| Gene name: | HAS2 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | Lung |
| Cell name: | Fibroblast |
| Gene ID: | 3037 |
| Category: | protein coding |
| Phenotype: | Lung fibrosis |
| Experimental category: | L |
| PMID: | 26987798 |
| Experiment: | Flow cytometry//BrdU assay//SA-β-gal activity assay//Knockdown |
| Description: | Deletion of HAS2 markedly suppressed the proliferation of fibrotic fibroblasts. Flow cytometry analysis revealed that HAS2 depletion significantly increased the proportion of cells in G1 phase.there was less BrdU incorporation in HAS2 siRNA transfected fibroblasts. Most interestingly, the proportion of cells with positive SA-β-gal staining was dramatically increased following HAS2 depletion. |
| Regulatory pathway: | P27-CDK2-SKP2 |
| R-AG-Pathway: | -- |
| Official symbol(s): | PSMD9-CDK2-SKP2 |
| Pathway experiment: | Western blot//Knockdown |
| Pathway description: | p27 protein levels were significantly increased in HAS2 deficient fibrotic fibroblasts at various time points after HAS2 siRNA transfection . Characterization of p27 in the presence of cycloheximide revealed that down-regulation of HAS2 increased p27 protein stability .CDK4 and cyclin B levels were also decreased in HAS2 deficient fibrotic fibroblasts.We observed a decrease (~ 30%) in SKP2 expression in HAS2 deficient fibrotic fibroblasts compared with control transfectants. We found that CDK2 protein levels were dramatically down-regulated upon HAS2 knock down in fibrotic fibroblasts ,which supported the hypothesis that HAS2 deletion-induced proliferative inhibition was through p27 accumulation and its effector pathway. |
Annotation:
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