| Gene name: | DLK1 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | WI-38 |
| Experiment: | SA-β-gal activity assay//Flow cytometry//Knockdown |
| Description: | Cells infected with the Sh-hDLK2 lentiviral construct exhibited a significantly slower rate of proliferation when compared to control cells,suggesting that depletion of DLK inhibited cell proliferation.Our results showed that loss of DLK results in a diminution of cells in S phase, an increased proportion (～20%) of cells in G1 phase and an unchanged percent-age of cells in the G2/M phase.More than 70% of cells infected with the lentivirus expressing a human DLK shRNA (Sh-hDLK2) showed elevated SA-β-Gal activity, whereas control cells failed to exhibit β-Gal staining. |
| Regulatory pathway: | ERK//P53-P21 |
| R-AG-Pathway: | --//-- |
| Official symbol(s): | MAPK1//TP53-CDKN1A |
| Pathway experiment: | Western blot//Knockdown |
| Pathway description: | In DLK-depleted cells, we noted a substantial decrease in ERK phosphorylation level relative to control , indicating that ERK activity in WI-38 cells is dependent on DLK. we observed that p53 and p21 expression was significantly up-regulated in DLK-depleted cells as compared to cells infected with the control lentiviruses. |
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