English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Inhibitors of casein kinase 2 (CK2), a regulator of cell proliferation andmediator of the DNA damage response, are being evaluated in clinical trials forthe treatment of cancers. Apigenin was capable of inhibiting the activation ofCK2 following γ irradiation in LN18 and U87 malignant glioma cells. Apigenin andsiRNA-mediated CK2 protein depletion further inhibited NF-κB activation and alteredthe Tyr68 phosphorylation of Chk2 kinase, a DNA damage response checkpoint kinase,following irradiation. However, CK2 inhibition did not decrease the ability ofthese glioma cells to repair double-strand DNA breaks, as assessed by COMET assaysand γ-H2Ax staining. Likewise, apigenin and siRNA-induced depletion of CK2 failedto sensitize glioma cells to the cytotoxic effect of 2 to 10 G-rays of γ irradiation,as assessed by clonogenic assays. These results contrast with those found in othercancer types, and urge to prudence regarding the inclusion of malignant gliomapatients in clinical trials that assess the radiosensitizing role of CK2 inhibitorsin solid cancers.

Casein kinase 2 inhibition modulates the DNA damage response but fails to radiosensitize malignant glioma cells