We elucidated that cell cycle progression and cell growth are separable and distinct. Furthermore, mTOR controls mammalian cell size and cell cycle progression via its downstream targets. Although both cell size and cell cycle progression are controlled by mTOR and mTOR-dependent signaling pathways, the nutrient responsive signaling molecule is centrally positioned to couple cell growth with cell division when the cells are cultured under the same conditions in which nutrients are restricted. With the evidence that cell cycle progression is dependent on a sufficient level of cell growth, mTOR primarily drives cell growth and as a secondary consequence, promotes cell cycle progression. In vivo, the fiber size in Landrace pigs was larger, whereas there were fewer fibers in Lantang pigs. The SC cell size in Landrace pigs was also larger than in Lantang pigs in vitro. There was a negative correlation between the pulmonary resistance in asthma mice and the levels of Clofentezine CTNNAL1 mRNA in the 8-day time course after the OVA challenge. It is conceivable that CTNNAL1 contributes to BEC constitutive adhesion. In vitro experiments showed that the rate of repair and proliferation of HBEC was slowed down after HBEC was treated with CTNNAL1 ASO, and CTNNAL1 expression was explicitly increased on the cells in wound edges. Those data indicate that CTNNAL1 might be involved in growth regulation and may be beneficial for the recovery of bronchial epithelium damage. In an attempt to identify the response of CTNNAL1 to acute stress, we observed the CTNNAL1 expression under an ozone stressed condition. As shown in this study, CTNNAL1 mRNA was increased both in lungs and in cultured HBEC with the acute ozone stress. Taken together, our results suggest that CTNNAL1 is involved in maintaining the Cefetamet pivoxil HCl integrity of the airway epithelium and down regulation of CTNNAL1 expression might contribute to epithelial dysfunction and asthma development. CTNNAL1 upregulation under acute stress conditions might be a protective response. The next question is the mechanisms regarding the regulation of CTNNAL1 expression in HBECs. Although several studies have shown the significance of altered CTNNAL1 expression, and the exon-intron organization and boundary sequences flanking 19 exons of the human CTNNAL1 gene have been reported recently, the mechanism underlying the regulation of CTNNAL1 expression has not been elucidated yet. In order to explore the mechanisms of transcriptional regulation of the CTNNAL1 gene, we identified some potential DNA-binding proteins that can be recruited to CTNNAL1 promoter region and may play roles in the regulation of the transcription of CTNNAL1 gene in this study.