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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
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  12. Analytics And Tracking
  13. Libraries
  14. Hosting Providers
  15. CDN Services

We began analyzing https://www.nature.com/articles/nrc.2015.17, but it redirected us to https://www.nature.com/articles/nrc.2015.17. The analysis below is for the second page.

Title[redir]:
Thirty years of BCL-2: translating cell death discoveries into novel cancer therapies | Nature Reviews Cancer
Description:
Research on the BCL-2-regulated apoptotic pathway has led to the development of small molecules called BH3-mimetics that bind to pro-survival BCL-2 proteins to induce apoptosis of malignant cells. This Timeline article describes the history of research on the BCL-2 family of proteins and their roles in cancer. The

Matching Content Categories {📚}

  • Education
  • Science
  • 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.
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How Does Doi.org Make Money? {💸}

We're unsure if the website is profiting.

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 could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {🔍}

pubmed, google, scholar, cas, article, cell, bcl, central, apoptosis, cancer, nature, death, family, strasser, cells, protein, science, mcl, bim, proteins, gene, bax, sci, human, proc, natl, acad, usa, mice, biol, survival, bclxl, bhonly, abt, mitochondrial, apoptotic, development, mol, lymphoma, oncogene, expression, lymphoid, proapoptotic, inhibitor, research, nat, cory, dev, leukemia, bak,

Topics {✒️}

permissions reprints nature portfolio privacy policy mammalian interleukin-1b-converting enzyme bcr-abl-expressing hematopoietic progenitor genome-wide array-based cgh author information authors advertising myc-driven b-cell lymphomagenesis bcl-2high/mcl-1low profile hemopoietic-specific early-response gene bcl-xl/bim fragment complex medical research council bcl-xl-bak peptide complex timeline article focuses partially bis-cpg-dependent bcr/abl+ leukemic cells medical research social media bcl-2-expressing breast tumors peri-implantation embryonic lethality somatic copy-number alteration targeted high-affinity inhibitor selective bcl-xl inhibitor anti-apoptotic context md organ-specific autoimmune disease death-inducing protein shares pro-survival bcl-2 proteins pre-b-cell leukemia potentiates sorafenib-induced apoptosis acute myeloid leukemia survival-promoting proteins bcl-2 human b-lymphoblastoid cells cellular survival-promoting proteins drug-treated cells die mammalian proto-oncogene bcl-2 p53-independent mechanisms inhibitable research microrna-125b promotes apoptosis hormone-resistant prostate cancer bcl-2-specific bh3 mimetic fas-induced hepatocellular apoptosis personal data bax channel-forming activity pro-apoptotic bcl-2 protein mir-193b regulates mcl-1 tyrosine kinase inhibitors p53-mediated apoptotic response bcl-2-related gene outer mitochondrial membrane

Questions {❓}

  • How do BCL-2 proteins induce mitochondrial outer membrane permeabilization?

Schema {🗺️}

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         headline:Thirty years of BCL-2: translating cell death discoveries into novel cancer therapies
         description:Research on the BCL-2-regulated apoptotic pathway has led to the development of small molecules called BH3-mimetics that bind to pro-survival BCL-2 proteins to induce apoptosis of malignant cells. This Timeline article describes the history of research on the BCL-2 family of proteins and their roles in cancer. The 'hallmarks of cancer' are generally accepted as a set of genetic and epigenetic alterations that a normal cell must accrue to transform into a fully malignant cancer. It follows that therapies designed to counter these alterations might be effective as anti-cancer strategies. Over the past 30 years, research on the BCL-2-regulated apoptotic pathway has led to the development of small-molecule compounds, known as 'BH3-mimetics', that bind to pro-survival BCL-2 proteins to directly activate apoptosis of malignant cells. This Timeline article focuses on the discovery and study of BCL-2, the wider BCL-2 protein family and, specifically, its roles in cancer development and therapy.
         datePublished:2016-01-29T00:00:00Z
         dateModified:2016-01-29T00:00:00Z
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      headline:Thirty years of BCL-2: translating cell death discoveries into novel cancer therapies
      description:Research on the BCL-2-regulated apoptotic pathway has led to the development of small molecules called BH3-mimetics that bind to pro-survival BCL-2 proteins to induce apoptosis of malignant cells. This Timeline article describes the history of research on the BCL-2 family of proteins and their roles in cancer. The 'hallmarks of cancer' are generally accepted as a set of genetic and epigenetic alterations that a normal cell must accrue to transform into a fully malignant cancer. It follows that therapies designed to counter these alterations might be effective as anti-cancer strategies. Over the past 30 years, research on the BCL-2-regulated apoptotic pathway has led to the development of small-molecule compounds, known as 'BH3-mimetics', that bind to pro-survival BCL-2 proteins to directly activate apoptosis of malignant cells. This Timeline article focuses on the discovery and study of BCL-2, the wider BCL-2 protein family and, specifically, its roles in cancer development and therapy.
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Social Networks {👍}(2)

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Mail Servers:

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CDN Services {📦}

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