External factors: | CAPERα-TBX3 repressor complex |
Aging type: | Prevent |
Aging characteristic: |
Category: | Other |
Phenotype: | Aging |
Experiment: | Knockdown//SA-β-gal activity assay//Immunostaining//qRT-PCR//Western blot |
Description: | Knockdown of either protein resulted in a dramatic increase in senescence associated β-galatosidase activity.This effect is specific because it occurs with two different shRNAs and is rescued by overexpression of CAPERα and Tbx3. Expression of senescence mediators was increased and conversely, expression of cell growth and cell cycle promoting genes was similarly decreased by CAPERα and TBX3 KD . |
Target gene: | LNCRNA UCA1 |
R-EF-Target gene: | Downregulation |
Official symbol(s): | LNCRNA UCA1 |
Target gene experiment: | qRT-PCR//CHIP-PCR |
Target gene description: | We found that shRNA KD of CAPERα or TBX3 in primary HFFS recapitulated the increase in UCA1 transcripts seen in HEK293 cells.After TBX3 KD, activating chromatin marks replaced repressive ones and markedly less CAPERα was bound. CAPERα KD also led to loss of repressive marks on UCA1/A3 , although TBX3 remained bound . |
Regulatory pathway: | p16-Rb |
R-EF-Pathway: | Downregulation |
Official symbol(s): | CDKN2A-RB1 |
Pathway experiment: | Knockdown//SA-β-gal activity assay//qRT-PCR |
Pathway description: | Increased expression of CDKN2A-p16INK (henceforth referred to as p16INK) and decreased PCNA, E2F1 and 2, CDK2, CDK4, CDC2 transcripts indicate that CAPERα/TBX3 represses the p16/RB pathway in proliferating HFFs.In contrast, shRNA-mediated KD of either RB or p16 rescued these phenotypes in TBX3 and CAPERα KD cells . |
Annotation: