Here's how DOI.ORG makes money* and how much!

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

DOI . ORG {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Doi.org Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. Social Networks
  11. External Links
  12. Analytics And Tracking
  13. Javascript Libraries
  14. Hosting Providers

We began analyzing https://www.nature.com/articles/s41419-019-1370-2, but it redirected us to https://www.nature.com/articles/s41419-019-1370-2. The analysis below is for the second page.

Title[redir]:
Cell death pathways in pathogenic trypanosomatids: lessons of (over)kill | Cell Death & Disease
Description:
Especially in tropical and developing countries, the clinically relevant protozoa Trypanosoma cruzi (Chagas disease), Trypanosoma brucei (sleeping sickness) and Leishmania species (leishmaniasis) stand out and infect millions of people worldwide leading to critical social-economic implications. Low-income populations are mainly affected by these three illnesses that are neglected by the pharmaceutical industry. Current anti-trypanosomatid drugs present variable efficacy with remarkable side effects that almost lead to treatment discontinuation, justifying a continuous search for alternative compounds that interfere with essential and specific parasite pathways. In this scenario, the triggering of trypanosomatid cell death machinery emerges as a promising approach, although the exact mechanisms involved in unicellular eukaryotes are still unclear as well as the controversial biological importance of programmed cell death (PCD). In this review, the mechanisms of autophagy, apoptosis-like cell death and necrosis found in pathogenic trypanosomatids are discussed, as well as their roles in successful infection. Based on the published genomic and proteomic maps, the panel of trypanosomatid cell death molecules was constructed under different experimental conditions. The lack of PCD molecular regulators and executioners in these parasites up to now has led to cell death being classified as an unregulated process or incidental necrosis, despite all morphological evidence published. In this context, the participation of metacaspases in PCD was also not described, and these proteases play a crucial role in proliferation and differentiation processes. On the other hand, autophagic phenotype has been described in trypanosomatids under a great variety of stress conditions (drugs, starvation, among others) suggesting that this process is involved in the turnover of damaged structures in the protozoa and is not a cell death pathway. Death mechanisms of pathogenic trypanosomatids may be involved in pathogenesis, and the identification of parasite-specific regulators could represent a rational and attractive alternative target for drug development for these neglected diseases.

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?

🏙️ Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 76,871,996 visitors per month in the current month.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Doi.org Make Money? {💸}

We see no obvious way the site makes money.

Not all websites focus on profit; some are designed to educate, connect people, or share useful tools. People create websites for numerous reasons. And this could be one such example. Doi.org might be plotting its profit, but the way they're doing it isn't detectable yet.

Keywords {🔍}

pubmed, article, google, scholar, death, cell, cas, autophagy, trypanosomatids, central, autophagic, atg, cruzi, trypanosoma, apoptosis, parasite, disease, brucei, programmed, leishmania, pcd, differentiation, pathway, nature, protozoa, necrosis, molecular, parasites, mitochondrial, pathogenic, drugs, molecules, apoptotic, apoptosislike, role, mechanisms, chagas, process, pathways, stress, drug, forms, membrane, activity, parasitol, leishmaniasis, treatment, metacaspases, dna, processes,

Topics {✒️}

nature portfolio drug discovery research molecular tools research priorities cysteine-dependent aspartate-directed proteases enzymatic kits author information authors previous data showed open questions nature 390 nature 407 nature 403 nature 406 nature reprints bcl-xl anti-apoptotic proteins article menna-barreto india fadd-homologous ice/ced-3 innovative semi-synthetic thiosemicarbazone ethics declarations conflict l-arginine-dependent suppression controversial data lysosomal hydrolase-dependent degradation papes/fundação oswaldo cruz int/neglected_diseases/2010report/en/ promising anti-protozoan peptide central nervous system death-inducing signaling complex int/neglected_diseases/diseases/en/ large-scale proteomic studies ros-dependent cell death high ros content author correspondence original author pro-apoptotic nuclease activity critical social-economic implications metacaspase-independent death pathway open complement system-based therapeutics morphological evidence published plasma membrane disruption molecules trigger/suppress autophagy dr de duve rio de janeiro autophagy-independent cell death natural stimuli de messias-reason human african trypanosomiasis menna-barreto

