External factors
| External factors: |
Temsirolimus |
| 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. |
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Regulatory relationship
| 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. |
| R-EF-Pathway:
|
Downregulation |
| Official symbol(s): |
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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. |
Aging network
Annotation:
The green line represents Upregulation.
The purple line represents Downregulation.
The orange line represents Activation.
The yellow line represents Inhibition.
The gray line represents Unclear.