Knockout Cell Lines

This study completed the Chinese Liver Cancer Atlas (CLCA) and three newly identified potential driver events were also selected for detailed functional verification. It was found that mutations in the above genes were sufficient to cause significant changes in gene expression levels (Among them, PPP1R12B, KCNJ12, FGA knockout cells and overexpression lentiviruses carrying mutations were all constructed by Ubigene), and were involved in regulating various malignant phenotypes of hepatocellular carcinoma, These results confirm the validity of the new driving events found based on data analysis.View details>>

to study the regulation mechanism of cGAS activity in order to prevent and treat viral diseases, a research team leading by Prof. Zhao[1] in Shandong University used the HeLa cell line with STING1 gene knockout constructed by Ubigene as the key cell model, and found out that the two conformations of DNA (B-DNA and Z-DNA) had different affinity with cGAS; The endogenous metabolism of small molecules spermine, spermidine and polyamine catabolism key enzyme SAT1 regulates cGAS activity by inducing DNA conformational transition. This research reveals a additional mechanism for preventing abnormal cytoDNA recognition and providing promising therapeutic targets for the treatment of diseases involving improper cGAS activation. View details>>

In this study, the HCT116 cell line with TP53 gene knocked out constructed by Ubigene was used. By analyzing the crystal structure of the complex of p53 and the anti-apoptotic protein BCL-2, and combining biochemical and cellular experiments, this study revealed a new mechanism of p53 interacting with BCL-2 protein and promoting apoptosis, that is, p53 forms a complex with BCL-2 by directly occupying the BH3-binding pocket of BCL-2, and antagonizes BCL-2 activity by releasing pro-apoptotic BCL-2 family proteins located in the pocket, thereby promoting apoptosis[2].These structural and functional data provide a new idea for further understanding the complex regulatory mechanism of p53-mediated mitochondrial apoptosis, and also provide an important basis for developing anticancer therapeutic strategies that target protein-protein interactions to activate apoptosis. View details>>

ZNF protein was confirmed as a key factor regulating the genome integrity of mammalian cells. In order to explore the possibility that ZFP can be used as an effector of DNA repair based on homologous recombination (HR), Jean Yves Masson[3] team of Laval University used the ZNF432 knockout U2OS cell line constructed by Ubigene to carry out a series of experiments, and found that ZNF432 deletion in cancer cells would accelerate DNA repair, lead to the weakening of PARPi effect, and make ovarian cancer cells develop drug resistance, confirming that ZNF432 is a new HR inhibitor, which successfully broadened the new way to study the efficacy of PARPi. View details>>

This study reveals the regulatory role of small nucleolar RNA SNORD17 and p53 pathway in hepatocellular carcinoma, which provides a new potential target for the treatment of hepatocellular carcinoma[5] . The researchers utilized SNORD17 knockout Hep G2 cell line (constructed by Ubigene) as the key cell model. After applied with in vitro and in vivo tests, they found out that in HCC cell lines, the knockout of SNORD17 gene can significantly inhibit cell proliferation, clone formation and G1/S phase transition. View details>>

This article explores a new mechanism for GSTP1 affecting the osteoclast cell-related bone homeostasis through combining with a large number of in vivo and in vitro experiments, based on the Pik3r1 knockout RAW264.7 cell model constructed by Ubigene. It was the first time to interpret that the cell fate of osteoclasts is determined by S-glutathionylation via a redox-autophagy which is mediated by GSTP1. View details>>