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"24 The absence of p53 increases cell proliferation in vivo and accelerates atherosclerosis.26 Besides, it is proved that p53 deficiency enhances the LPS-induced ALI in vivo.25 Caveolin-1 is identified a novel transduction factor and involved in the progression of pulmonary emphysema by activating ATM-p53-p21 pathway.28 Moreover, in COPD patients, p53/p21 pathway can be activated by up-regulating USP7 to mediate cell premature senescence."
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"The collective results indicate that USP7 deubiquitinates and stabilizes PRMT1 under high glucose conditions.Based on the finding that p53 overexpression induced downregulation of USP7 in A549 and H1299 cells (Fig. 5L) and USP7 expression was significantly increased upon the addition of pifithrin-α when cells were grown under glucose insufficiency (Fig. 5M), we further investigated the involvement of USP7 in modulation of PRMT1 by p53."