Gene name: | SGK1 |
Aging type: | Prevent |
Aging characteristic: |
Tissue type: | -- |
Cell name: | HUVEC,SGK1WT |
Gene ID: | 6446 |
Category: | protein coding |
Phenotype: | Atherosclerosis |
Experimental category: | L |
PMID: | 26230157 |
Experiment: | SA-β-gal activity assay//Telomerase activity assay |
Description: | Infected HUVEC lines have been cultured until the last stage of senescence, represented as arrest of cellular proliferation (PDL16). During serial passages of HUVEC, the activity of SA-β-gal in control pLPCX and in SGK1Δ60 increased by ~5-6-fold from PDL6 to PDL16. SGK1WT was able to significantly reduce SA-β-gal activity (by 2-fold) compared with SGK1Δ60 and pLPCX cellular groups at PDL8 (p<0.0005). SGK1WT cells showed a significant increase in telomerase activity at PDL8 compared with both PDL6 (p<0.05), and PDL13 (p<0.005). |
Target gene: | HTERT |
Official symbol(s): | HTERT |
R-AG-Target gene: | -- |
Subcategory: | Unclear |
Target gene experiment: | Co-IP//Pull-down assay//Flow cytometry//Immunostaining |
Target gene description: | We found that SGK1 co-immunoprecipitates with hTERT in all cellular constructs, proving a protein-protein interaction. However, a different shift was observed between total SGK1Δ60 and hTERT immunoprecipitate, suggesting that hTERT interacts only with SGK1 full length,and further supporting the previously reported inactivity of SGK1Δ60 in delay endothelial aging. To confirm these results we performed a GST pull-down assay which established the direct interaction between SGK1 and hTERT, similarly to what we observed with previous used methodology.However, a significant decrease in ROS production was evident in the cells overexpressing SGK1WT compared with both control, and SGK1Δ60 construct (p<0.005). |
Regulatory pathway: | -- |
R-AG-Pathway: | -- |
Pathway experiment: | -- |
Pathway description: | -- |
Annotation:
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