| Gene name: | FASLG |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | CRC29 |
| Gene ID: | 356 |
| Category: | protein coding |
| Phenotype: | Colorectal cancer |
| Experimental category: | HL |
| PMID: | 28300842 |
| Experiment: | SA-β-gal activity assay//Flow cytometry//Colony formation assay |
| Description: | We found that chronic CD95L exposure suppressed the colony-forming potential of five out of nine of these cultures by more than 50% .FACS analysis of PI-stained cells did show a marked increase in the number of cells in G2.We found that CD95L stimulation induced expression of senescence-associated β-galactosi-dase (SA-β-GAL). |
| Target gene: | CASPASE |
| Official symbol(s): | CASPASE |
| R-AG-Target gene: | Activation |
| Subcategory: | Unclear |
| Target gene experiment: | Western blot |
| Target gene description: | A time course experiment showed that induction of γH2AX following CD95L stimulation paralleled caspase-8 and caspase-3 activation, starting already 2?h following ligand stimulation. |
| Regulatory pathway: | P53 |
| R-AG-Pathway: | -- |
| Official symbol(s): | TP53 |
| Pathway experiment: | Knockdown//SA-β-gal activity assay//Western blot |
| Pathway description: | Knockdown of p53 did not prevent upstream events like caspase-8 and caspase-3 activation, iCAD processing or DNA damage induction. Rather, p53 knockdown increased CD95L-induced DNA damage, which is in line with its function as a ‘guardian of the genome' by activating genes involved in cell cycle arrest and DNA repair.26 Despite the increased DNA damage in CD95L-stimulated p53 knockdown cells, these cells did not enter senescence and largely retained their clone-forming potential . |
Annotation:
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