DOI . ORG {}

Analyzed Page
Matching Content Categories
CMS
Monthly Traffic Estimate
How Does Doi.org Make Money
Keywords
Topics
Questions
Schema
Social Networks
External Links
Analytics And Tracking
Libraries
Hosting Providers
CDN Services

We began analyzing https://www.nature.com/articles/6603354, but it redirected us to https://www.nature.com/articles/6603354. The analysis below is for the second page.

Title[redir]:
Insulin receptor substrates mediate distinct biological responses to insulin-like growth factor receptor activation in breast cancer cells | British Journal of Cancer
Description:
Activation of the type I insulin-like growth factor receptor (IGF-IR) regulates several aspects of the malignant phenotype, including cancer cell proliferation and metastasis. Phosphorylation of adaptor proteins downstream of IGF-IR may couple IGF action to specific cancer phenotypes. In this study, we sought to determine if insulin receptor substrate-1 and -2 (IRS-1 and -2) mediate distinct biological effects in breast cancer cells. Insulin receptor substrate-1 and IRS-2 were expressed in T47D-YA breast cancer cells, which lack IRS-1 and -2 expression, yet retain functional IGF-IR. In the absence of IRS-1 and -2 expression, IGF-IR activation was unable to stimulate proliferation or motility in T47D-YA cells. Expression of IRS-1 resulted in IGF-I-stimulated proliferation, but did not affect motility. In contrast, expression of IRS-2 enhanced IGF-I-stimulated motility, but did not stimulate proliferation. The αIR-3, an inhibitor of the IGF-IR, was unable to affect these IGF-stimulated phenotypes unless IRS-1 or -2 was expressed. Thus, IGF-IR alone is unable to regulate important breast cancer cell phenotypes. In these cells, IRS proteins are required for and mediate distinct aspects of IGF-IR-stimulated behaviour. As multiple agents targeting the IGF-IR are currently in early clinical trials, IRS expression should be considered as a potential biomarker for IGF-IR responsiveness.

Matching Content Categories {📚}

Science
Education
Telecommunications

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month

Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Doi.org Make Money? {💸}

We can't tell how the site generates income.

Not all websites are made for profit; some exist to inform or educate users. Or any other reason why people make websites. And this might be the case. Doi.org has a secret sauce for making money, but we can't detect it yet.

Keywords {🔍}

cells, irs, cell, igfir, cancer, breast, growth, igfi, receptor, expression, tdya, article, google, scholar, tdyairs, cas, motility, insulin, substrate, insulinlike, data, activation, sfm, proliferation, yee, shown, figure, signalling, human, factor, usa, pathways, mapk, zhang, igfistimulated, lines, tdwt, protein, signaling, treated, proteins, αir, nature, mediate, functional, response, biological, adaptor, clinical, treatment,

Topics {✒️}

nature portfolio translational research privacy policy inhibit igf-i-stimulated entry nature 318 nature advertising growth factor-i-stimulated proliferation t47d-ya/irs-1 cells exhibited igf-i-stimulated cell proliferation measured igf-i-stimulated motility analysed igf-i-stimulated proliferation establish igf-ir-mediated monolayer mediate igf-ir-stimulated proliferation igf-i-activated igf-ir author information authors 0/ reprints t47d-ya/irs-1 cell clones t47d-ya/irs-2 cell clones induce igf-ir-mediated stimulation igf-ir-stimulated cell motility igf-ir-mediated cell motility igf-i-stimulated proliferation short-interfering rna constructs open bar pr-b-null-cell line investigate igf-ir-mediated proliferation igf-i-stimulated growth triple-negative breast cancer igf-i-stimulated motility mda-mb-231bo cells mda-mb-435 cell lines assessed anchorage-independent growth author correspondence igf-i-stimulated increase igf-ii influencing stability igf-ir stimulated proliferation igf-ir-stimulated proliferation antiprogestin-occupied b-receptors igf-ir signal transduction predict igf-ir dependency growth factor-mediated signaling high progesterone-receptor levels mediating igf-ir action 2 short-interfering rna anti-igf-ir agent igf-ir-mediated motility gold particle-coated coverslips disrupt igf-ir signalling igf-ir-stimulated behaviour

