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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. External Links
  11. Analytics And Tracking
  12. Libraries
  13. Hosting Providers
  14. CDN Services

We began analyzing https://link.springer.com/article/10.1007/s11064-008-9835-1, but it redirected us to https://link.springer.com/article/10.1007/s11064-008-9835-1. The analysis below is for the second page.

Title[redir]:
Parp and Cell Death or Protection in Rat Primary Astroglial Cell Cultures Under LPS/IFNγ Induced Proinflammatory Conditions | Neurochemical Research
Description:
The enzyme poly(ADP-ribose)polymerase (PARP) has a leader role in the DNA damage survey mechanisms by its nick-sensor function, but it is also involved in the early events of the programmed cell death, particularly during inflammatory injury, as a coactivator of NF-kB. In the present study, we evaluated the PARP involvement in the mechanisms of protection and/or cell death in rat astroglial cell cultures during the early phase of proinflammatory commitment after lipopolysaccharide and interferon gamma treatment. According with the recent findings that PARP-1 phosphorylation by MAPK/ERK-2 pathway seems to modulate PARP activation, in time course experiments we demonstrated that a very early PARP activation and expression is able to trigger a cell death pathway, DNA damage independent, during strong proinflammatory insults, maintaining its role of guardian of the genome stability only during the normal cell cycling.

Matching Content Categories {📚}

  • Education
  • Telecommunications
  • Science

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


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How Does Doi.org Make Money? {💸}

We can't see how the site brings in money.

While profit motivates many websites, others exist to inspire, entertain, or provide valuable resources. Websites have a variety of goals. And this might be one of them. Doi.org might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

article, google, scholar, pubmed, cas, polyadpribose, polymerase, cell, parp, dna, death, res, damage, activation, sci, brain, role, expression, dois, biol, pathway, adpribose, neurochem, cells, biochem, chem, pharmacol, neurosci, rat, poly, mice, acad, usa, inhibition, inhibitor, astroglial, cultures, giuffridastella, nicoletti, access, apoptosis, cerebral, nitric, proc, natl, doipnas, wang, repair, doijbcm, gene,

Topics {✒️}

γ-irradiated balb/3t3 fibroblasts month download article/chapter dna double-strand breaks glucocorticoid-mediated cell lysis parp-1 reduces alpha-synuclein ca2+/mg2+-dependent endonuclease extracellular signal-regulated kinases mek/erk pathway extracellular signal-regulated kinase nf-κb transcriptional activation defective nf-kappab activation mnng-treated hela cells growth-phase-dependent response parp-1-induced cell death polymerase-1-dependent cell death erk signaling pathway redox-dependent transcriptional regulation nitric oxide donors article spina-purrello dna strand breaks anna maria giuffrida-stella full article pdf de menissier murcia lps-stimulated j774 cell death pathway mapk/erk-2 pathway glutamate-induced neurotoxicity astroglial cell cultures related subjects privacy choices/manage cookies dna damage response pro-apoptotic factors necrotic death induced differential gene expression vivo oxidative stress glial inos expression necrotic cell death nf-kb activation adp-ribose polymerase-1 regulates programmed cell death strong proinflammatory insults dual-key mechanism inducing neuronal death conditions privacy policy parp-1 nhej pathway dna damage independent oxidative dna damage apoptotic neuronal death stalled replication forks parp1-dependent kinetics

Questions {❓}

  • Chiarugi A (2002) Poly(ADP-ribose) polymerase: killer or conspirator?
  • Nicoletti VG, Giuffrida-Stella AM (2003) Role of PARP under stress conditions: cell death or protection?
  • Shall S, De Murcia G (2000) Poly(ADP-ribose) polimerase-1: what we have learned from the deficient mouse model?

Schema {🗺️}

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         description:The enzyme poly(ADP-ribose)polymerase (PARP) has a leader role in the DNA damage survey mechanisms by its nick-sensor function, but it is also involved in the early events of the programmed cell death, particularly during inflammatory injury, as a coactivator of NF-kB. In the present study, we evaluated the PARP involvement in the mechanisms of protection and/or cell death in rat astroglial cell cultures during the early phase of proinflammatory commitment after lipopolysaccharide and interferon gamma treatment. According with the recent findings that PARP-1 phosphorylation by MAPK/ERK-2 pathway seems to modulate PARP activation, in time course experiments we demonstrated that a very early PARP activation and expression is able to trigger a cell death pathway, DNA damage independent, during strong proinflammatory insults, maintaining its role of guardian of the genome stability only during the normal cell cycling.
         datePublished:2008-08-29T00:00:00Z
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      headline:Parp and Cell Death or Protection in Rat Primary Astroglial Cell Cultures Under LPS/IFNγ Induced Proinflammatory Conditions
      description:The enzyme poly(ADP-ribose)polymerase (PARP) has a leader role in the DNA damage survey mechanisms by its nick-sensor function, but it is also involved in the early events of the programmed cell death, particularly during inflammatory injury, as a coactivator of NF-kB. In the present study, we evaluated the PARP involvement in the mechanisms of protection and/or cell death in rat astroglial cell cultures during the early phase of proinflammatory commitment after lipopolysaccharide and interferon gamma treatment. According with the recent findings that PARP-1 phosphorylation by MAPK/ERK-2 pathway seems to modulate PARP activation, in time course experiments we demonstrated that a very early PARP activation and expression is able to trigger a cell death pathway, DNA damage independent, during strong proinflammatory insults, maintaining its role of guardian of the genome stability only during the normal cell cycling.
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External Links {🔗}(309)

Analytics and Tracking {📊}

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Libraries {📚}

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Emails and Hosting {✉️}

Mail Servers:

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CDN Services {📦}

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