| Gene name: | ZNF148 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | NCI-H460 |
| Gene ID: | 7707 |
| Category: | protein coding |
| Phenotype: | Lung cancer |
| Experimental category: | L |
| PMID: | 19583777 |
| Experiment: | Knockdown//SA-β-gal activity assay |
| Description: | Knockdown of endogenous ZBP-89 promoted NCI-H460 cell senescence, a 1.5-fold increase in SA-β-gal activity was seen after 7 days of ZBP-89i transfection, whereas overexpression of ZBP- 89 led to a reverse effect. In addition, cells transfected with ZBP-89i exhibited phenotypic changes that are typical of cells undergoing replicative senescence. |
| Target gene: | P16 |
| Official symbol(s): | P16 |
| R-AG-Target gene: | Downregulation |
| Subcategory: | Binding to promoter |
| Target gene experiment: | SA-β-gal activity assay//Western blot//Luciferase reporter assay//RT-PCR |
| Target gene description: | ZBP-89 restrained senescence of NCI-H460 cells through p16 repression. Representative photomicrographs of the SA-β-gal staining at day 7 after ZBP-89i transfection, or ZBP-89i plus p16i transfection. An irrelevant siRNA vector was used as the control.Western blotting demon- strated that p16 protein expression was decreased on ZBP-89 ectopic expression, whereas it was enhanced。Western blotting demonstrated that p16 protein expression was decreased on ZBP-89 ectopic expression, whereas it was enhanced by knockdown of the endogenous ZBP-89 in NCI- H460 cells by knockdown of the endogenous ZBP-89 in NCI- H460 cells .Overexpression of ZBP-89 greatly inhibited p16 promoter activity。The p16 mRNA level was decreased on ectopic expression of ZBP-89, but increased by knockdown of endoge- nous ZBP-89. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
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