Questions {❓}

This raises an important question: what molecular attributes will likely be predictive of tumour dependence on IGF-IR?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Insulin receptor substrates mediate distinct biological responses to insulin-like growth factor receptor activation in breast cancer cells
         description:Activation of the type I insulin-like growth factor receptor (IGF-IR) regulates several aspects of the malignant phenotype, including cancer cell proliferation and metastasis. Phosphorylation of adaptor proteins downstream of IGF-IR may couple IGF action to specific cancer phenotypes. In this study, we sought to determine if insulin receptor substrate-1 and -2 (IRS-1 and -2) mediate distinct biological effects in breast cancer cells. Insulin receptor substrate-1 and IRS-2 were expressed in T47D-YA breast cancer cells, which lack IRS-1 and -2 expression, yet retain functional IGF-IR. In the absence of IRS-1 and -2 expression, IGF-IR activation was unable to stimulate proliferation or motility in T47D-YA cells. Expression of IRS-1 resulted in IGF-I-stimulated proliferation, but did not affect motility. In contrast, expression of IRS-2 enhanced IGF-I-stimulated motility, but did not stimulate proliferation. The Î±IR-3, an inhibitor of the IGF-IR, was unable to affect these IGF-stimulated phenotypes unless IRS-1 or -2 was expressed. Thus, IGF-IR alone is unable to regulate important breast cancer cell phenotypes. In these cells, IRS proteins are required for and mediate distinct aspects of IGF-IR-stimulated behaviour. As multiple agents targeting the IGF-IR are currently in early clinical trials, IRS expression should be considered as a potential biomarker for IGF-IR responsiveness.
         datePublished:2006-10-17T00:00:00Z
         dateModified:2011-11-16T00:00:00Z
         pageStart:1220
         pageEnd:1228
         sameAs:https://doi.org/10.1038/sj.bjc.6603354
         keywords:
            insulin-like growth factor-I
            type I insulin-like growth factor receptor
            insulin receptor substrate
            proliferation
            motility
            Biomedicine
            general
            Cancer Research
            Epidemiology
            Molecular Medicine
            Oncology
            Drug Resistance
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.bjc.6603354/MediaObjects/41416_2006_Article_BF6603354_Fig1_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.bjc.6603354/MediaObjects/41416_2006_Article_BF6603354_Fig2_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.bjc.6603354/MediaObjects/41416_2006_Article_BF6603354_Fig3_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.bjc.6603354/MediaObjects/41416_2006_Article_BF6603354_Fig4_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.bjc.6603354/MediaObjects/41416_2006_Article_BF6603354_Fig5_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.bjc.6603354/MediaObjects/41416_2006_Article_BF6603354_Fig6_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.bjc.6603354/MediaObjects/41416_2006_Article_BF6603354_Fig7_HTML.jpg
         isPartOf:
            name:British Journal of Cancer
            issn:
               1532-1827
               0007-0920
            volumeNumber:95
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Nature Publishing Group UK
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:S A Byron
               affiliation:
                     name:University of Minnesota Cancer Center
                     address:
                        name:Department of Pharmacology, University of Minnesota Cancer Center, Minneapolis, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:K B Horwitz
               affiliation:
                     name:University of Colorado Health Science Center
                     address:
                        name:Department of Medicine, University of Colorado Health Science Center, Denver, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:J K Richer
               affiliation:
                     name:University of Colorado Health Science Center
                     address:
                        name:Department of Medicine, University of Colorado Health Science Center, Denver, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:C A Lange
               affiliation:
                     name:University of Minnesota Cancer Center
                     address:
                        name:Department of Pharmacology, University of Minnesota Cancer Center, Minneapolis, USA
                        type:PostalAddress
                     type:Organization
                     name:University of Minnesota Cancer Center
                     address:
                        name:Department of Medicine, University of Minnesota Cancer Center, Minneapolis, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:X Zhang
               affiliation:
                     name:University of Minnesota Cancer Center
                     address:
                        name:Department of Medicine, University of Minnesota Cancer Center, Minneapolis, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:D Yee
               affiliation:
                     name:University of Minnesota Cancer Center
                     address:
                        name:Department of Pharmacology, University of Minnesota Cancer Center, Minneapolis, USA
