| Gene name: | CDKN2A |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | AECII |
| Gene ID: | 1029 |
| Category: | protein coding |
| Phenotype: | Chronic obstructive pulmonary disease |
| Experimental category: | HL |
| PMID: | 31428695 |
| Experiment: | SA-β-gal activity assay//Knockdown//EdU assay |
| Description: | In vivo cell proliferation was assessed by EdU incorporation. Deleting p16 significantly increased cell proliferation from 3.6% to 5.3%.When exposed to CSE, the percentage of senescent p16+/+ AECIIs increased as assessed by flow β-gal activity. Deletion of p16 completely prevented the CSE-induced senescence of AECII (p16+/+ CS vs. p16?/? CS). |
| Target gene: | CYCLIN D |
| Official symbol(s): | CYCLIN D |
| R-AG-Target gene: | -- |
| Subcategory: | Unclear |
| Target gene experiment: | Western blot |
| Target gene description: | There was a much larger increase in cyclin D in p16?/?compared with p16+/+lungs upon CS exposure, supporting the observation of enhanced cell proliferation and regeneration in p16?/?lung. |
| Regulatory pathway: | IGF-1-AKT1 |
| R-AG-Pathway: | -- |
| Official symbol(s): | IGF1-AKT1 |
| Pathway experiment: | qRT-PCR//Western blot//Knockdown |
| Pathway description: | Deletion of p16 increased IGF1 mRNA and protein. This translated to a 7.83-fold increase in IGF1 protein in p16?/? lung compared with p16+/+.Similarly, total Akt was substantially elevated in p16?/? lungs and increased with CS. |
Annotation:
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