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  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
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We are analyzing https://link.springer.com/article/10.1007/s12640-011-9277-4.

Title:
Role of Cell Cycle Re-Entry in Neurons: A Common Apoptotic Mechanism of Neuronal Cell Death | Neurotoxicity Research
Description:
Currently, there is no effective treatment for neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease. Thus, a major focus of neuroscience research is to examine the mechanisms involved in neuronal loss in order to identify potential drug targets. Recent results indicate that DNA damage and re-entry into the cell cycle may constitute a common pathway in apoptosis in neurological diseases. The role of the cell cycle in such disorders is supported by data on the brain of patients who showed an increase in cell-cycle protein expression. Indeed, studies performed in neuronal cell preparations indicate that oxidative stress could be the main mechanism responsible for cell cycle re-entry. DNA damage and repair after oxidative stress may activate the enzyme ataxia telangiectasia mutated, which is a cell-cycle regulator. Once the cell cycle is activated, the increase in the expression of transcription factor E2F-1 could induce neuronal apoptosis. Furthermore, the potential routes involved in E2F-1 induced apoptosis could be p53-dependent or p53-independent. Under this E2F-1 hypothesis of cell death, multiple mitochondria-dependent pathways may be activated, including caspase and caspase-independent signaling cascades. Finally, given that cyclin-dependent kinase inhibitory drugs have neuroprotective and anti-apoptotic effects in experimental models, their potential application for the treatment of neurological disorders should be taken into account.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Telecommunications
  • Science

Content Management System {📝}

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 {📈}

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? {💸}

We're unsure how the site profits.

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 earning cash quietly, but we haven't detected the monetization method.

Keywords {🔍}

google, scholar, pubmed, cas, cell, cycle, disease, death, neuronal, apoptosis, alzheimers, neurons, neurosci, res, park, dna, cyclindependent, cdk, smith, biol, activation, role, brain, mol, camins, expression, article, verdaguer, cellcycle, kinase, lee, kinases, reentry, pallàs, pathway, transcription, proteins, chem, neurochem, cerebellar, granule, zhu, neurodegeneration, slack, damage, protein, factor, inhibition, sci, target,

Topics {✒️}

ta-promoter-derived deltan’-p73 transcript cyclin-dependent kinases cdk2 ataxia telangiectasia-p53–e2f-1 pathway month download article/chapter traumatic brain injury cyclin-dependent kinase inhibitors cell cycle-related proteins 1-methyl-4-phenylpyridinium-induced apoptosis b-amyloid-treated cortical neurons transcription factor e2f1/rb promotes e2f1-induced apoptosis potassium withdrawal-induced apoptosis b-myb promoter activity death-receptor-mediated apoptosis increased deltan-p73 expression kainic acid-induced apoptosis jordan-sciutto kl e2f-dependent gene repression kainic acid-induced death ischemia/hypoxic neuronal death cell-cycle protein expression dna damage-induced apoptosis calpain/cdk5/p25 pathway sh-sy5y neuroblastoma cells e2f1 mediates apoptosis facultat de biologia cyclin-dependent kinases cyclin dependent kinases phase cell-cycle regulators multiple mitochondria-dependent pathways g1 cell-cycle control neural-specific regulatory subunit cyclin-dependent kinase 5 e2f1 mediates death caspase-independent signaling cascades neuronal apoptosis evoked transcription factor e2f-1 cell cycle pathway e2f1 induces apoptosis cell cycle proteins e2f-1 induced apoptosis e2f-1-induced apoptosis potassium-induced apoptosis transcription factor e2f1 neuronal death evoked e2f1-induced apoptosis cell death induced neuronal death induced cerebellar granule cells related subjects

Questions {❓}

  • Chong ZZ, Li F, Maiese K (2005) Employing new cellular therapeutic targets for Alzheimer’s disease: a change for the better?
  • Copani A, Uberti D, Sortino MA, Bruno V, Nicoletti F, Memo M (2001) Activation of cell-cycle-associated proteins in neuronal death: a mandatory or dispensable path?
  • Kruman II (2004) Why do neurons enter the cell cycle?
  • Tsai LH, Lee MS, Cruz J (2004) Cdk5, a therapeutic target for Alzheimer’s disease?
  • Vincent I, Rosado M, Davies P (1996) Mitotic mechanisms in Alzheimer’s disease?

