In Stock Cell Lines
Homo sapiens (Human)
Liver
Adherent
The RB1CC1 Knockout Hep-G2 Cell Line provides a CRISPR/Cas9-edited loss-of-function model for studying autophagy and mTOR signaling in a human hepatocellular carcinoma background. RB1CC1 scaffold protein is essential for assembly of the ULK1-ATG13-FIP200 complex, and its disruption impairs downstream events such as Beclin1 recruitment, LC3 lipidation, and p62 degradation. This cell line is ideal for autophagy mechanism studies, liver cancer research, and drug metabolism screening using assays like LC3 western blotting, autophagic flux monitoring, and CYP activity analysis. It supports investigations into RB1CC1-mediated regulation of cell proliferation and hepatocyte function.
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NME6 Knockout Hela Polyclonal Cells
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MC3R Knockout MCF7 Polyclonal Cells
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Rabbit Liver Sinusoidal Endothelial Cells
Cat. No. ARP0722
The RB1CC1 Knockout Hep-G2 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the human Hep-G2 hepatocellular carcinoma line. This model features targeted disruption of the RB1CC1 gene, which encodes a key scaffold protein essential for autophagy initiation. The engineered line provides a stable loss-of-function platform for investigating the cellular consequences of RB1CC1 deficiency in a liver cancer context.
Hep-G2 is a widely used human liver epithelial cell line originally derived from a 15-year-old male with hepatocellular carcinoma. These cells retain many differentiated hepatic functions, making them a standard in vitro system for studying liver metabolism, drug metabolism, and hepatocarcinogenesis. Their well-characterized phenotype and robust growth make them suitable for gene-editing applications aimed at dissecting signaling pathways that regulate liver cell physiology and pathology.
RB1CC1, also known as FIP200, functions as a molecular scaffold within the ULK1-ATG13-FIP200 complex, which is a critical regulator of autophagy induction. This complex is activated upstream by nutrient-sensing kinases such as mTOR and AMPK, and it is under transcriptional control by TFEB. Once assembled, RB1CC1 facilitates the recruitment of downstream effectors including Beclin1, VPS34, and ATG14 to promote autophagosome nucleation and LC3 lipidation, while also mediating the degradation of autophagic cargo receptors like p62/SQSTM1. Through these interactions, RB1CC1 integrates signals from mTOR and AMPK pathways to coordinate autophagic flux with cellular energy status and growth factor availability.
Disruption of RB1CC1 in the Hep-G2 background is predicted to severely impair autophagy, leading to accumulation of damaged organelles and protein aggregates, and dysregulation of mTOR signaling. In hepatocellular carcinoma cells, autophagy plays dual roles in tumor suppression and promotion, and RB1CC1 loss may sensitize cells to nutrient stress or alter proliferative capacity. This model thus allows researchers to dissect autophagy-dependent versus autophagy-independent functions of RB1CC1 in liver cancer cell survival, metabolism, and drug response, providing a physiologically relevant hepatic environment.
The RB1CC1 Knockout Hep-G2 Cell Line is a versatile tool for a wide range of experimental applications. It is particularly suited for autophagy mechanism studies using LC3-II and p62 western blotting, LC3 immunofluorescence, and autophagic flux assays. In liver cancer research, the line enables cell proliferation assays, drug sensitivity testing, and CYP activity assays to evaluate metabolic competence and hepatotoxicity. Additionally, it serves as an ideal model for gene-editing method development in hepatic systems. For further details or inquiries regarding this product, please contact Ascent Research.
