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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 began analyzing https://www.nature.com/articles/jhg2006100, but it redirected us to https://www.nature.com/articles/jhg2006100. The analysis below is for the second page.

Title[redir]:
The potential role of DFNA5, a hearing impairment gene, in p53-mediated cellular response to DNA damage | Journal of Human Genetics
Description:
The tumor suppressor p53 plays a crucial role in the cellular response to DNA damage by transcriptional activation of numerous downstream genes. Although a considerable number of p53 target genes have been reported, the precise mechanism of p53-regulated tumor suppression still remains to be elucidated. Here, we report a novel role of the DFNA5 gene in p53-mediated etoposide-induced cell death. The DFNA5 gene has been previously reported to be responsible for autosomal-dominant, nonsyndromic hearing impairment. The expression of the DFNA5 gene was strongly induced by exogenous and endogenous p53. The chromatin immunoprecipitation assay indicated that a potential p53-binding sequence is located in intron 1 of the DFNA5 gene. Furthermore, the reporter gene assay revealed that the sequence displays p53-dependent transcriptional activity. The ectopic expression of DFNA5 enhanced etoposide-induced cell death in the presence of p53; however, it was inhibited in the absence of p53. Finally, the expression of DFNA5 mRNA was remarkably induced by gamma-ray irradiation in the colon of p53(+/+) mice but not in that of p53(−/−) mice. These results suggest that DFNA5 plays a role in the p53-regulated cellular response to genotoxic stress probably by cooperating with p53.

Matching Content Categories {📚}

  • Science
  • Education
  • Telecommunications

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

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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 if the website is profiting.

While many websites aim to make money, others are created to share knowledge or showcase creativity. People build websites for various reasons. This could be one of them. Link.springer.com might be earning cash quietly, but we haven't detected the monetization method.

Keywords {🔍}

dfna, cells, expression, cell, gene, dna, article, google, scholar, cas, fig, response, pbs, cancer, protein, role, damage, apoptosis, analysis, mrna, nature, cellular, mice, hearing, function, human, impairment, death, assay, pdependent, antibody, nakamura, arakawa, etoposideinduced, hepg, wildtype, genes, pregulated, line, apoptotic, target, pwaf, infected, van, mutant, sequences, reported, sequence, presence, results,

Topics {✒️}

nature portfolio si-mscv-puro-h1r-p53ri retrovirus permissions reprints privacy policy si-mscv-puro-h1r retrovirus open reading frame mrna purification kits advertising include cell-cycle-regulating proteins nature 404 nature 408 nature p53-dependent cell-cycle checkpoint pcr-blunt ii-topo plasmid etoposide-resistant mewo-eto-1 cells social media pcr-blunt ii-topo etoposide-induced cell death author information authors p53-inducible ubiquitin-protein ligase genotoxin-induced cell death parental mewo-eto-1 cells semi-quantitative rt-pcr analysis tumor suppressor p53 etoposide-induced dna damage dna damage-induced apoptosis author correspondence predictive p53 binding-sites brain-specific p53-target gene p53-regulated tumor suppression dna damage-repair proteins hiroshi egami & hideo baba induce p53-dependent apoptosis induce p53-dependent apotosis ecori-digested dna fragment hepg2-p53-cont cells subjected lung-cancer cell line consensus p53-binding sequence regulates p53-dependent apoptosis gsdme-mediated pyroptosis promotes semi-quantitative rt-pcr 4 mg/ml bromophenol blue gamma-irradiation-induced apoptosis mouse anti-flag antibody etoposide-induced apoptotic cells p53-dependent apoptotic pathway g418-resistant colonies grown p53-independent ceramide formation pyroptosis cell death p53-mediated cellular response

Questions {❓}

  • Furthermore, does DFNA5 mediate the p53-regulated cellular response outside the cochlea?
  • How do we explain such contrasting dual roles of DFNA5 in the cellular response to DNA damage?
  • The most important question is how and where does DFNA5 function as a mediator of p53?
  • Van Laer L, Vrijiens K, Thys S et al (2004) DFNA5: hearing impairment exon instead of hearing impairment gene?

