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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
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  6. Keywords
  7. Topics
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We are analyzing https://link.springer.com/article/10.1007/s00705-006-0821-0.

Title:
Modulation of apoptosis by human papillomavirus (HPV) oncoproteins | Archives of Virology
Description:
The regulation of host-mediated apoptosis by the E6 and E7 oncoproteins has garnered attention because it is believed to be an important strategy employed by high-risk (HR)-human papillomaviruses (HPVs) to evade immune surveillance. Additionally, the revelation that E5 can protect cells from tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis suggests that it may also play a role in undermining host defense mechanisms. Cellular transformation is an unintended consequence of persistent infection by HR-HPVs, and it is therefore likely that the primary function of E5, E6 and E7 is to regulate cell survival throughout the normal viral life cycle in order to ensure viral replication and promote the spread of progeny. The purpose of this article is to review the literature on the regulation of host-mediated apoptosis by E5, E6 and E7 that describes the mechanisms employed by HR-HPVs to persist in the host and create the conditions necessary for cellular transformation.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
  • Politics
  • Law & Government

Content Management System {πŸ“}

What CMS is link.springer.com built with?

Custom-built

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

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of link.springer.com audience?

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


Based on our best estimate, this website will receive around 8,170,236 visitors per month in the current month.

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How Does Link.springer.com Make Money? {πŸ’Έ}

We can't figure out the monetization strategy.

Not every website is profit-driven; some are created to spread information or serve as an online presence. Websites can be made for many reasons. This could be one of them. Link.springer.com could be secretly minting cash, but we can't detect the process.

Keywords {πŸ”}

cas, google, scholar, pubmed, article, human, papillomavirus, type, protein, apoptosis, hpv, oncogene, virol, oncoprotein, cell, cells, cancer, proteins, sjonc, banks, oncoproteins, biol, jvi, cervical, virus, gene, activity, factor, duerksenhughes, tumor, chem, science, van, regulation, highrisk, papilloma, chen, howley, binds, death, degradation, lee, usa, transformation, access, interaction, mol, res, keratinocytes, expression,

Topics {βœ’οΈ}

kenter cj melief cervical intraepithelial neoplasia month download article/chapter dimaio es hwang parkhurst pj duerksen-hughes nakagawa jm huibregtse tumor necrosis factor johnson cm simbulan-rosenthal ifn-alpha-induced apoptosis nader dj mccance 16-kilodalton pore-forming protein hong jj chen duerksen-hughes pj inactivates growth-inhibitory insulin human virus oncoproteins scheffner pm howley hubert sl giannini schlegel dj mccance stromal macrophage/dendrocyte populations life cycle dc%2bd3sxitl2ksg%3d%3d 10 dc%2bd3mxhsfckuw%3d%3d 10 dc%2bd2cxhsfomsq%3d%3d 10 van deurs duerksen-hughes rights epithelial cell line stoppler mc stoppler hpv-tumor diagnosis high-risk papillomaviruses bind mannhardt sa weinzimer specific protein recognition pdz ligand domain ubiquitin-mediated degradation human papillomavirus immortalization interferon regulatory factor-3 krishna ej androphy papillomavirus e6 oncoproteins dyson pm howley vidal pm howley tong pm howley full article pdf intraepithelial langerhans’ cells type 16 virus brien ms campo transcriptional coactivator cbp/p300 ensure viral replication squamous intraepithelial lesions pitot pf lambert e7 oncoprotein associates tata-binding protein

Schema {πŸ—ΊοΈ}

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         headline:Modulation of apoptosis by human papillomavirus (HPV) oncoproteins
         description:The regulation of host-mediated apoptosis by the E6 and E7 oncoproteins has garnered attention because it is believed to be an important strategy employed by high-risk (HR)-human papillomaviruses (HPVs) to evade immune surveillance. Additionally, the revelation that E5 can protect cells from tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis suggests that it may also play a role in undermining host defense mechanisms. Cellular transformation is an unintended consequence of persistent infection by HR-HPVs, and it is therefore likely that the primary function of E5, E6 and E7 is to regulate cell survival throughout the normal viral life cycle in order to ensure viral replication and promote the spread of progeny. The purpose of this article is to review the literature on the regulation of host-mediated apoptosis by E5, E6 and E7 that describes the mechanisms employed by HR-HPVs to persist in the host and create the conditions necessary for cellular transformation.
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      headline:Modulation of apoptosis by human papillomavirus (HPV) oncoproteins
      description:The regulation of host-mediated apoptosis by the E6 and E7 oncoproteins has garnered attention because it is believed to be an important strategy employed by high-risk (HR)-human papillomaviruses (HPVs) to evade immune surveillance. Additionally, the revelation that E5 can protect cells from tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis suggests that it may also play a role in undermining host defense mechanisms. Cellular transformation is an unintended consequence of persistent infection by HR-HPVs, and it is therefore likely that the primary function of E5, E6 and E7 is to regulate cell survival throughout the normal viral life cycle in order to ensure viral replication and promote the spread of progeny. The purpose of this article is to review the literature on the regulation of host-mediated apoptosis by E5, E6 and E7 that describes the mechanisms employed by HR-HPVs to persist in the host and create the conditions necessary for cellular transformation.
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External Links {πŸ”—}(290)

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