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Description du livre Etat : New. N° de réf. du vendeur ABLIING23Apr0316110076879
Description du livre PAP. Etat : New. New Book. Shipped from UK. THIS BOOK IS PRINTED ON DEMAND. Established seller since 2000. N° de réf. du vendeur L0-9783838120522
Description du livre Etat : New. PRINT ON DEMAND Book; New; Fast Shipping from the UK. No. book. N° de réf. du vendeur ria9783838120522_lsuk
Description du livre PF. Etat : New. N° de réf. du vendeur 6666-IUK-9783838120522
Description du livre Taschenbuch. Etat : Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -While investigating the involvement of REV3, the catalytic subunit of TLS Polymerase zeta (Pol zeta) in the development of chemotherapy resistance, it was found that inhibition of REV3 expression per se suppresses colony formation of cancer cells whereas normal cells were less affected. It was confirmed that inhibition of REV3 in various cancer cell lines leads to a growth inhibition, due to accumulation of persistent DNA damage, subsequently leading to the activation of the ATM-dependent DNA damage response (DDR) cascade. Inhibition of REV3 in p53-proficient cancer cells results in a G1-arrest and senescence. In contrast, the inhibition of REV3 in p53-deficient or p53-knockout cancer cells results in a growth inhibition and a G2/M-arrest whereas a small fraction of the p53-deficient or p53-knockout cancer cells can overcome the G2/M-arrest, which results in mitotic slippage and aneuploidy. It is shown for the first time that inhibition of a TLS Pol confers synthetic sickness/lethality specifically in cancer cells. The inhibition REV3 per se suppresses cancer cell growth whereas normal cells are less affected, thus identifying REV3 as a potential target for a cancer-specific therapy. 92 pp. Englisch. N° de réf. du vendeur 9783838120522
Description du livre Taschenbuch. Etat : Neu. nach der Bestellung gedruckt Neuware - Printed after ordering - While investigating the involvement of REV3, the catalytic subunit of TLS Polymerase zeta (Pol zeta) in the development of chemotherapy resistance, it was found that inhibition of REV3 expression per se suppresses colony formation of cancer cells whereas normal cells were less affected. It was confirmed that inhibition of REV3 in various cancer cell lines leads to a growth inhibition, due to accumulation of persistent DNA damage, subsequently leading to the activation of the ATM-dependent DNA damage response (DDR) cascade. Inhibition of REV3 in p53-proficient cancer cells results in a G1-arrest and senescence. In contrast, the inhibition of REV3 in p53-deficient or p53-knockout cancer cells results in a growth inhibition and a G2/M-arrest whereas a small fraction of the p53-deficient or p53-knockout cancer cells can overcome the G2/M-arrest, which results in mitotic slippage and aneuploidy. It is shown for the first time that inhibition of a TLS Pol confers synthetic sickness/lethality specifically in cancer cells. The inhibition REV3 per se suppresses cancer cell growth whereas normal cells are less affected, thus identifying REV3 as a potential target for a cancer-specific therapy. N° de réf. du vendeur 9783838120522
Description du livre PAP. Etat : New. New Book. Delivered from our UK warehouse in 4 to 14 business days. THIS BOOK IS PRINTED ON DEMAND. Established seller since 2000. N° de réf. du vendeur L0-9783838120522
Description du livre Etat : New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. Autor/Autorin: Knobel Philip AlexanderDissertation and study of Biology at the University of Zurich, Switzerland. Postdoctoral fellow at the Institute for Research in Biomedicine in Barcelona, Spain.While investigating the involvement of REV3, . N° de réf. du vendeur 5406406