ArticleThe Biochemical journal2002
Interaction of protein tyrosine phosphatase (PTP) 1B with its substrates is influenced by two distinct binding domains.
Article in The Biochemical journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 33 citations in OpenAlex.
- Identification of miRNA-mRNA Co-expression by network analysis in dengue virus infection.Virusdisease · 2025Article
- The ER tether VAPA is required for proper cell motility and anchors ER-PM contact sites to focal adhesions.eLife · 2024Article
- Medicinal Aspects of PTP1B Inhibitors as Anti-Breast Cancer Agents: An Overview.Current medicinal chemistry · 2024Review
- Ventromedial hypothalamus-specific Ptpn1 deletion exacerbates diet-induced obesity in female mice.The Journal of clinical investigation · 2014Article
- Deficiency of PTP1B in leptin receptor-expressing neurons leads to decreased body weight and adiposity in mice.Endocrinology · 2012Article
- ER-bound protein tyrosine phosphatase PTP1B interacts with Src at the plasma membrane/substrate interface.PloS one · 2012Article
- PTP1B: a double agent in metabolism and oncogenesis.Trends in biochemical sciences · 2010Review
- HF diets increase hypothalamic PTP1B and induce leptin resistance through both leptin-dependent and -independent mechanisms.American journal of physiology. Endocrinology and metabolism · 2009Article
- PTP-1B is an essential positive regulator of platelet integrin signaling.The Journal of cell biology · 2005Article
- Redox paradox: insulin action is facilitated by insulin-stimulated reactive oxygen species with multiple potential signaling targets.Diabetes · 2005Review
- The NAD(P)H oxidase homolog Nox4 modulates insulin-stimulated generation of H2O2 and plays an integral role in insulin signal transduction.Molecular and cellular biology · 2004Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have shown previously that protein tyrosine phosphatase (PTP) 1B interacts with insulin receptor and negatively regulates insulin signalling by an N-terminal binding domain [Dadke, Kusari and Chernoff (2000) J. Biol. Chem. 275, 23642-23647] and it also negatively regulates integrin signalling through a proline-rich region present in the C-terminus [Liu, Hill and Chernoff (1996) J. Biol. Chem. 271, 31290-31295; Liu, Sells and Chernoff (1998) Curr. Biol. 8, 173-176]. Here we show that PTP1B mutants that are defective in Src homology 3 domain binding fully retain the ability to inhibit insulin signalling, whereas mutants defective in insulin-receptor binding fully retain the ability to inhibit integrin signalling. In contrast, both the C-terminal proline-rich region and the tandem tyrosine residues present in the N-terminal region are required for the activation of Src family kinases. These data show that PTP1B can independently regulate insulin and integrin signals, and that Src might represent a convergence point for regulating signal transduction by this phosphatase.
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