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

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14740%2F17%3A00094367" target="_blank" >RIV/00216224:14740/17:00094367 - isvavai.cz</a>

Alternative codes found

RIV/61989592:15110/17:73578951 RIV/00098892:_____/17:N0000004

Result on the web

<a href="http://www.tandfonline.com/doi/abs/10.1080/10428194.2016.1187276?journalCode=ilal20" target="_blank" >http://www.tandfonline.com/doi/abs/10.1080/10428194.2016.1187276?journalCode=ilal20</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1080/10428194.2016.1187276" target="_blank" >10.1080/10428194.2016.1187276</a>

Result language

angličtina

Original language name

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

Original language description

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.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

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OECD FORD branch

30200 - Clinical medicine

Project

Result was created during the realization of more than one project. More information in the Projects tab.

Continuities

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Publication year

2017

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

LEUKEMIA & LYMPHOMA

ISSN

1042-8194

e-ISSN

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Volume of the periodical

58

Issue of the periodical within the volume

1

Country of publishing house

GB - UNITED KINGDOM

Number of pages

5

Pages from-to

199-203

UT code for WoS article

000387484400027

EID of the result in the Scopus database

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