| Gene name: | LRP8 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | Smooth muscle cell |
| Gene ID: | 7804 |
| Category: | protein coding |
| Phenotype: | Cardiovascular disease |
| Experimental category: | L |
| PMID: | 31412739 |
| Experiment: | SA-β-gal activity assay//Knockdown |
| Description: | In contrast, smooth muscle cells isolated from the aorta or the carotid arteries of Lrp8?/? mice displayed very slow growth rate under the same culturing conditions with significant reduction in population doubling after the first passage. The number of senescence-associated β-galactosidase positive Lrp8?/? cells after 8 days in culture with 10% FBS (≈25%–30%) was higher than the ≈5% to 8% of senescence observed in Lrp8+/+ cells. |
| Target gene: | CDC20-PP2A |
| Official symbol(s): | CDC20 |
| R-AG-Target gene: | -- |
| Subcategory: | Unclear |
| Target gene experiment: | CHIP//Western blot |
| Target gene description: | We used coimmunoprecipitation to analyze the CDC20-PP2A complex formation in Lrp8+/+ and Lrp8?/? smooth muscle cells and found that binding of the regulatory PP2A-B56α subunit to CDC20 does not require apoER2, while binding of the PP2A-C (catalytic subunit of PP2A) to CDC20 requires apoER2 expression . More importantly, while no direct interaction of CDC20 with apoER2 was detected, we observed binding of apoER2 to PP2AC in coimmunoprecipitation experiments with apoER2 antibodies. Since CDC20 interaction with PP2A and aurora kinase dephosphorylation are necessary steps for cell cycle exit,35,36 these data, together with the observation of a trend toward increased CDC20 level in Lrp8?/? smooth muscle cells, is consistent with the interpretation that apoER2 deficiency suppresses PP2A-C interaction with CDC20, thereby preventing its activation to cause cytokinesis impairment and cell cycle arrest. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
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