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LINK . SPRINGER . COM {}

  1. Analyzed Page
  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/s10495-008-0200-2.

Title:
The tubulin-depolymerising agent combretastatin-4 induces ectopic aster assembly and mitotic catastrophe in lung cancer cells H460 | Apoptosis
Description:
The relationship between microtubular dynamics, dismantling of pericentriolar components and induction of apoptosis was analysed after exposure of H460 non-small lung cancer cells to anti-mitotic drugs. The microtubule destabilising agent, combretastatin-A4 (CA-4) led to microtubular array disorganization, arrest in mitosis and abnormal metaphases, accompanied by the presence of numerous centrosome-independent “star-like” structures containing tubulin and aggregates of pericentrosomal matrix components like γ-tubulin, pericentrin and ninein, whereas the structural integrity of centrioles was not affected by treatment. On the contrary, in condition of prolonged exposure or high concentrations of CA-4 such aggregates never formed. Treatment with 7.5 nM CA-4, which produced a high frequency “star-like” aggregates, was accompanied by mitotic catastrophe commitment characterized by translocation of the proapoptotic Bim protein to mitochondria activation of caspases-3/9 and DNA fragmentation as a result of either prolonged metaphase arrest or attempt of cells to divide. Drug concentrations which fail to block cells at mitosis were also unable to activate apotosis. A detailed time-course analysis of cell cycle arrest and apoptosis indicated that after CA-4 washout the number of metaphases with “star-like” structures decreased as a function of time and arrested cells proceeded in anaphase. After 4 h, the multiple α- and γ-tubulin aggregates coalesced into two well-defined spindles in a bipolar mitotic spindle organization. Overall, our findings suggest that the maintenance of microtubular integrity plays a relevant role in stabilising the pericentriolar matrix, whose dismantling can be associated with apoptosis after exposure to microtubule depolymerising agents.
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 7,626,432 visitors per month in the current month.

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How Does Link.springer.com Make Money? {💸}

We don’t know how the website earns money.

Some websites aren't about earning revenue; they're built to connect communities or raise awareness. There are numerous motivations behind creating websites. This might be one of them. Link.springer.com could be secretly minting cash, but we can't detect the process.

Keywords {🔍}

google, scholar, cas, article, pubmed, cell, cells, mitotic, biol, microtubule, centrosome, apoptosis, catastrophe, sci, gammatubulin, cancer, spindle, role, agents, microtubules, combretastatin, access, centrosomal, privacy, cookies, content, induces, cenciarelli, tanzarella, vitale, antoccia, arrest, mitosis, ninein, death, rev, centrosomes, bornens, function, publish, search, agent, lung, crateri, arancia, dynamics, tubulin, aggregates, γtubulin, pericentrin,

Topics {✒️}

month download article/chapter multidrug-resistant cancer therapy radiation-induced cell death radiation-induced mitotic catastrophe diazepam-induced mitotic failure microtubule-organizing centers abnormal microtubule minus-end anchorage gamma-tubulin complexes x-irradiated mammalian cells stefania meschini & giuseppe arancia microtubule depolymerising agents arsenite-induced mitotic arrest microtubule destabilising agent numerous centrosome-independent “star proapoptotic bim protein γ-tubulin aggregates coalesced p53 transcription-dependent full article pdf gamma-tubulin form microtubulin binding sites article apoptosis aims privacy choices/manage cookies microtubule-interfering agents microtubule-damaging agents gamma-tubulin distribution cell cycle arrest kinetochore-microtubule attachment tubulin superfamily encoded alpha tubulin acetylation ilio vitale article cenciarelli minus-end capture antonio antoccia multinucleated cells induced combretastatin-a4 incresased microtubule stability independent processes linked sigma-tau anti-mitotic drugs developing anticancer agents microtubular array disorganization arrested cells proceeded european economic area microtubular integrity plays n-substituted isatins vande woude gf adenomatous polyposis coli crest patient sera mitochondrial membrane permeabilization università roma tre

Questions {❓}

  • Roninson IB, Broude EV, Chang BD (2007) If not apoptosis then what?