Questions {❓}

  • Are apoptotic-like and autophagic pathways good drug targets in trypanosomatids?
  • Are protozoan metacaspases potential parasite killers?
  • Autophagosomes: biogenesis from scratch?
  • Autophagy in cell death: an innocent convict?
  • Autophagy: dual roles in life and death?
  • Blocking autophagy to prevent parasite differentiation: a possible new strategy for fighting parasitic infections?
  • Cell death in Leishmania induced by stress and differentiation: programmed cell death or necrosis?
  • Cell death in parasitic protozoa: regulated or incidental?
  • Kinetoplastida: model organisms for simple autophagic pathways?
  • Necrosis: a specific form of programmed cell death?
  • Programmed cell death in trypanosomatids: a way to maximize their biological fitness?
  • Stairway to heaven or hell?
  • What are the molecular mechanisms involved in protozoan autophagy?
  • What is the real biological relevance of programmed cell death in protozoa?
  • Which molecules participate in apoptotic-like activation/regulation in trypanosomatids?
  • Which molecules trigger/suppress autophagy in these protozoa?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Cell death pathways in pathogenic trypanosomatids: lessons of (over)kill
         description:Especially in tropical and developing countries, the clinically relevant protozoa Trypanosoma cruzi (Chagas disease), Trypanosoma brucei (sleeping sickness) and Leishmania species (leishmaniasis) stand out and infect millions of people worldwide leading to critical social-economic implications. Low-income populations are mainly affected by these three illnesses that are neglected by the pharmaceutical industry. Current anti-trypanosomatid drugs present variable efficacy with remarkable side effects that almost lead to treatment discontinuation, justifying a continuous search for alternative compounds that interfere with essential and specific parasite pathways. In this scenario, the triggering of trypanosomatid cell death machinery emerges as a promising approach, although the exact mechanisms involved in unicellular eukaryotes are still unclear as well as the controversial biological importance of programmed cell death (PCD). In this review, the mechanisms of autophagy, apoptosis-like cell death and necrosis found in pathogenic trypanosomatids are discussed, as well as their roles in successful infection. Based on the published genomic and proteomic maps, the panel of trypanosomatid cell death molecules was constructed under different experimental conditions. The lack of PCD molecular regulators and executioners in these parasites up to now has led to cell death being classified as an unregulated process or incidental necrosis, despite all morphological evidence published. In this context, the participation of metacaspases in PCD was also not described, and these proteases play a crucial role in proliferation and differentiation processes. On the other hand, autophagic phenotype has been described in trypanosomatids under a great variety of stress conditions (drugs, starvation, among others) suggesting that this process is involved in the turnover of damaged structures in the protozoa and is not a cell death pathway. Death mechanisms of pathogenic trypanosomatids may be involved in pathogenesis, and the identification of parasite-specific regulators could represent a rational and attractive alternative target for drug development for these neglected diseases.
         datePublished:2019-01-30T00:00:00Z
         dateModified:2019-01-30T00:00:00Z
         pageStart:1
         pageEnd:11
         license:http://creativecommons.org/licenses/by/4.0/
         sameAs:https://doi.org/10.1038/s41419-019-1370-2
         keywords:
            Cell death
            Parasitic infection
            Life Sciences
            general
            Biochemistry
            Cell Biology
            Immunology
            Cell Culture
            Antibodies
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41419-019-1370-2/MediaObjects/41419_2019_1370_Fig1_HTML.png
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41419-019-1370-2/MediaObjects/41419_2019_1370_Fig2_HTML.png
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41419-019-1370-2/MediaObjects/41419_2019_1370_Fig3_HTML.png
         isPartOf:
            name:Cell Death & Disease
            issn:
               2041-4889
            volumeNumber:10
            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:Rubem Figueiredo Sadok Menna-Barreto
               affiliation:
                     name:Laboratory of Cell Biology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation
                     address:
                        name:Laboratory of Cell Biology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Manguinhos, Brazil
