Gene name: | TAGLN |
Aging type: | Accelerate |
Aging characteristic: |
Tissue type: | -- |
Cell name: | HepG2 |
Experiment: | Colony formation assay//SA-β-gal activity assay |
Description: | SM22a overexpression significantly induced the inhibition of cell growth of HepG2 cells. Conversely, when SM22a-overexpressing cells were transfected with siRNA, which suppresses the expression of SM22a, the cell growth was partially restored to that of control cells.These results suggest that SM22a is closely involved in regulation of cell growth and senescence. |
Target gene: | MT-1G |
Official symbol(s): | MT1G |
R-AG-Target gene: | Upregulation |
Subcategory: | Unclear |
Target gene experiment: | RT-PCR//Western blot |
Target gene description: | In two selected SM22a-overexpressing clones, the levels of MT-1G were also elevated. |
Regulatory pathway: | P16-PRB |
R-AG-Pathway: | Activation |
Official symbol(s): | CDKN2A-RB1 |
Pathway experiment: | RT-PCR//Western blot |
Pathway description: | SM22a overexpression resulted in a significant elevation of p16INK4a when analyzed by RT-PCR and Western blot. In wild-type HepG2 cells, serine 780 and 807/811 residues of pRB were highly phosphorylated. However, SM22a overexpression in these cells significantly inhibited the phosphorylation of serine 780 and 807/811 residues in pRB, which may prevent the detachment of E2F from pRB and thus suppress cell proliferation. Phosphorylation of serine 608 residue in pRB was also significantly inhibited. On the other hand, when SM22a-overexpressing cells were transfected again with siRNA to suppress SM22a expression, serine 608, 780, and 807/811 residues in pRB were re-phosphorylated, thereby restoring cell growth to a certain level. |
Annotation:
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