| Gene name: | EGFR |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | A549 |
| Experiment: | SA-β-gal activity assay//Western blot |
| Description: | Examination of p53 wild-type cells revealed several features of senescence, including morphologic characteristics indicating premature differentiation and expression of senescence-associated β-galactosidase as well as increased levels of trimethylated histone H3K9 . |
| Target gene: | P53 |
| Official symbol(s): | P53 |
| R-AG-Target gene: | -- |
| Subcategory: | Unclear |
| Target gene experiment: | SA-β-gal activity assay//Western blot |
| Target gene description: | Examination of p53 wild-type cells revealed several features of senescence, including morphologic characteristics indicating premature differentiation and expression of senescence-associated β-galactosidase as well as increased levels of trimethylated histone H3K9. |
| Regulatory pathway: | MEK-ERK |
| R-AG-Pathway: | -- |
| Official symbol(s): | MAP2K7-MAPK1 |
| Pathway experiment: | Cell viability assay//Cell Proliferation assay//SA-β-gal activity assay |
| Pathway description: | Using A549, ABC1, and HCC44 cells as representative examples, we observed that treatment with a MEK inhibitor indeed increased the fraction of cells with residual g-H2AX foci by 8.2% to 18.1%, which was comparable with the effects of EGFR inhibition in A549 cells. MEK inhibition also caused p21 induction, radiosensitization, cellular senescence, and did not further enhance the radiosensitizing effects of erlotinib,implicating the MEK–ERK pathway as one common effector pathway of radioresistance downstream of EGFR. |
Annotation:
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