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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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