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@article{1387483, author = {Kafkova Raskova, Leona and Navrkalová, Veronika and Jarosova, Marie and Loja, Tomáš and Černá, Jana and Kucerova, Jana and Kriegova, Eva and Prochazka, Vit and Novak, Zdenek and Simkova, Dana and Pospíšilová, Šárka and Divoky, Vladimir}, article_location = {Oxon}, article_number = {1}, doi = {http://dx.doi.org/10.1080/10428194.2016.1187276}, keywords = {PROTEIN EXPRESSION; ATM; APOPTOSIS; SURVIVAL; MYC}, language = {eng}, issn = {1042-8194}, journal = {LEUKEMIA & LYMPHOMA}, title = {Ability to downregulate the level of cyclin-dependent kinase inhibitor p27(Kip1) after DNA damage is retained in chronic lymphocytic leukemia cells with functional ATM/p53 signaling pathway}, url = {http://www.tandfonline.com/doi/abs/10.1080/10428194.2016.1187276?journalCode=ilal20}, volume = {58}, year = {2017} }
TY - JOUR ID - 1387483 AU - Kafkova Raskova, Leona - Navrkalová, Veronika - Jarosova, Marie - Loja, Tomáš - Černá, Jana - Kucerova, Jana - Kriegova, Eva - Prochazka, Vit - Novak, Zdenek - Simkova, Dana - Pospíšilová, Šárka - Divoky, Vladimir PY - 2017 TI - Ability to downregulate the level of cyclin-dependent kinase inhibitor p27(Kip1) after DNA damage is retained in chronic lymphocytic leukemia cells with functional ATM/p53 signaling pathway JF - LEUKEMIA & LYMPHOMA VL - 58 IS - 1 SP - 199-203 EP - 199-203 PB - TAYLOR & FRANCIS LTD SN - 10428194 KW - PROTEIN EXPRESSION KW - ATM KW - APOPTOSIS KW - SURVIVAL KW - MYC UR - http://www.tandfonline.com/doi/abs/10.1080/10428194.2016.1187276?journalCode=ilal20 L2 - http://www.tandfonline.com/doi/abs/10.1080/10428194.2016.1187276?journalCode=ilal20 N2 - The activity of the key DNA-damage response (DDR) kinases, ATR and ATM, is largely compromised in chronic lymphocytic leukemia (CLL) cells. While noncycling CLL cells lack ATR protein expression,[1] ATM is commonly targeted for inactivation by genetic abnormalities of the ATM gene.[2] It has been shown that checkpoint pathways, which operate in cycling somatic cells and target Cdk2 kinase activity, are to some extent activated in arrested CLL cells after DNA damage as well;[3] however, the impact of these pathways is questionable, as it could be hampered by predominantly cytoplasmic localization of Cdk2 in CLL cells.[4] Nevertheless, DDR plays a key role in sensitivity of CLL to chemotherapy. Another stress-response kinase, p38 MAP kinase (p38MAPK), was shown to promote CLL cells survival.[5] In multiple cell types, p38MAPK activates different cell cycle checkpoints (mainly through regulation of cyclindependent kinase (Cdk) inhibitors p21Cip1 and p27Kip1), and also ATM/ATR-dependent G2/M checkpoint signaling through MAPKAP kinase-2 activity.[6] While relationship between ATM/p53 and p21Cip1 expression in CLL was studied,[7] the association of ATM kinase activity with the levels of p27Kip1 after DNA damage has not been elucidated in CLL cells. ER -
KAFKOVA RASKOVA, Leona, Veronika NAVRKALOVÁ, Marie JAROSOVA, Tomáš LOJA, Jana ČERNÁ, Jana KUCEROVA, Eva KRIEGOVA, Vit PROCHAZKA, Zdenek NOVAK, Dana SIMKOVA, Šárka POSPÍŠILOVÁ and Vladimir DIVOKY. Ability to downregulate the level of cyclin-dependent kinase inhibitor p27(Kip1) after DNA damage is retained in chronic lymphocytic leukemia cells with functional ATM/p53 signaling pathway. \textit{LEUKEMIA \&{} LYMPHOMA}. Oxon: TAYLOR \&{} FRANCIS LTD, 2017, vol.~58, No~1, p.~199-203. ISSN~1042-8194. Available from: https://dx.doi.org/10.1080/10428194.2016.1187276.
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