (Baltimore, Md.) · 2013Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Recent studies reveal that COP1 suppresses the expression of gluconeogenetic genes and prohibits hepatic glucose production. To get more insight into COP1 in hepatic cells, we examined the impact of COP1 on insulin-responsive genes and insulin signaling. We found that COP1 increased the responsiveness of insulin-modulated genes to insulin in that it promoted the expression of insulin-induced genes and inhibited that of insulin-suppressed genes and that COP1 enhanced insulin signaling as it promoted phosphorylation of Akt and ERK as well as tyrosine phosphorylation of IRβ induced by insulin. To delineate the mechanism under which COP1 modulates insulin signaling, we examined the possibility that COP1 modulates the activity of PTP1B, the major insulin receptor tyrosine phosphatase. The results indicated that COP1 physically interacted with PTP1B and suppressed PTP1B phosphatase activity as well as the association of PTP1B with IRβ. We suggest that COP1 is a positive regulator of hepatic insulin signaling.
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Registered trials
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