'Knock down' of DNA polymerase beta by RNA interference: recapitulation of null phenotype. Polosina, Y. Y., Rosenquist, T. A., Grollman, A. P., & Miller, H. DNA repair, 3(11):1469-74, 11, 2004.
'Knock down' of DNA polymerase beta by RNA interference: recapitulation of null phenotype. [link]Mendeley  'Knock down' of DNA polymerase beta by RNA interference: recapitulation of null phenotype. [link]Paper  doi  abstract   bibtex   
DNA polymerase beta (pol beta) is the major DNA polymerase involved in the base excision repair (BER) pathway in mammalian cells and, as a consequence, BER is severely compromised in cells lacking pol beta. Pol beta null (-/-) mouse embryos are not viable and pol beta null cells are hypersensitive to alkylating agents. Using RNA interference (RNAi) technology in mouse cells, we have reduced the pol beta protein and mRNA to undetectable levels. Pol beta knockdown cell lines display a pattern of hypersensitivity to DNA damaging agents similar to that observed in pol beta null cells. Generation of pol beta knock down cells makes it possible to combine the pol beta null phenotype with deficiencies in other DNA repair proteins, thereby helping to elucidate the role of pol beta and its interactions with other proteins in mammalian cells.
@article{ mendeley_4996784452,
  isauthor = {1},
  abstract = {DNA polymerase beta (pol beta) is the major DNA polymerase involved in the base excision repair (BER) pathway in mammalian cells and, as a consequence, BER is severely compromised in cells lacking pol beta. Pol beta null (-/-) mouse embryos are not viable and pol beta null cells are hypersensitive to alkylating agents. Using RNA interference (RNAi) technology in mouse cells, we have reduced the pol beta protein and mRNA to undetectable levels. Pol beta knockdown cell lines display a pattern of hypersensitivity to DNA damaging agents similar to that observed in pol beta null cells. Generation of pol beta knock down cells makes it possible to combine the pol beta null phenotype with deficiencies in other DNA repair proteins, thereby helping to elucidate the role of pol beta and its interactions with other proteins in mammalian cells.},
  month = {11},
  canonical_id = {3ed26e50-6d00-11df-a474-0026b95e3e23},
  added = {1339234570},
  year = {2004},
  keywords = {Animals, Base Sequence, Bleomycin, Bleomycin: toxicity, Cell Line, Cisplatin, Cisplatin: toxicity, DNA Damage, DNA Polymerase beta, DNA Polymerase beta: deficiency, DNA Polymerase beta: genetics, DNA Polymerase beta: metabolism, DNA Repair, DNA, Complementary, DNA, Complementary: genetics, Hydrogen Peroxide, Hydrogen Peroxide: toxicity, Methyl Methanesulfonate, Methyl Methanesulfonate: toxicity, Methylene Blue, Methylene Blue: toxicity, Mice, Phenotype, RNA Interference, RNA, Messenger, RNA, Messenger: genetics, RNA, Messenger: metabolism, Ultraviolet Rays, Ultraviolet Rays: adverse effects},
  isstarred = {0},
  id = {4996784452},
  discipline = {Computer and Information Science},
  journal = {DNA repair},
  title = {'Knock down' of DNA polymerase beta by RNA interference: recapitulation of null phenotype.},
  day = {2},
  deletionpending = {0},
  version = {1339234654},
  pmid = {15380102},
  number = {11},
  url_mendeley = {http://www.mendeley.com//research/knock-down-dna-polymerase-beta-rna-interference-recapitulation-null-phenotype//},
  volume = {3},
  isread = {0},
  author = {Yaroslava Y {Polosina} and Thomas A {Rosenquist} and Arthur P {Grollman} and Holly {Miller}},
  pages = {1469-74},
  doi = {10.1016/j.dnarep.2004.05.011},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/15380102},
  type = {Journal Article},
  issn = {1568-7864},
  modified = {1339234654},
  subdiscipline = {Information Science},
  journal = {DNA repair},
  dateaccessed = {09/06/12}
}

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