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We began analyzing https://www.tandfonline.com/doi/full/10.1128/MCB.21.15.5082-5093.2001, but it redirected us to https://www.tandfonline.com/doi/full/10.1128/MCB.21.15.5082-5093.2001. The analysis below is for the second page.

Title[redir]:
Identification of Insulin Receptor Substrate 1 (IRS-1) and IRS-2 as Signaling Intermediates in the α6β4 Integrin-Dependent Activation of Phosphoinositide 3-OH Kinase and Promotion of Invasion: Molecular and Cellular Biology: Vol 21 , No 15 - Get Access
Description:
Expression of the α6β4 integrin increases the invasive potential of carcinoma cells by a mechanism that involves activation of phosphoinositide 3-OH kinase (PI3K). In the present study, we investig...

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access, journals, sciences, open, taylor, francis, search, online, article, irs, browse, journal, studies, log, articles, find, environment, science, activation, pik, group, page, publish, health, social, cart, read, issue, receptor, integrin, pdf, technology, information, register, signaling, kinase, proteins, content, close, menu, select, calls, papers, suggester, publishing, guidance, author, services, bioscience, earth,

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social care medicine journals bioscience molecular downloaded article pdf twitter page taylor harvard medical school article /doi/full/10 francis group journal search calls α6β4 integrin-dependent activation downloaded article pdfs cart search limited period α6β4-dependent phosphorylation advanced search molecular find guidance insulin receptor subst journals books receive personalised research crossref citations access rights institution access read lists articles published online consensus binding motif excellent technical assistance nih grant ca81325 army grant damd17–97-1–7313 applicable share back citing articles based journals browse cellular biology list α6β4-dependent promotion open organize signaling complexes α6β4 integrin increases cytoplasmic adapter proteins intrinsic kinase activity information promote carcinoma invasion β4 cytoplasmic domain issue 15 identification development identification journals a date register article https α6β4 integrin tyrosine residue register log crossref icon author services

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      articleSection:Cell Growth and Development
      name:Identification of Insulin Receptor Substrate 1 (IRS-1) and IRS-2 as Signaling Intermediates in the Î±6Î²4 Integrin-Dependent Activation of Phosphoinositide 3-OH Kinase and Promotion of Invasion
      headline:Identification of Insulin Receptor Substrate 1 (IRS-1) and IRS-2 as Signaling Intermediates in the Î±6Î²4 Integrin-Dependent Activation of Phosphoinositide 3-OH Kinase and Promotion of Invasion
      abstract:Expression of the Î±6Î²4 integrin increases the invasive potential of carcinoma cells by a mechanism that involves activation of phosphoinositide 3-OH kinase (PI3K). In the present study, we investigated the signaling pathway by which the Î±6Î²4 integrin activates PI3K. Neither the Î±6 nor the Î²4 cytoplasmic domain contains the consensus binding motif for PI3K, pYMXM, indicating that additional proteins are likely to be involved in the activation of this lipid kinase by the Î±6Î²4 integrin. We identified insulin receptor substrate 1 (IRS-1) and IRS-2 as signaling intermediates in the activation of PI3K by the Î±6Î²4 integrin. IRS-1 and IRS-2 are cytoplasmic adapter proteins that do not contain intrinsic kinase activity but rather function by recruiting proteins to surface receptors, where they organize signaling complexes. Ligation of the Î±6Î²4 receptor promotes tyrosine phosphorylation of IRS-1 and IRS-2 and increases their association with PI3K, as determined by coimmunoprecipitation. Moreover, we identified a tyrosine residue in the cytoplasmic domain of the Î²4 subunit, Y1494, that is required for Î±6Î²4-dependent phosphorylation of IRS-2 and activation of PI3K in response to receptor ligation. Most importantly, Y1494 is essential for the ability of the Î±6Î²4 integrin to promote carcinoma invasion. Taken together, these results imply a key role for the IRS proteins in the Î±6Î²4-dependent promotion of carcinoma invasion.
      description:Expression of the Î±6Î²4 integrin increases the invasive potential of carcinoma cells by a mechanism that involves activation of phosphoinositide 3-OH kinase (PI3K). In the present study, we investigated the signaling pathway by which the Î±6Î²4 integrin activates PI3K. Neither the Î±6 nor the Î²4 cytoplasmic domain contains the consensus binding motif for PI3K, pYMXM, indicating that additional proteins are likely to be involved in the activation of this lipid kinase by the Î±6Î²4 integrin. We identified insulin receptor substrate 1 (IRS-1) and IRS-2 as signaling intermediates in the activation of PI3K by the Î±6Î²4 integrin. IRS-1 and IRS-2 are cytoplasmic adapter proteins that do not contain intrinsic kinase activity but rather function by recruiting proteins to surface receptors, where they organize signaling complexes. Ligation of the Î±6Î²4 receptor promotes tyrosine phosphorylation of IRS-1 and IRS-2 and increases their association with PI3K, as determined by coimmunoprecipitation. Moreover, we identified a tyrosine residue in the cytoplasmic domain of the Î²4 subunit, Y1494, that is required for Î±6Î²4-dependent phosphorylation of IRS-2 and activation of PI3K in response to receptor ligation. Most importantly, Y1494 is essential for the ability of the Î±6Î²4 integrin to promote carcinoma invasion. Taken together, these results imply a key role for the IRS proteins in the Î±6Î²4-dependent promotion of carcinoma invasion.
      author:
            type:Person
            name:Leslie M. Shaw
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      datePublished:2023-03-28
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