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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
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We began analyzing https://link.springer.com/article/10.1007/s00018-009-0177-1, but it redirected us to https://link.springer.com/article/10.1007/s00018-009-0177-1. The analysis below is for the second page.

Title[redir]:
Nonsense-mediated mRNA decay in human cells: mechanistic insights, functions beyond quality control and the double-life of NMD factors | Cellular and Molecular Life Sciences
Description:
Nonsense-mediated decay is well known by the lucid definition of being a RNA surveillance mechanism that ensures the speedy degradation of mRNAs containing premature translation termination codons. However, as we review here, NMD is far from being a simple quality control mechanism; it also regulates the stability of many wild-type transcripts. We summarise the abundance of research that has characterised each of the NMD factors and present a unified model for the recognition of NMD substrates. The contentious issue of how and where NMD occurs is also discussed, particularly with regard to P-bodies and SMG6-driven endonucleolytic degradation. In recent years, the discovery of additional functions played by several of the NMD factors has further complicated the picture. Therefore, we also review the reported roles of UPF1, SMG1 and SMG6 in other cellular processes.

Matching Content Categories {📚}

  • Education
  • Science
  • Telecommunications

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?

🏙️ Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 98,426,998 visitors per month in the current month.

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How Does Doi.org Make Money? {💸}

We can't tell how the site generates income.

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. Doi.org has a revenue plan, but it's either invisible or we haven't found it.

Keywords {🔍}

google, scholar, pubmed, cas, article, mrna, decay, nonsensemediated, cell, biol, mol, rna, upf, protein, human, translation, smg, surveillance, maquat, nonsense, mammalian, complex, genes, nat, embo, nmd, mrnas, gene, pathway, dev, factors, termination, sci, yeast, cells, genet, izaurralde, mutations, required, factor, degradation, proteins, jacobson, staufen, control, usa, pathways, kim, regulation, hentze,

Topics {✒️}

month download article/chapter nicole kleinschmidt & oliver mühlemann phosphatidylinositol kinase-related kinase nonsense-mediated decay pathway trigger nonsense-mediated decay nonsense-mediated mrna decay nonsense-mediated decay approaches wt1-mediated transcriptional activation nonsense codon-mediated decay interferon-gamma-receptor deficiency nonsense-mediated decay factors stress-induced signaling pathways exon-junction complex assembly exon-exon junction complex cap-binding protein 1-mediated sec trna[ser]sec rna-mediated gene silencing cis-acting sequence elements unstable beta-globin mrna mrna exon-exon junctions exon-junction complex components post-transcriptional pathways upf3-mediated regulatory switch c-terminal pabc domain multipurpose rna-decay machine full article pdf ovarian rna-binding protein post-transcriptional control elongation factor recruitment smg-1-upf1-erf1-erf3 complex nonsense-mediated decay smg6-driven endonucleolytic degradation ruiz-echevarria mj eukaryotic mrna turnover wild-type protein exon junction complex upf protein complex high-throughput sequencing colon cancer cells mrnp domain organization mammalian mrna turnover eukaryotic mrna decapping pre-mrna splicing cystic fibrosis caused mrna decay solves elicit mrna decay mrna surveillance complex mrna decay pathways beta-globin mrna exon-exon junctions

Questions {❓}

  • Hilleren P, Parker R (1999) mRNA surveillance in eukaryotes: kinetic proofreading of proper translation termination as assessed by mRNP domain organization?
  • Kerem E (2004) Pharmacologic therapy for stop mutations: how much CFTR activity is enough?
  • Kerr TP, Sewry CA, Robb SA, Roberts RG (2001) Long mutant dystrophins and variable phenotypes: evasion of nonsense-mediated decay?
  • Li S, Wilkinson MF (1998) Nonsense surveillance in lymphocytes?
  • McGlincy NJ, Smith CW (2008) Alternative splicing resulting in nonsense-mediated mRNA decay: what is the meaning of nonsense?

Schema {🗺️}

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         description:Nonsense-mediated decay is well known by the lucid definition of being a RNA surveillance mechanism that ensures the speedy degradation of mRNAs containing premature translation termination codons. However, as we review here, NMD is far from being a simple quality control mechanism; it also regulates the stability of many wild-type transcripts. We summarise the abundance of research that has characterised each of the NMD factors and present a unified model for the recognition of NMD substrates. The contentious issue of how and where NMD occurs is also discussed, particularly with regard to P-bodies and SMG6-driven endonucleolytic degradation. In recent years, the discovery of additional functions played by several of the NMD factors has further complicated the picture. Therefore, we also review the reported roles of UPF1, SMG1 and SMG6 in other cellular processes.
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      headline:Nonsense-mediated mRNA decay in human cells: mechanistic insights, functions beyond quality control and the double-life of NMD factors
      description:Nonsense-mediated decay is well known by the lucid definition of being a RNA surveillance mechanism that ensures the speedy degradation of mRNAs containing premature translation termination codons. However, as we review here, NMD is far from being a simple quality control mechanism; it also regulates the stability of many wild-type transcripts. We summarise the abundance of research that has characterised each of the NMD factors and present a unified model for the recognition of NMD substrates. The contentious issue of how and where NMD occurs is also discussed, particularly with regard to P-bodies and SMG6-driven endonucleolytic degradation. In recent years, the discovery of additional functions played by several of the NMD factors has further complicated the picture. Therefore, we also review the reported roles of UPF1, SMG1 and SMG6 in other cellular processes.
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