| External factors: | Temsirolimus |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Hutchinson-Gilford progeria syndrome |
| Experiment: | Immunocytochemistry//SA-β-gal activity assay//Cell viability assay |
| Description: | Immunocytochemistry:temsirolimus significantly stimulated autophagy in both normal and HGPS fibroblasts.viability assays:viability assays confirmed that temsirolimus increased the number of viable cells in HGPS culturesSA-β-gal activity assay:In the presence of temsirolimus, the number of β-Gal-positive cells was decreased in both control (2.0%) and HGPS (5.9%) cultures.Immunocytochemistry:Temsirolimus treatment induced a decreased number of γH2A.X-positive HGPS nuclei (36.1%) signifying a reduction in DNA damage. |
| Target gene: | PROGERIN |
| R-EF-Target gene: | Downregulation |
| Official symbol(s): | PROGERIN |
| Target gene experiment: | Western blot |
| Target gene description: | Western blot analyses of long-term cultures showed reduced levels of progerin in HGPS cells treated for 85 days. |
| Regulatory pathway: | mTOR |
| R-EF-Pathway: | Downregulation |
| Official symbol(s): | MTOR |
| Pathway experiment: | Western blot |
| Pathway description: | As expected, temsirolimus lowered the phosphorylated 4E-BP1 and S6RP protein levels, indicating that the mTOR-signaling pathway was inhibited. |
Annotation: