Here's how NATURE.COM makes money* and how much!

*Please read our disclaimer before using our estimates.
Loading...

NATURE . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Nature.com Make Money
  6. How Much Does Nature.com Make
  7. Keywords
  8. Topics
  9. Questions
  10. Schema
  11. External Links
  12. Analytics And Tracking
  13. Libraries
  14. Hosting Providers
  15. CDN Services

We are analyzing https://www.nature.com/articles/cmi2017135.

Title:
The chemokine MCP-1 (CCL2) in the host interaction with cancer: a foe or ally? | Cellular & Molecular Immunology
Description:
Macrophages are one of the most abundant leukocyte populations infiltrating tumor tissues and can exhibit both tumoricidal and tumor-promoting activities. In 1989, we reported the purification of monocyte chemoattractant protein-1 (MCP-1) from culture supernatants of mitogen-activated peripheral blood mononuclear cells and tumor cells. MCP-1 is a potent monocyte-attracting chemokine, identical to the previously described lymphocyte-derived chemotactic factor or tumor-derived chemotactic factor, and greatly contributes to the recruitment of blood monocytes into sites of inflammatory responses and tumors. Because in vitro-cultured tumor cells often produce significant amounts of MCP-1, tumor cells are considered to be the main source of MCP-1. However, various non-tumor cells in the tumor stroma also produce MCP-1 in response to stimuli. Studies performed in vitro and in vivo have provided evidence that MCP-1 production in tumors is a consequence of complex interactions between tumor cells and non-tumor cells and that both tumor cells and non-tumor cells contribute to the production of MCP-1. Although MCP-1 production was once considered to be a part of host defense against tumors, it is now believed to regulate the vicious cycle between tumor cells and macrophages that promotes the progression of tumors.
Website Age:
30 years and 10 months (reg. 1994-08-11).

Matching Content Categories {πŸ“š}

  • Education
  • Health & Fitness
  • Science

Content Management System {πŸ“}

What CMS is nature.com built with?

Custom-built

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

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of nature.com 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 Nature.com Make Money? {πŸ’Έ}


Display Ads {🎯}


The website utilizes display ads within its content to generate revenue. Check the next section for further revenue estimates.

Ads are managed by yourbow.com. Particular relationships are as follows:

Direct Advertisers (10)
google.com, pmc.com, doceree.com, yourbow.com, audienciad.com, onlinemediasolutions.com, advibe.media, aps.amazon.com, getmediamx.com, onomagic.com

Reseller Advertisers (38)
conversantmedia.com, rubiconproject.com, pubmatic.com, appnexus.com, openx.com, smartadserver.com, lijit.com, sharethrough.com, video.unrulymedia.com, google.com, yahoo.com, triplelift.com, onetag.com, sonobi.com, contextweb.com, 33across.com, indexexchange.com, media.net, themediagrid.com, adform.com, richaudience.com, sovrn.com, improvedigital.com, freewheel.tv, smaato.com, yieldmo.com, amxrtb.com, adyoulike.com, adpone.com, criteo.com, smilewanted.com, 152media.info, e-planning.net, smartyads.com, loopme.com, opera.com, mediafuse.com, betweendigital.com

How Much Does Nature.com Make? {πŸ’°}


Display Ads {🎯}

$63,100 per month
Our analysis indicates Nature.com generates between $42,042 and $115,616 monthly online from display ads.

Keywords {πŸ”}

pubmed, google, scholar, cas, article, cancer, cells, monocyte, central, chemoattractant, protein, cell, mcp, tumor, immunol, human, yoshimura, nature, macrophage, macrophages, breast, res, ccl, expression, chemokine, chemotactic, factor, access, gene, content, metastasis, natl, monocytes, tumors, usa, analysis, molecular, host, leonard, mol, biol, receptors, cookies, recruitment, vitro, vivo, production, matsushima, nat, clin,

Topics {βœ’οΈ}

nature portfolio permissions reprints privacy policy granulocyte/macrophage colony-stimulating factor advertising nf-kb/rel subunit specificity nature 2009 nature 2015 nature 2011 nature 2014 nature chemically defined media platelet-derived growth factor macrophage-csf-dependent macrophage responses lymphocyte-derived chemotactic factor tumor-derived chemotactic factor lymphocyte-derived chemotactic factors development monocyte-derived macrophage subpopulation facilitate breast-tumour metastasis short-lived intermediary reactions cell-free substances formed lymphoid cell-antigen interaction ccl2/ccr2 signalling recruits potent monocyte-attracting chemokine author information authors tumor-promoting activities autocrine tumor-promoting network social media ccl2 mediates cross-talk monocyte chemoattractant protein-1 monocyte-chemoattractant protein-1 malignant pleural effusion personal data vitro-cultured tumor cells transformed cells stimulated springerlink instant access lewis lung carcinoma host defense cytokines data protection permissions macrophage chemoattractant protein-1 destructive cascade mediated author correspondence author declares monocyte chemoattractant proteins monocyte secretory protein inflammatory chemokines ccl2 human breast cancer fibrosarcoma cell growth

Questions {❓}

  • The chemokine MCP-1 (CCL2) in the host interaction with cancer: a foe or ally?
  • The chemokine MCP-1 (CCL2) in the host interaction with cancer: a foe or ally?