Schema {🗺️}

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         description:Currently, there is no effective treatment for neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease. Thus, a major focus of neuroscience research is to examine the mechanisms involved in neuronal loss in order to identify potential drug targets. Recent results indicate that DNA damage and re-entry into the cell cycle may constitute a common pathway in apoptosis in neurological diseases. The role of the cell cycle in such disorders is supported by data on the brain of patients who showed an increase in cell-cycle protein expression. Indeed, studies performed in neuronal cell preparations indicate that oxidative stress could be the main mechanism responsible for cell cycle re-entry. DNA damage and repair after oxidative stress may activate the enzyme ataxia telangiectasia mutated, which is a cell-cycle regulator. Once the cell cycle is activated, the increase in the expression of transcription factor E2F-1 could induce neuronal apoptosis. Furthermore, the potential routes involved in E2F-1 induced apoptosis could be p53-dependent or p53-independent. Under this E2F-1 hypothesis of cell death, multiple mitochondria-dependent pathways may be activated, including caspase and caspase-independent signaling cascades. Finally, given that cyclin-dependent kinase inhibitory drugs have neuroprotective and anti-apoptotic effects in experimental models, their potential application for the treatment of neurological disorders should be taken into account.
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      headline:Role of Cell Cycle Re-Entry in Neurons: A Common Apoptotic Mechanism of Neuronal Cell Death
      description:Currently, there is no effective treatment for neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease. Thus, a major focus of neuroscience research is to examine the mechanisms involved in neuronal loss in order to identify potential drug targets. Recent results indicate that DNA damage and re-entry into the cell cycle may constitute a common pathway in apoptosis in neurological diseases. The role of the cell cycle in such disorders is supported by data on the brain of patients who showed an increase in cell-cycle protein expression. Indeed, studies performed in neuronal cell preparations indicate that oxidative stress could be the main mechanism responsible for cell cycle re-entry. DNA damage and repair after oxidative stress may activate the enzyme ataxia telangiectasia mutated, which is a cell-cycle regulator. Once the cell cycle is activated, the increase in the expression of transcription factor E2F-1 could induce neuronal apoptosis. Furthermore, the potential routes involved in E2F-1 induced apoptosis could be p53-dependent or p53-independent. Under this E2F-1 hypothesis of cell death, multiple mitochondria-dependent pathways may be activated, including caspase and caspase-independent signaling cascades. Finally, given that cyclin-dependent kinase inhibitory drugs have neuroprotective and anti-apoptotic effects in experimental models, their potential application for the treatment of neurological disorders should be taken into account.
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                     name:Unitat de Bioquimica, Facultat de Medicina i Ciències de la Salut, Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Universitat Rovira i Virgili, Reus, Spain
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                  address:
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      name:Ester Verdaguer
      affiliation:
            name:Universitat de Barcelona
            address:
               name:Departament de Biologia Cel·lular, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain
               type:PostalAddress
            type:Organization
      name:Carme Auladell
      affiliation:
            name:Universitat de Barcelona
            address:
               name:Departament de Biologia Cel·lular, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain
               type:PostalAddress
            type:Organization
      name:Javier G. Pizarro
      affiliation:
            name:Centros de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Institut de Biomedicina (IBUB), Universitat de Barcelona, Nucli Universitari de Pedralbes
            address:
               name:Unitat de Farmacologia i Farmacognòsia, Facultat de Farmàcia, Centros de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Institut de Biomedicina (IBUB), Universitat de Barcelona, Nucli Universitari de Pedralbes, Barcelona, Spain
               type:PostalAddress
            type:Organization
      name:Carlos Beas-Zarate
      affiliation:
            name:Universidad de Guadalajara and División de Neurociencias, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS)
            address:
               name:Departamento de Biología Celular y Molecular, C.U.C.B.A, Universidad de Guadalajara and División de Neurociencias, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Guadalajara, Mexico
               type:PostalAddress
            type:Organization
      name:Mercè Pallàs
      affiliation:
            name:Centros de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Institut de Biomedicina (IBUB), Universitat de Barcelona, Nucli Universitari de Pedralbes
            address:
               name:Unitat de Farmacologia i Farmacognòsia, Facultat de Farmàcia, Centros de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Institut de Biomedicina (IBUB), Universitat de Barcelona, Nucli Universitari de Pedralbes, Barcelona, Spain
               type:PostalAddress
            type:Organization
      name:Antoni Camins
      affiliation:
            name:Centros de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Institut de Biomedicina (IBUB), Universitat de Barcelona, Nucli Universitari de Pedralbes
            address:
               name:Unitat de Farmacologia i Farmacognòsia, Facultat de Farmàcia, Centros de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Institut de Biomedicina (IBUB), Universitat de Barcelona, Nucli Universitari de Pedralbes, Barcelona, Spain
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Unitat de Bioquimica, Facultat de Medicina i Ciències de la Salut, Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Universitat Rovira i Virgili, Reus, Spain
      name:Unitat de Farmacologia i Farmacognòsia, Facultat de Farmàcia, Centros de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Institut de Biomedicina (IBUB), Universitat de Barcelona, Nucli Universitari de Pedralbes, Barcelona, Spain
      name:Unitat de Bioquimica, Facultat de Medicina i Ciències de la Salut, Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Universitat Rovira i Virgili, Reus, Spain
      name:Departament de Biologia Cel·lular, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain
      name:Departament de Biologia Cel·lular, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain
      name:Unitat de Farmacologia i Farmacognòsia, Facultat de Farmàcia, Centros de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Institut de Biomedicina (IBUB), Universitat de Barcelona, Nucli Universitari de Pedralbes, Barcelona, Spain
      name:Departamento de Biología Celular y Molecular, C.U.C.B.A, Universidad de Guadalajara and División de Neurociencias, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Guadalajara, Mexico
      name:Unitat de Farmacologia i Farmacognòsia, Facultat de Farmàcia, Centros de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Institut de Biomedicina (IBUB), Universitat de Barcelona, Nucli Universitari de Pedralbes, Barcelona, Spain
      name:Unitat de Farmacologia i Farmacognòsia, Facultat de Farmàcia, Centros de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Institut de Biomedicina (IBUB), Universitat de Barcelona, Nucli Universitari de Pedralbes, Barcelona, Spain
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