Schema {🗺️}

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         description:The tumor suppressor p53 plays a crucial role in the cellular response to DNA damage by transcriptional activation of numerous downstream genes. Although a considerable number of p53 target genes have been reported, the precise mechanism of p53-regulated tumor suppression still remains to be elucidated. Here, we report a novel role of the DFNA5 gene in p53-mediated etoposide-induced cell death. The DFNA5 gene has been previously reported to be responsible for autosomal-dominant, nonsyndromic hearing impairment. The expression of the DFNA5 gene was strongly induced by exogenous and endogenous p53. The chromatin immunoprecipitation assay indicated that a potential p53-binding sequence is located in intron 1 of the DFNA5 gene. Furthermore, the reporter gene assay revealed that the sequence displays p53-dependent transcriptional activity. The ectopic expression of DFNA5 enhanced etoposide-induced cell death in the presence of p53; however, it was inhibited in the absence of p53. Finally, the expression of DFNA5 mRNA was remarkably induced by gamma-ray irradiation in the colon of p53(+/+) mice but not in that of p53(−/−) mice. These results suggest that DFNA5 plays a role in the p53-regulated cellular response to genotoxic stress probably by cooperating with p53.
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      headline:The potential role of DFNA5, a hearing impairment gene, in p53-mediated cellular response to DNA damage
      description:The tumor suppressor p53 plays a crucial role in the cellular response to DNA damage by transcriptional activation of numerous downstream genes. Although a considerable number of p53 target genes have been reported, the precise mechanism of p53-regulated tumor suppression still remains to be elucidated. Here, we report a novel role of the DFNA5 gene in p53-mediated etoposide-induced cell death. The DFNA5 gene has been previously reported to be responsible for autosomal-dominant, nonsyndromic hearing impairment. The expression of the DFNA5 gene was strongly induced by exogenous and endogenous p53. The chromatin immunoprecipitation assay indicated that a potential p53-binding sequence is located in intron 1 of the DFNA5 gene. Furthermore, the reporter gene assay revealed that the sequence displays p53-dependent transcriptional activity. The ectopic expression of DFNA5 enhanced etoposide-induced cell death in the presence of p53; however, it was inhibited in the absence of p53. Finally, the expression of DFNA5 mRNA was remarkably induced by gamma-ray irradiation in the colon of p53(+/+) mice but not in that of p53(−/−) mice. These results suggest that DFNA5 plays a role in the p53-regulated cellular response to genotoxic stress probably by cooperating with p53.
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      affiliation:
            name:National Cancer Center Research Institute
            address:
               name:Center for Medical Genomics, National Cancer Center Research Institute, Tokyo, Japan
               type:PostalAddress
            type:Organization
      name:Tohru Kiyono
      affiliation:
            name:National Cancer Center Research Institute
            address:
               name:Virology Division, National Cancer Center Research Institute, Tokyo, Japan
               type:PostalAddress
            type:Organization
      name:Hiroshi Egami
      affiliation:
            name:Kumamoto University
            address:
               name:Department of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, Kumamoto, Japan
               type:PostalAddress
            type:Organization
      name:Hideo Baba
      affiliation:
            name:Kumamoto University
            address:
               name:Department of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, Kumamoto, Japan
               type:PostalAddress
            type:Organization
      name:Hirofumi Arakawa
      affiliation:
            name:National Cancer Center Research Institute
            address:
               name:Cancer Medicine and Biophysics Division, National Cancer Center Research Institute, Tokyo, Japan
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Cancer Medicine and Biophysics Division, National Cancer Center Research Institute, Tokyo, Japan
      name:Department of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, Kumamoto, Japan
      name:Cancer Medicine and Biophysics Division, National Cancer Center Research Institute, Tokyo, Japan
      name:Cancer Medicine and Biophysics Division, National Cancer Center Research Institute, Tokyo, Japan
      name:Cancer Medicine and Biophysics Division, National Cancer Center Research Institute, Tokyo, Japan
      name:Cancer Medicine and Biophysics Division, National Cancer Center Research Institute, Tokyo, Japan
      name:Cancer Medicine and Biophysics Division, National Cancer Center Research Institute, Tokyo, Japan
      name:Cancer Medicine and Biophysics Division, National Cancer Center Research Institute, Tokyo, Japan
      name:Cancer Transcriptome Project, National Cancer Center Research Institute, Tokyo, Japan
      name:Center for Medical Genomics, National Cancer Center Research Institute, Tokyo, Japan
      name:Center for Medical Genomics, National Cancer Center Research Institute, Tokyo, Japan
      name:Virology Division, National Cancer Center Research Institute, Tokyo, Japan
      name:Department of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, Kumamoto, Japan
      name:Department of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, Kumamoto, Japan
      name:Cancer Medicine and Biophysics Division, National Cancer Center Research Institute, Tokyo, Japan

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