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:The chemokine MCP-1 (CCL2) in the host interaction with cancer: a foe or ally?
         description:Macrophages are one of the most abundant leukocyte populations infiltrating tumor tissues and can exhibit both tumoricidal and tumor-promoting activities. In 1989, we reported the purification of monocyte chemoattractant protein-1 (MCP-1) from culture supernatants of mitogen-activated peripheral blood mononuclear cells and tumor cells. MCP-1 is a potent monocyte-attracting chemokine, identical to the previously described lymphocyte-derived chemotactic factor or tumor-derived chemotactic factor, and greatly contributes to the recruitment of blood monocytes into sites of inflammatory responses and tumors. Because in vitro-cultured tumor cells often produce significant amounts of MCP-1, tumor cells are considered to be the main source of MCP-1. However, various non-tumor cells in the tumor stroma also produce MCP-1 in response to stimuli. Studies performed in vitro and in vivo have provided evidence that MCP-1 production in tumors is a consequence of complex interactions between tumor cells and non-tumor cells and that both tumor cells and non-tumor cells contribute to the production of MCP-1. Although MCP-1 production was once considered to be a part of host defense against tumors, it is now believed to regulate the vicious cycle between tumor cells and macrophages that promotes the progression of tumors.
         datePublished:2018-01-29T00:00:00Z
         dateModified:2018-01-29T00:00:00Z
         pageStart:335
         pageEnd:345
         sameAs:https://doi.org/10.1038/cmi.2017.135
         keywords:
            chemokines
            cytokines
            inflammation
            macrophages
            tumor microenvironment
            Biomedicine
            general
            Immunology
            Medical Microbiology
            Microbiology
            Antibodies
            Vaccine
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fcmi.2017.135/MediaObjects/41423_2018_80_Fig1_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fcmi.2017.135/MediaObjects/41423_2018_80_Fig2_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fcmi.2017.135/MediaObjects/41423_2018_80_Fig3_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fcmi.2017.135/MediaObjects/41423_2018_80_Fig4_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fcmi.2017.135/MediaObjects/41423_2018_80_Fig5_HTML.jpg
         isPartOf:
            name:Cellular & Molecular Immunology
            issn:
               2042-0226
               1672-7681
            volumeNumber:15
            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:Teizo Yoshimura
               affiliation:
                     name:Okayama University
                     address:
                        name:Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Kita-ku, Japan
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:The chemokine MCP-1 (CCL2) in the host interaction with cancer: a foe or ally?
      description:Macrophages are one of the most abundant leukocyte populations infiltrating tumor tissues and can exhibit both tumoricidal and tumor-promoting activities. In 1989, we reported the purification of monocyte chemoattractant protein-1 (MCP-1) from culture supernatants of mitogen-activated peripheral blood mononuclear cells and tumor cells. MCP-1 is a potent monocyte-attracting chemokine, identical to the previously described lymphocyte-derived chemotactic factor or tumor-derived chemotactic factor, and greatly contributes to the recruitment of blood monocytes into sites of inflammatory responses and tumors. Because in vitro-cultured tumor cells often produce significant amounts of MCP-1, tumor cells are considered to be the main source of MCP-1. However, various non-tumor cells in the tumor stroma also produce MCP-1 in response to stimuli. Studies performed in vitro and in vivo have provided evidence that MCP-1 production in tumors is a consequence of complex interactions between tumor cells and non-tumor cells and that both tumor cells and non-tumor cells contribute to the production of MCP-1. Although MCP-1 production was once considered to be a part of host defense against tumors, it is now believed to regulate the vicious cycle between tumor cells and macrophages that promotes the progression of tumors.
      datePublished:2018-01-29T00:00:00Z
      dateModified:2018-01-29T00:00:00Z
      pageStart:335
      pageEnd:345
      sameAs:https://doi.org/10.1038/cmi.2017.135
      keywords:
         chemokines
         cytokines
         inflammation
         macrophages
         tumor microenvironment
         Biomedicine
         general
         Immunology
         Medical Microbiology
         Microbiology
         Antibodies
         Vaccine
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fcmi.2017.135/MediaObjects/41423_2018_80_Fig1_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fcmi.2017.135/MediaObjects/41423_2018_80_Fig2_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fcmi.2017.135/MediaObjects/41423_2018_80_Fig3_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fcmi.2017.135/MediaObjects/41423_2018_80_Fig4_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fcmi.2017.135/MediaObjects/41423_2018_80_Fig5_HTML.jpg
      isPartOf:
         name:Cellular & Molecular Immunology
         issn:
            2042-0226
            1672-7681
         volumeNumber:15
         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:Teizo Yoshimura
            affiliation:
                  name:Okayama University
                  address:
                     name:Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Kita-ku, Japan
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Cellular & Molecular Immunology
      issn:
         2042-0226
         1672-7681
      volumeNumber:15
Organization:
      name:Nature Publishing Group UK
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Okayama University
      address:
         name:Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Kita-ku, Japan
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Teizo Yoshimura
      affiliation:
            name:Okayama University
            address:
               name:Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Kita-ku, Japan
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Kita-ku, Japan
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {πŸ”—}(314)

Analytics and Tracking {πŸ“Š}

  • Google Tag Manager

Libraries {πŸ“š}

  • Prism.js
  • Zoom.js

Emails and Hosting {βœ‰οΈ}

Mail Servers:

  • mxa-002c5801.gslb.pphosted.com
  • mxb-002c5801.gslb.pphosted.com

Name Servers:

  • pdns1.ultradns.net
  • pdns2.ultradns.net
  • pdns3.ultradns.org
  • pdns4.ultradns.org
  • pdns5.ultradns.info
  • pdns6.ultradns.co.uk

CDN Services {πŸ“¦}

  • Crossref

4.43s.