Dotiwala Farokh (6 results)

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    • Language: English

      Published by LAP LAMBERT Academic Publishing, 2015

      383830277X / 9783838302775

      • Softcover

      Seller: preigu, Osnabrück, Germanypreigu

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      Taschenbuch. Condition: Neu. Nuclear and cytoplasmic control of the DNA damage checkpoint | A new way of looking at cell cycle control | Farokh Dotiwala | Taschenbuch | 188 S. | Englisch | 2015 | LAP LAMBERT Academic Publishing | EAN 9783838302775 | Verantwortliche Person für die EU: preigu GmbH & Co. KG, Lengericher Landstr. 19, 49078 Osnabrück, mail[at]preigu[dot]de | Anbieter: preigu.

    • Language: English

      Published by LAP Lambert Academic Publishing, 2009

      383830277X / 9783838302775

      • Softcover

      Seller: Mispah books, Redhill, SURRE, United KingdomMispah books

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      Paperback. Condition: Like New. LIKE NEW. SHIPS FROM MULTIPLE LOCATIONS. book.

    • Language: English

      Published by LAP LAMBERT Academic Publishing Jun 2009, 2009

      383830277X / 9783838302775

      • Softcover
      • Print on Demand

      Seller: BuchWeltWeit Ludwig Meier e.K., Bergisch Gladbach, GermanyBuchWeltWeit Ludwig Meier e.K.

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      Taschenbuch. Condition: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -Cell cycle checkpoints are the means by which cells maintain their genomic integrity and resist factors that are potentially mutagenic. It is well known that there are different checkpoints for different stresses a cell could face, one of them being the DNA damage checkpoint. For long the activity of this checkpoint was thought to be limited to the nucleus. In this and other emerging studies it has now been established that the DNA damage checkpoint can regulate cell cycle arrest, nuclear positioning and movement by controlling cytoplasmic factors and events. This study establishes a novel regulatory mechanism of the DNA damage checkpoint involving vesicular transport system and cytoplasmic, non-proteosomal protein degradation. The study also focuses on the connection between the spindle assembly checkpoint (SAC) and the DNA damage checkpoint. To study this we generate an acentric chromosome with a single DNA double strand break on it. We find that budding yeast cells that have one chromosome with conditional GAL1-Cen centromere turned off cannot activate the SAC and both the sister chromatids of this chromosome get preferentially segregated to the mother cell. 188 pp. Englisch.

    • Language: English

      Published by LAP Lambert Academic Publishing, 2009

      383830277X / 9783838302775

      • Softcover
      • Print on Demand

      Seller: moluna, Greven, Germanymoluna

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      Condition: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. Cell cycle checkpoints are the means by which cells maintain their genomic integrity and resist factors that are potentially mutagenic. It is well known that there are different checkpoints for different stresses a cell could face, one of them being the DNA.

    • Language: English

      Published by LAP LAMBERT Academic Publishing Jun 2009, 2009

      383830277X / 9783838302775

      • Softcover
      • Print on Demand

      Seller: buchversandmimpf2000, Emtmannsberg, BAYE, Germanybuchversandmimpf2000

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      Taschenbuch. Condition: Neu. This item is printed on demand - Print on Demand Titel. Neuware -Cell cycle checkpoints are the means by which cells maintain their genomic integrity and resist factors that are potentially mutagenic. It is well known that there are different checkpoints for different stresses a cell could face, one of them being the DNA damage checkpoint. For long the activity of this checkpoint was thought to be limited to the nucleus. In this and other emerging studies it has now been established that the DNA damage checkpoint can regulate cell cycle arrest, nuclear positioning and movement by controlling cytoplasmic factors and events. This study establishes a novel regulatory mechanism of the DNA damage checkpoint involving vesicular transport system and cytoplasmic, non-proteosomal protein degradation. The study also focuses on the connection between the spindle assembly checkpoint (SAC) and the DNA damage checkpoint. To study this we generate an acentric chromosome with a single DNA double strand break on it. We find that budding yeast cells that have one chromosome with conditional GAL1-Cen centromere turned off cannot activate the SAC and both the sister chromatids of this chromosome get preferentially segregated to the mother cell.VDM Verlag, Dudweiler Landstraße 99, 66123 Saarbrücken 188 pp. Englisch.

    • Language: English

      Published by LAP LAMBERT Academic Publishing, 2009

      383830277X / 9783838302775

      • Softcover
      • Print on Demand

      Seller: AHA-BUCH GmbH, Einbeck, GermanyAHA-BUCH GmbH

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      Taschenbuch. Condition: Neu. nach der Bestellung gedruckt Neuware - Printed after ordering - Cell cycle checkpoints are the means by which cells maintain their genomic integrity and resist factors that are potentially mutagenic. It is well known that there are different checkpoints for different stresses a cell could face, one of them being the DNA damage checkpoint. For long the activity of this checkpoint was thought to be limited to the nucleus. In this and other emerging studies it has now been established that the DNA damage checkpoint can regulate cell cycle arrest, nuclear positioning and movement by controlling cytoplasmic factors and events. This study establishes a novel regulatory mechanism of the DNA damage checkpoint involving vesicular transport system and cytoplasmic, non-proteosomal protein degradation. The study also focuses on the connection between the spindle assembly checkpoint (SAC) and the DNA damage checkpoint. To study this we generate an acentric chromosome with a single DNA double strand break on it. We find that budding yeast cells that have one chromosome with conditional GAL1-Cen centromere turned off cannot activate the SAC and both the sister chromatids of this chromosome get preferentially segregated to the mother cell.