Abstract: The present disclosure relates to a composition for preventing or treating fibrosis including an inhibitor of cyclin-dependent kinase 17 (CDK17) expression or activity. According to the present disclosure, the inhibitor of CDK17 expression or activity significantly reduces collagen production and cell activity and viability in activated hepatic stellate cells (liver fibrosis cell model), renal tubular epithelial cells (renal fibrosis cell model) in which fibrosis is induced by TGF-? treatment, and alveolar epithelial cells (lung fibrosis cell model) in which fibrosis is induced by TGF-? treatment, indicating that the composition of the present disclosure has an excellent effect in preventing or treating fibrosis.

Abstract: A semiconductor device is provided. The semiconductor device includes a first stacked structure including a plurality of first insulating patterns and a plurality of first semiconductor patterns alternately stacked on a substrate, the first stacked structure extending in a first direction parallel to an upper surface of the substrate, a first conductive pattern on one side surface of the first stacked structure, the first conductive pattern extending in a second direction crossing the upper surface of the substrate, and a first ferroelectric layer between the first stacked structure and the first conductive pattern, the first ferroelectric layer extending in the second direction, wherein each of the first semiconductor patterns includes a first impurity region, a first channel region and a second impurity region which are sequentially arranged along the first direction.

Abstract: The present disclosure relates to a novel use of CMTR1 having the activity of enhancing the production and function of siRNA, and more particularly, to a composition for enhancing the production of siRNA including a cap1 2?-O-ribose methyltransferase (CMTR1) protein as an active ingredient, and a composition for enhancing the gene silencing activity by siRNA, and also to a method for producing siRNA for gene silencing in vitro. According to the present disclosure, the CMTR1 may enhance the production of siRNA for gene silencing and at the same time, ultimately enhance the production and function of siRNA without artificial chemical modification of siRNA by enhancing the formation of holo-RNA-induced silencing complex (RISC) that acts on silencing of a target gene in an RNAi mechanism. Therefore, the CMTR1 of the present disclosure can be usefully used in the development of pharmaceuticals using siRNA as a therapeutic agent.

Abstract: The present invention relates to a composition or cell therapeutic agent for preventing or treating liver fibrosis, containing an exosome or exosome-derived ribonucleic acid. The exosome or ribonucleic acid derived therefrom, of the present invention, has effects of inhibiting activities of hepatic stellate cells and Kupffer cells and reducing the expression of ?-SMA and inhibits the progression of liver fibrosis by inhibiting the deposition of collagen, thereby being effectively usable as a cell therapeutic agent for the prevention or treatment of liver fibrosis.

Abstract: The present disclosure relates to a composition for preventing or treating fibrosis including an inhibitor of cyclin-dependent kinase 17 (CDK17) expression or activity. According to the present disclosure, the inhibitor of CDK17 expression or activity significantly reduces collagen production and cell activity and viability in activated hepatic stellate cells (liver fibrosis cell model), renal tubular epithelial cells (renal fibrosis cell model) in which fibrosis is induced by TGF-? treatment, and alveolar epithelial cells (lung fibrosis cell model) in which fibrosis is induced by TGF-? treatment, indicating that the composition of the present disclosure has an excellent effect in preventing or treating fibrosis.

Abstract: The present invention relates to a composition or cell therapeutic agent for preventing or treating liver fibrosis, containing an exosome or exosome-derived ribonucleic acid. The exosome or ribonucleic acid derived therefrom, of the present invention, has effects of inhibiting activities of hepatic stellate cells and Kupffer cells and reducing the expression of ?-SMA and inhibits the progression of liver fibrosis by inhibiting the deposition of collagen, thereby being effectively usable as a cell therapeutic agent for the prevention or treatment of liver fibrosis.