| Gene name: | HOPX |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | HBEC,Y-BE |
| Gene ID: | 84525 |
| Category: | protein coding |
| Phenotype: | Lung cancer |
| Experimental category: | HL |
| PMID: | 25345926 |
| Experiment: | SA-β-gal activity assay//Cell morphological analysis |
| Description: | SA-β-Gal staining showed that HOPX transfectant cells displayed cellular enlargement and flattening as well as positivity for SA-β-Gal staining. Additionally, cells exhibited senescence-associated nuclear properties, including elevation of SAHF and accumulation of p-H2AX (gamma-H2AX, Ser139). Forced expression of HOPX in immortalized human bronchial epithelial cells Y-BE led to increased SA-β-Gal staining activity, while knockdown of HOPX in HBECs resulted in decreased SA-β-Gal positive staining, indicating that HOPX-mediated senescence is not restricted to malignant cells. |
| Regulatory pathway: | RAS-MAPK//AKT |
| R-AG-Pathway: | Activation//Downregulation |
| Official symbol(s): | KRAS-MAPK//AKT1 |
| Pathway experiment: | Western blot |
| Pathway description: | We found that ectopic expression of HOPX resulted in activation of Ras in both HOPX-positive transfectants HOPX-3 and HOPX-V5-7, as revealed by Ras GTPase assay, which in turn led to activation/phosphorylation of ERK and p38, two major players of the MAPK pathway.Overexpression of HOPX led to inactivation of Akt and down-regulation of MDM2, a negative regulator of p53, as well as the p53 downstream target p21.Decreased expression of HOPX led to reversed effects on the Ras/MAPK pathway and the Akt pathway, with reduced phosphorylated levels of ERK and p38, as well as increased phosphorylated levels of Akt, MDM2, and down-regulation of p21. |
Annotation:
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