External factors: | BIBR1532 |
Aging type: | Accelerate |
Aging characteristic: |
Category: | Chemical compounds |
Phenotype: | Lung cancer |
Experiment: | SA-β-gal activity assay//Flow cytometry |
Description: | After a total dose of 8 Gy of conventional fractionation radiation (2 Gy over 4 fractions), SA-β-gal-positive cells were significantly increased when cells were treated with BIBR1532 . BIBR1532 significantly decreased IR-induced G2/M cell cycle arrest after irradiation in both non-small cell lung cancer (NSCLC) cell lines. |
Regulatory pathway: | ATM-CHK1 |
R-EF-Pathway: | Downregulation |
Official symbol(s): | ATM-CHK1 |
Pathway experiment: | Western blot//Flow cytometry |
Pathway description: | In NSCLC cells, BIBR1532 significantly inhibited radiation-induced ATM/CHK1 phosphorylation.BIBR1532 treatment also inhibited IR-induced G2/M cell cycle arrest. |
Annotation: