| Gene name: | PIM1 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | Heart left ventricle |
| Cell name: | hCPC |
| Gene ID: | 5292 |
| Category: | protein coding |
| Phenotype: | Heart failure |
| Experimental category: | HL |
| PMID: | 25882843 |
| Experiment: | SA-β-gal activity assay//Cell morphological analysis |
| Description: | SA β-gal positive cells were least prevalent in Nuc-Pim1 hCPCs, with a ?30.25% decrease (p < 0.001) as compared with Nuc-GFP.Longer, spindle-shaped hCPCs were evident after Nuc-Pim1 modification as measured by the length to width ratio and cell roundness. Concurrently, Nuc-Pim1 modification increased the Hayflick limit of hCPCs as compared with PimWT, prolonging the post-mitotic phenotype as demonstrated by the extended expansion capability of modified cells .PimWT and Mito-Pim1 modification resulted in a reduction of SA β-gal+ cells. |
| Target gene: | P53//P16//NS |
| Official symbol(s): | P53//P16//KRAS |
| R-AG-Target gene: | Downregulation//Downregulation//Upregulation |
| Subcategory: | Unclear |
| Target gene experiment: | Western blot//qPCR |
| Target gene description: | Gene and protein expression of the cell cycle arrest/senescence marker p53 decreased after Nuc-Pim1 modification with a 1.15-fold reduction of mRNA and a 1.45-fold reduction of protein, as measured by qPCR and immunoblot analysis, respectively.Concurrent down-regulation of the p16 gene and protein expression occurred in Nuc-Pim1 hCPCs as evident by 1.85- and 1.96-fold reductions, respectively. A highly significant increase in NS gene expression resulted from Nuc-Pim1 expression in hCPCs (2.59-fold, p < 0.001) compared with PimWT and Mito-Pim1, as measured by qPCR analysis. Concurrent up-regulation of Ns protein expression was also detected in Nuc-Pim1 hCPCs (2.17-fold, p < 0.01) compared with controls . |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
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