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We are analyzing https://link.springer.com/article/10.1007/s10059-013-0172-0.

Title:
Induction of mitochondrial dysfunction by poly(ADP-ribose) polymer: Implication for neuronal cell death | Molecules and Cells
Description:
Poly(ADP-ribose) polymerase-1 (PARP-1) mediates neuronal cell death in a variety of pathological conditions involving severe DNA damage. Poly(ADP-ribose) (PAR) polymer is a product synthesized by PARP-1. Previous studies suggest that PAR polymer heralds mitochondrial apoptosis-inducing factor (AIF) release and thereby, signals neuronal cell death. However, the details of the effects of PAR polymer on mitochondria remain to be elucidated. Here we report the effects of PAR polymer on mitochondria in cells in situ and isolated brain mitochondria in vitro. We found that PAR polymer causes depolarization of mitochondrial membrane potential and opening of the mitochondrial permeability transition pore early after injury. Furthermore, PAR polymer specifically induces AIF release, but not cytochrome c from isolated brain mitochondria. These data suggest PAR polymer as an endogenous mitochondrial toxin and will further our understanding of the PARP-1-dependent neuronal cell death paradigm.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
  • Telecommunications
  • Science

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 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {πŸ’Έ}

The income method remains a mystery to us.

Many websites are intended to earn money, but some serve to share ideas or build connections. Websites exist for all kinds of purposes. This might be one of them. Link.springer.com might be cashing in, but we can't detect the method they're using.

Keywords {πŸ”}

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Topics {βœ’οΈ}

month download article/chapter seong-woon yu apoptosis-inducing factor substitutes eun-kyoung kim peripheral-type benzodiazepine receptor polymer-induced cell death cells seung-hoon baek polymerase-1-dependent cell death mitochondrial permeability transition apoptosis-inducing factor apoptosis inducing factor neuronal cell death dna damage signaling full article pdf privacy choices/manage cookies quantitative fluorescent indicator mitochondrial membrane potentials endogenous mitochondrial toxin apoptotic cell death conditions privacy policy related subjects mitochondrial membrane potential outer membrane permeabilization previous studies suggest european economic area ischemic rat hepatocytes cellular stress signaling article baek article molecules flow cytometric analysis accepting optional cookies j-aggregate formation daegu gyeongbuk institute isolated brain mitochondria rat brain mitochondria main content log authors correspondence journal finder publish article log cell death cell death 2009 article cite polymer access mitochondrial dysfunction par polymer personal data ca2+-overload enhanced apoptosis induces cleavage privacy policy

Schema {πŸ—ΊοΈ}

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         headline:Induction of mitochondrial dysfunction by poly(ADP-ribose) polymer: Implication for neuronal cell death
         description:Poly(ADP-ribose) polymerase-1 (PARP-1) mediates neuronal cell death in a variety of pathological conditions involving severe DNA damage. Poly(ADP-ribose) (PAR) polymer is a product synthesized by PARP-1. Previous studies suggest that PAR polymer heralds mitochondrial apoptosis-inducing factor (AIF) release and thereby, signals neuronal cell death. However, the details of the effects of PAR polymer on mitochondria remain to be elucidated. Here we report the effects of PAR polymer on mitochondria in cells in situ and isolated brain mitochondria in vitro. We found that PAR polymer causes depolarization of mitochondrial membrane potential and opening of the mitochondrial permeability transition pore early after injury. Furthermore, PAR polymer specifically induces AIF release, but not cytochrome c from isolated brain mitochondria. These data suggest PAR polymer as an endogenous mitochondrial toxin and will further our understanding of the PARP-1-dependent neuronal cell death paradigm.
         datePublished:2013-08-29T00:00:00Z
         dateModified:2013-08-29T00:00:00Z
         pageStart:258
         pageEnd:266
         sameAs:https://doi.org/10.1007/s10059-013-0172-0
         keywords:
            apoptosis-inducing factor
            mitochondria
            neuronal cell death
            poly(ADP-ribose) polymer
            Cell Biology
            Biochemistry
            general
            Biomedicine
            Biotechnology
         image:
         isPartOf:
            name:Molecules and Cells
            issn:
               0219-1032
               1016-8478
            volumeNumber:36
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer Netherlands
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                        name:Department of Brain Science, Daegu Gyeongbuk Institute of Science and Technology (DGIST), 711-873, Korea
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      headline:Induction of mitochondrial dysfunction by poly(ADP-ribose) polymer: Implication for neuronal cell death
      description:Poly(ADP-ribose) polymerase-1 (PARP-1) mediates neuronal cell death in a variety of pathological conditions involving severe DNA damage. Poly(ADP-ribose) (PAR) polymer is a product synthesized by PARP-1. Previous studies suggest that PAR polymer heralds mitochondrial apoptosis-inducing factor (AIF) release and thereby, signals neuronal cell death. However, the details of the effects of PAR polymer on mitochondria remain to be elucidated. Here we report the effects of PAR polymer on mitochondria in cells in situ and isolated brain mitochondria in vitro. We found that PAR polymer causes depolarization of mitochondrial membrane potential and opening of the mitochondrial permeability transition pore early after injury. Furthermore, PAR polymer specifically induces AIF release, but not cytochrome c from isolated brain mitochondria. These data suggest PAR polymer as an endogenous mitochondrial toxin and will further our understanding of the PARP-1-dependent neuronal cell death paradigm.
      datePublished:2013-08-29T00:00:00Z
      dateModified:2013-08-29T00:00:00Z
      pageStart:258
      pageEnd:266
      sameAs:https://doi.org/10.1007/s10059-013-0172-0
      keywords:
         apoptosis-inducing factor
         mitochondria
         neuronal cell death
         poly(ADP-ribose) polymer
         Cell Biology
         Biochemistry
         general
         Biomedicine
         Biotechnology
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            name:Seung-Hoon Baek
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                  name:Ajou University
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                     name:College of Pharmacy, Ajou University, Suwon, Korea
                     type:PostalAddress
                  type:Organization
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            name:Ok-Nam Bae
            affiliation:
                  name:Hanyang University
                  address:
                     name:College of Pharmacy, Hanyang University, Ansan, Korea
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                     name:Department of Brain Science, Daegu Gyeongbuk Institute of Science and Technology (DGIST), 711-873, Korea
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               name:College of Pharmacy, Hanyang University, Ansan, Korea
               type:PostalAddress
            type:Organization
      name:Eun-Kyoung Kim
      affiliation:
            name:Daegu Gyeongbuk Institute of Science and Technology (DGIST)
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               name:Department of Brain Science, Daegu Gyeongbuk Institute of Science and Technology (DGIST), 711-873, Korea
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Seong-Woon Yu
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            name:Daegu Gyeongbuk Institute of Science and Technology (DGIST)
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               name:Department of Brain Science, Daegu Gyeongbuk Institute of Science and Technology (DGIST), 711-873, Korea
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