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Cell death pathways in pathogenic trypanosomatids: lessons of (over)kill
      description:Especially in tropical and developing countries, the clinically relevant protozoa Trypanosoma cruzi (Chagas disease), Trypanosoma brucei (sleeping sickness) and Leishmania species (leishmaniasis) stand out and infect millions of people worldwide leading to critical social-economic implications. Low-income populations are mainly affected by these three illnesses that are neglected by the pharmaceutical industry. Current anti-trypanosomatid drugs present variable efficacy with remarkable side effects that almost lead to treatment discontinuation, justifying a continuous search for alternative compounds that interfere with essential and specific parasite pathways. In this scenario, the triggering of trypanosomatid cell death machinery emerges as a promising approach, although the exact mechanisms involved in unicellular eukaryotes are still unclear as well as the controversial biological importance of programmed cell death (PCD). In this review, the mechanisms of autophagy, apoptosis-like cell death and necrosis found in pathogenic trypanosomatids are discussed, as well as their roles in successful infection. Based on the published genomic and proteomic maps, the panel of trypanosomatid cell death molecules was constructed under different experimental conditions. The lack of PCD molecular regulators and executioners in these parasites up to now has led to cell death being classified as an unregulated process or incidental necrosis, despite all morphological evidence published. In this context, the participation of metacaspases in PCD was also not described, and these proteases play a crucial role in proliferation and differentiation processes. On the other hand, autophagic phenotype has been described in trypanosomatids under a great variety of stress conditions (drugs, starvation, among others) suggesting that this process is involved in the turnover of damaged structures in the protozoa and is not a cell death pathway. Death mechanisms of pathogenic trypanosomatids may be involved in pathogenesis, and the identification of parasite-specific regulators could represent a rational and attractive alternative target for drug development for these neglected diseases.
      datePublished:2019-01-30T00:00:00Z
      dateModified:2019-01-30T00:00:00Z
      pageStart:1
      pageEnd:11
      license:http://creativecommons.org/licenses/by/4.0/
      sameAs:https://doi.org/10.1038/s41419-019-1370-2
      keywords:
         Cell death
         Parasitic infection
         Life Sciences
         general
         Biochemistry
         Cell Biology
         Immunology
         Cell Culture
         Antibodies
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41419-019-1370-2/MediaObjects/41419_2019_1370_Fig1_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41419-019-1370-2/MediaObjects/41419_2019_1370_Fig2_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41419-019-1370-2/MediaObjects/41419_2019_1370_Fig3_HTML.png
      isPartOf:
         name:Cell Death & Disease
         issn:
            2041-4889
         volumeNumber:10
         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:Rubem Figueiredo Sadok Menna-Barreto
            affiliation:
                  name:Laboratory of Cell Biology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation
                  address:
                     name:Laboratory of Cell Biology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Manguinhos, Brazil
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Cell Death & Disease
      issn:
         2041-4889
      volumeNumber:10
Organization:
      name:Nature Publishing Group UK
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Laboratory of Cell Biology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation
      address:
         name:Laboratory of Cell Biology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Manguinhos, Brazil
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Rubem Figueiredo Sadok Menna-Barreto
      affiliation:
            name:Laboratory of Cell Biology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation
            address:
               name:Laboratory of Cell Biology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Manguinhos, Brazil
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Laboratory of Cell Biology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Manguinhos, Brazil

Social Networks {👍}(1)

External Links {🔗}(832)

Analytics and Tracking {📊}

  • Google Analytics
  • Google Tag Manager
  • Google Universal Analytics

Javascript Libraries {📚}

  • Prism.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
7.64s.