| Gene name: | SRSF3 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | 293T,HUVEC,MEF,NIH-3T3 |
| Experiment: | SA-β-gal activity assay//Knockdown//CCK-8 assay//Flow cytometry//qRT-PCR |
| Description: | RNA interferences using two shRNAs targeting SRSF3 caused increased senescenceassociated β-galactosidase (SA-β-gal) staining in both human (293T and HUVEC) and mouse (MEF and NIH3T3) cells. In addition, SRSF3-KD reduced cell growth rate in tested cell lines.Notably, SRSF3-KD caused a common decrease of S phase percentage in both 293T and MEF cells. What’s more,knockdown of SRSF3 in human and mouse cells also led to the decreased expression of MKI67, a molecular marker for cell proliferation. |
| Target gene: | PTEN |
| Official symbol(s): | PTEN |
| R-AG-Target gene: | -- |
| Subcategory: | Unclear |
| Target gene experiment: | Luciferase reporter assay//Western blot |
| Target gene description: | As knockdown of SRSF3 induced 3′ UTR shortening of PTEN and transcripts with shortened 3′ UTR of PTEN generated more protein than those with the longer one, one would expect that SRSF3-KD can increase the protein level of PTEN.Consistently, SRSF3 knockdown with two shRNAs both led to higher PTEN protein abundance in human 293T and HUVEC cells . |
| Regulatory pathway: | PI3K-AKT |
| R-AG-Pathway: | -- |
| Official symbol(s): | PIK3CA-AKT1 |
| Pathway experiment: | Knockdown//Western blot |
| Pathway description: | Furthermore, SRSF3 knockdown attenuated the abundance of p-AKT but not that of the total AKT,coinciding with the result of PTEN upregulation. |
Annotation:
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