3results about How to "Improve induction ability" patented technology

This invention belongs to the field of biomedicine and regenerative medicine technology. It discloses a chimeric polypeptide, related biomaterials, and their application in inducing cardiomyocytes. The chimeric polypeptide is obtained through family homologous domain substitution and is selected from the following groups: (1) a MEF2 chimeric polypeptide with MEF2C protein as the backbone, wherein the N-terminal and C-terminal transcriptional activation domains are replaced by homologous regions of MEF2B and MEF2D, respectively; (2) a GATA chimeric polypeptide with GATA4 protein as the backbone, wherein the N-terminal transcriptional activation domain is replaced by homologous regions of GATA1 and GATA6. This invention also provides the nucleic acid encoding the polypeptide, the construct, and a method for efficiently inducing fibroblast reprogramming into cardiomyocytes under in vitro conditions. When the chimeric polypeptide of this invention is used alone or in combination, the induced cells exhibit calcium ion oscillations earlier and have higher maturity.

This invention relates to the field of breast cancer therapeutics, providing a novel application of *Dendrobium nobile*, specifically the application of dendrobine in the preparation of breast cancer therapeutics. This invention verifies that dendrobine can significantly inhibit breast cancer cell viability. The inhibitory effect of dendrobine on the migration and proliferation of T47D breast cancer cells and its ability to induce cell death increases with increasing dosage. Simultaneously, cloning experiments also show that dendrobine significantly inhibits the colony-forming ability of breast cancer cells. ROS and JC-1 experiments also show that dendrobine induces mitochondrial dysfunction and increases ROS levels. Western blot experiments show that under dendrobine treatment, the expression levels of ferroptosis markers GPX4 and Nrf2 are significantly reduced. Dendrobine can promote ferroptosis in breast cancer cells and inhibit their cell viability by inducing mitochondrial dysfunction, and it holds promise as a breast cancer therapeutic drug specifically targeting ferroptosis.