Gene name: | MYC |
Aging type: | Accelerate |
Aging characteristic: |
Tissue type: | -- |
Cell name: | IMR-90 |
Experiment: | Crystal violet assay//SA-β-gal activity assay//BrdU assay//qRT-PCR//GSEA analysis |
Description: | Expression of the reprogramming factors (OSKM) in IMR90 human fibroblasts causes a senescence-like growth arrest that constitutes an intrinsic barrier to reprogramming (Banito et al. 2009). Similar to oncogenic RASG12V, the expression of OSKM induces the cyclin-dependent kinase (CDK) inhibitors (CDKIs) p15INK4b, p16INK4a, and p21CIP1, which are involved in implementing the stable growth arrest associated with senescence. Gene set enrichment analysis (GSEA) found signatures for senescence and the SASP significantly enriched in the transcriptome of cells expressing OSKM. |
Target gene: | CDKN1A//MYOT//MTOR//UBE2E1 |
Official symbol(s): | CDKN1A//MYOT//MTOR//UBE2E1 |
R-AG-Target gene: | --//--//--//-- |
Subcategory: | Unclear |
Target gene experiment: | Crystal violet staining//SA-β-gal activity assay//BrdU assay |
Target gene description: | The ability of shRNAs targeting CDKN1A, MYOT, MTOR, and UBE2E1 to prevent OSKM-induced senescence was confirmed by increased proliferation, a higher percentage of cells incorporating BrdU, and a decrease in the percentage of senescence-associated βgalactosidase (SA-β-Gal)-positive cells when compared with IMR90 cells infected with OSKM and a control vector . |
Regulatory pathway: | TGFβ |
R-AG-Pathway: | -- |
Official symbol(s): | TGFB1 |
Pathway experiment: | BrdU assay//Follow-up analysis |
Pathway description: | Moreover, inhibition of TGFBRI signaling blunted the growth arrest triggered by OSKM. In this regard, the scRNA-seq data and the follow-up analysis highlighted that TGF-β signaling was induced by OSKM . |
Annotation:
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