Schema {🗺️}

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         headline:The tubulin-depolymerising agent combretastatin-4 induces ectopic aster assembly and mitotic catastrophe in lung cancer cells H460
         description:The relationship between microtubular dynamics, dismantling of pericentriolar components and induction of apoptosis was analysed after exposure of H460 non-small lung cancer cells to anti-mitotic drugs. The microtubule destabilising agent, combretastatin-A4 (CA-4) led to microtubular array disorganization, arrest in mitosis and abnormal metaphases, accompanied by the presence of numerous centrosome-independent “star-like” structures containing tubulin and aggregates of pericentrosomal matrix components like γ-tubulin, pericentrin and ninein, whereas the structural integrity of centrioles was not affected by treatment. On the contrary, in condition of prolonged exposure or high concentrations of CA-4 such aggregates never formed. Treatment with 7.5 nM CA-4, which produced a high frequency “star-like” aggregates, was accompanied by mitotic catastrophe commitment characterized by translocation of the proapoptotic Bim protein to mitochondria activation of caspases-3/9 and DNA fragmentation as a result of either prolonged metaphase arrest or attempt of cells to divide. Drug concentrations which fail to block cells at mitosis were also unable to activate apotosis. A detailed time-course analysis of cell cycle arrest and apoptosis indicated that after CA-4 washout the number of metaphases with “star-like” structures decreased as a function of time and arrested cells proceeded in anaphase. After 4 h, the multiple α- and γ-tubulin aggregates coalesced into two well-defined spindles in a bipolar mitotic spindle organization. Overall, our findings suggest that the maintenance of microtubular integrity plays a relevant role in stabilising the pericentriolar matrix, whose dismantling can be associated with apoptosis after exposure to microtubule depolymerising agents.
         datePublished:2008-04-02T00:00:00Z
         dateModified:2008-04-02T00:00:00Z
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            Cancer Research
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      headline:The tubulin-depolymerising agent combretastatin-4 induces ectopic aster assembly and mitotic catastrophe in lung cancer cells H460
      description:The relationship between microtubular dynamics, dismantling of pericentriolar components and induction of apoptosis was analysed after exposure of H460 non-small lung cancer cells to anti-mitotic drugs. The microtubule destabilising agent, combretastatin-A4 (CA-4) led to microtubular array disorganization, arrest in mitosis and abnormal metaphases, accompanied by the presence of numerous centrosome-independent “star-like” structures containing tubulin and aggregates of pericentrosomal matrix components like γ-tubulin, pericentrin and ninein, whereas the structural integrity of centrioles was not affected by treatment. On the contrary, in condition of prolonged exposure or high concentrations of CA-4 such aggregates never formed. Treatment with 7.5 nM CA-4, which produced a high frequency “star-like” aggregates, was accompanied by mitotic catastrophe commitment characterized by translocation of the proapoptotic Bim protein to mitochondria activation of caspases-3/9 and DNA fragmentation as a result of either prolonged metaphase arrest or attempt of cells to divide. Drug concentrations which fail to block cells at mitosis were also unable to activate apotosis. A detailed time-course analysis of cell cycle arrest and apoptosis indicated that after CA-4 washout the number of metaphases with “star-like” structures decreased as a function of time and arrested cells proceeded in anaphase. After 4 h, the multiple α- and γ-tubulin aggregates coalesced into two well-defined spindles in a bipolar mitotic spindle organization. Overall, our findings suggest that the maintenance of microtubular integrity plays a relevant role in stabilising the pericentriolar matrix, whose dismantling can be associated with apoptosis after exposure to microtubule depolymerising agents.
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      dateModified:2008-04-02T00:00:00Z
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      pageEnd:669
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         CA-4
         Centrosome
         Ninein
         Gamma-tubulin
         Pericentrin
         Mitotic catastrophe
         Bim
         Cancer Research
         Cell Biology
         Oncology
         Biochemistry
         general
         Virology
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                  name:University “Roma Tre”
                  address:
                     name:Department of Biology, University “Roma Tre”, Rome, Italy
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                  type:Organization
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            name:Claudio Pisano
            affiliation:
                  name:SIGMA-TAU Industrie Farmaceutiche Riunite S.p.A
                  address:
                     name:SIGMA-TAU Industrie Farmaceutiche Riunite S.p.A, Pomezia, Italy
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                     type:PostalAddress
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            name:Stefania Meschini
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                  name:Istituto Superiore di Sanità
                  address:
                     name:Department of Technology and Health, Istituto Superiore di Sanità, Rome, Italy
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      address:
         name:Department of Biology, University “Roma Tre”, Rome, Italy
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         name:SIGMA-TAU Industrie Farmaceutiche Riunite S.p.A, Pomezia, Italy
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               name:Department of Biology, University “Roma Tre”, Rome, Italy
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      name:Claudio Pisano
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            name:SIGMA-TAU Industrie Farmaceutiche Riunite S.p.A
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               name:SIGMA-TAU Industrie Farmaceutiche Riunite S.p.A, Pomezia, Italy
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      name:Pasqualina Crateri
      affiliation:
            name:Istituto Superiore di Sanità
            address:
               name:Department of Technology and Health, Istituto Superiore di Sanità, Rome, Italy
               type:PostalAddress
            type:Organization
      name:Stefania Meschini
      affiliation:
            name:Istituto Superiore di Sanità
            address:
               name:Department of Technology and Health, Istituto Superiore di Sanità, Rome, Italy
               type:PostalAddress
            type:Organization
      name:Giuseppe Arancia
      affiliation:
            name:Istituto Superiore di Sanità
            address:
               name:Department of Technology and Health, Istituto Superiore di Sanità, Rome, Italy
               type:PostalAddress
            type:Organization
      name:Antonio Antoccia
      affiliation:
            name:University “Roma Tre”
            address:
               name:Department of Biology, University “Roma Tre”, Rome, Italy
               type:PostalAddress
            type:Organization
      email:[email protected]
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      name:Department of Biology, University “Roma Tre”, Rome, Italy
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      name:SIGMA-TAU Industrie Farmaceutiche Riunite S.p.A, Pomezia, Italy
      name:Department of Technology and Health, Istituto Superiore di Sanità, Rome, Italy
      name:Department of Technology and Health, Istituto Superiore di Sanità, Rome, Italy
      name:Department of Technology and Health, Istituto Superiore di Sanità, Rome, Italy
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