Summary of maternal SMC2 functions during oocyte growth, maturation and zygote development. In oocytes, the SMC2-deleted oocytes have defects in NSN-SN transition in GV stage, and further chromosome condensation. After fertilization, Depletion of maternal SMC2 causes abnormal nuclear morphology, impaired pronuclear function and accumulated DNA damage, which prevented the development of embryos beyond the zygote stage.

OTUD4 acts as a novel deubiquitinase of Snail1 in melanoma. The depletion of OTUD4 in melanoma cells markedly inhibited Snail1 stability and Snail1-driven malignant phenotypes both in vitro and in vivo.

PI3Kγ/Akt plays an important role in the physiological and mechanically induced maxillary. The absence of the PI3Kγ enzyme and the loss of its kinase activity increased maxillary bone mass and root volume. Accordingly, PI3Kγ^−/− mice exhibited a reduction in bone remodeling induced by mechanical loading with less OTM and opening of the maxillary suture. The mechanisms involve greater reduction of p-Akt protein, differentiation of osteoblasts, as demonstrated by cell counts and increased expression of Runx2 and Alp under steady-state conditions. Moreover, under mechanical stimulation, PI3Kγ^−/− mice showed lack of osteoclast responsiveness, which was possibly linked to a reduced expression of Rank and Il-6.

Primary cilium on most mammalian cells is a microtubule structure protruding from cell surface where many receptors and ion channels such as TRPV4 are localized. In this study, primary cilia of rat calvarial osteoblasts were found to become shorter and even disappeared when the cells were exposed to a random positioning machine-simulated microgravity, accompanied by increased expression and overactive Ca²⁺ channel of TRPV4, which induced overload Ca²⁺ influx, mitochondrial dysfunction, oxidative stress, and loss of osteogenesis. Protection of primary cilia by overexpression of miR-129-3p or moslosooflavone prevented the TRPV4-mediated overload Ca²⁺ influx and all above-mentioned changes, indicating that protection of primary cilia should be an effective countermeasure to the simulated microgravity-induced oxidative stress and loss of osteogenic potential of osteoblasts.