Gene name: | IFNG |
Aging type: | Accelerate |
Aging characteristic: |
Tissue type: | -- |
Cell name: | Melanocyte |
Experiment: | Flow cytometry//SA-β-gal activity assay |
Description: | IFN-γ significantly decreased the cell viability in a dose dependent manner. Cell cycle analysis results demonstrated that IFN-c at both concentrations caused the accumulation of melanocytes at G1 phase, while decreased the percentage of cells at S and G2/M phases.In contrast, melanocytes after persistent IFN-γ treatment became large, flat in shape with shorter and fewer dendrites, and some cells were highly pigmented.We also noticed a significantincrease of SA-β-gal stain ing, a marker of senescence, in melanocytes with 7 days of IFN-γ stimulation. |
Target gene: | P21/WAF1 |
Official symbol(s): | P21/WAF1 |
R-AG-Target gene: | Upregulation |
Subcategory: | Unclear |
Target gene experiment: | Western blot//SA-β-gal activity assay |
Target gene description: | Immunoblotting analysis indicated that protein level of p21 was greatly elevated with the increasing duration of IFN-γ treatment,while p16 level didn’t change during the experiment.P21 siRNA treatment suppressed the IFN-γ-induced increase of SA-β-gal staining. |
Regulatory pathway: | JAK2-STAT1 |
R-AG-Pathway: | -- |
Official symbol(s): | JAK2-STAT1 |
Pathway experiment: | MTS assay//Western blot//SA-β-gal activity assay//Flow cytometry |
Pathway description: | In the presence of IFN-γ, the cell viability of control siRNA transfected melanocytes was significantly inhibited. Significantly, JAK2 or STAT1 siRNA efficiently restored the viability of melanocytes. Immunoblotting results confirmed that JAK2 or STAT1 siRNA, but not JAK1 siRNA inhibited the increase of p21 induced by IFN-. Moreover, IFN-γ-induced SA-β-gal staining increase in melanocytes was blocked by JAK2 and STAT1 siRNAs.IFN-γ treatment caused obvious elevation of intracellular ROS, and the effect of IFN-γ was dose-dependent manner. |
Annotation:
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