                        type:PostalAddress
                     type:Organization
                     name:University of Minnesota Cancer Center
                     address:
                        name:Department of Medicine, University of Minnesota Cancer Center, Minneapolis, USA
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Insulin receptor substrates mediate distinct biological responses to insulin-like growth factor receptor activation in breast cancer cells
      description:Activation of the type I insulin-like growth factor receptor (IGF-IR) regulates several aspects of the malignant phenotype, including cancer cell proliferation and metastasis. Phosphorylation of adaptor proteins downstream of IGF-IR may couple IGF action to specific cancer phenotypes. In this study, we sought to determine if insulin receptor substrate-1 and -2 (IRS-1 and -2) mediate distinct biological effects in breast cancer cells. Insulin receptor substrate-1 and IRS-2 were expressed in T47D-YA breast cancer cells, which lack IRS-1 and -2 expression, yet retain functional IGF-IR. In the absence of IRS-1 and -2 expression, IGF-IR activation was unable to stimulate proliferation or motility in T47D-YA cells. Expression of IRS-1 resulted in IGF-I-stimulated proliferation, but did not affect motility. In contrast, expression of IRS-2 enhanced IGF-I-stimulated motility, but did not stimulate proliferation. The Î±IR-3, an inhibitor of the IGF-IR, was unable to affect these IGF-stimulated phenotypes unless IRS-1 or -2 was expressed. Thus, IGF-IR alone is unable to regulate important breast cancer cell phenotypes. In these cells, IRS proteins are required for and mediate distinct aspects of IGF-IR-stimulated behaviour. As multiple agents targeting the IGF-IR are currently in early clinical trials, IRS expression should be considered as a potential biomarker for IGF-IR responsiveness.
      datePublished:2006-10-17T00:00:00Z
      dateModified:2011-11-16T00:00:00Z
      pageStart:1220
      pageEnd:1228
      sameAs:https://doi.org/10.1038/sj.bjc.6603354
      keywords:
         insulin-like growth factor-I
         type I insulin-like growth factor receptor
         insulin receptor substrate
         proliferation
         motility
         Biomedicine
         general
         Cancer Research
         Epidemiology
         Molecular Medicine
         Oncology
         Drug Resistance
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.bjc.6603354/MediaObjects/41416_2006_Article_BF6603354_Fig1_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.bjc.6603354/MediaObjects/41416_2006_Article_BF6603354_Fig2_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.bjc.6603354/MediaObjects/41416_2006_Article_BF6603354_Fig3_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.bjc.6603354/MediaObjects/41416_2006_Article_BF6603354_Fig4_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.bjc.6603354/MediaObjects/41416_2006_Article_BF6603354_Fig5_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.bjc.6603354/MediaObjects/41416_2006_Article_BF6603354_Fig6_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.bjc.6603354/MediaObjects/41416_2006_Article_BF6603354_Fig7_HTML.jpg
      isPartOf:
         name:British Journal of Cancer
         issn:
            1532-1827
            0007-0920
         volumeNumber:95
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Nature Publishing Group UK
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:S A Byron
            affiliation:
                  name:University of Minnesota Cancer Center
                  address:
                     name:Department of Pharmacology, University of Minnesota Cancer Center, Minneapolis, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:K B Horwitz
            affiliation:
                  name:University of Colorado Health Science Center
                  address:
                     name:Department of Medicine, University of Colorado Health Science Center, Denver, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:J K Richer
            affiliation:
                  name:University of Colorado Health Science Center
                  address:
                     name:Department of Medicine, University of Colorado Health Science Center, Denver, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:C A Lange
            affiliation:
                  name:University of Minnesota Cancer Center
                  address:
                     name:Department of Pharmacology, University of Minnesota Cancer Center, Minneapolis, USA
                     type:PostalAddress
                  type:Organization
                  name:University of Minnesota Cancer Center
                  address:
                     name:Department of Medicine, University of Minnesota Cancer Center, Minneapolis, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:X Zhang
            affiliation:
                  name:University of Minnesota Cancer Center
                  address:
                     name:Department of Medicine, University of Minnesota Cancer Center, Minneapolis, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:D Yee
            affiliation:
                  name:University of Minnesota Cancer Center
                  address:
                     name:Department of Pharmacology, University of Minnesota Cancer Center, Minneapolis, USA
                     type:PostalAddress
                  type:Organization
                  name:University of Minnesota Cancer Center
                  address:
                     name:Department of Medicine, University of Minnesota Cancer Center, Minneapolis, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:British Journal of Cancer
      issn:
         1532-1827
         0007-0920
      volumeNumber:95
Organization:
      name:Nature Publishing Group UK
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University of Minnesota Cancer Center
      address:
         name:Department of Pharmacology, University of Minnesota Cancer Center, Minneapolis, USA
         type:PostalAddress
      name:University of Colorado Health Science Center
      address:
         name:Department of Medicine, University of Colorado Health Science Center, Denver, USA
         type:PostalAddress
      name:University of Colorado Health Science Center
      address:
         name:Department of Medicine, University of Colorado Health Science Center, Denver, USA
         type:PostalAddress
      name:University of Minnesota Cancer Center
      address:
         name:Department of Pharmacology, University of Minnesota Cancer Center, Minneapolis, USA
         type:PostalAddress
      name:University of Minnesota Cancer Center
      address:
         name:Department of Medicine, University of Minnesota Cancer Center, Minneapolis, USA
         type:PostalAddress
      name:University of Minnesota Cancer Center
      address:
         name:Department of Medicine, University of Minnesota Cancer Center, Minneapolis, USA
         type:PostalAddress
      name:University of Minnesota Cancer Center
      address:
         name:Department of Pharmacology, University of Minnesota Cancer Center, Minneapolis, USA
         type:PostalAddress
      name:University of Minnesota Cancer Center
      address:
         name:Department of Medicine, University of Minnesota Cancer Center, Minneapolis, USA
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:S A Byron
      affiliation:
            name:University of Minnesota Cancer Center
            address:
               name:Department of Pharmacology, University of Minnesota Cancer Center, Minneapolis, USA
               type:PostalAddress
            type:Organization
      name:K B Horwitz
      affiliation:
            name:University of Colorado Health Science Center
            address:
               name:Department of Medicine, University of Colorado Health Science Center, Denver, USA
               type:PostalAddress
            type:Organization
      name:J K Richer
      affiliation:
            name:University of Colorado Health Science Center
            address:
               name:Department of Medicine, University of Colorado Health Science Center, Denver, USA
               type:PostalAddress
            type:Organization
      name:C A Lange
      affiliation:
            name:University of Minnesota Cancer Center
            address:
               name:Department of Pharmacology, University of Minnesota Cancer Center, Minneapolis, USA
               type:PostalAddress
            type:Organization
            name:University of Minnesota Cancer Center
            address:
               name:Department of Medicine, University of Minnesota Cancer Center, Minneapolis, USA
               type:PostalAddress
            type:Organization
      name:X Zhang
      affiliation:
            name:University of Minnesota Cancer Center
            address:
               name:Department of Medicine, University of Minnesota Cancer Center, Minneapolis, USA
               type:PostalAddress
            type:Organization
      name:D Yee
      affiliation:
            name:University of Minnesota Cancer Center
            address:
               name:Department of Pharmacology, University of Minnesota Cancer Center, Minneapolis, USA
               type:PostalAddress
            type:Organization
            name:University of Minnesota Cancer Center
            address:
               name:Department of Medicine, University of Minnesota Cancer Center, Minneapolis, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Pharmacology, University of Minnesota Cancer Center, Minneapolis, USA
      name:Department of Medicine, University of Colorado Health Science Center, Denver, USA
      name:Department of Medicine, University of Colorado Health Science Center, Denver, USA
      name:Department of Pharmacology, University of Minnesota Cancer Center, Minneapolis, USA
      name:Department of Medicine, University of Minnesota Cancer Center, Minneapolis, USA
      name:Department of Medicine, University of Minnesota Cancer Center, Minneapolis, USA
      name:Department of Pharmacology, University of Minnesota Cancer Center, Minneapolis, USA
      name:Department of Medicine, University of Minnesota Cancer Center, Minneapolis, USA

Social Networks {👍}(1)

https://twitter.com/BrJCancer

External Links {🔗}(288)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Prism.js
Zoom.js

Emails and Hosting {✉️}

Mail Servers:

mx.zoho.eu
mx2.zoho.eu
mx3.zoho.eu

Name Servers:

josh.ns.cloudflare.com
zita.ns.cloudflare.com

CDN Services {📦}

Crossref

4.78s.