In Stock Cell Lines
Homo sapiens (Human)
Uterus (cervix)
Adherent
CRISPR/Cas9-edited RB1CC knockout HeLa cell line targeting the autophagy scaffold protein RB1CC (RB1CC1/FIP200). This model enables functional studies of ULK1 complex assembly, mTORC1-AMPK signaling, and cross-talk with cell cycle regulators such as RB1 and p53. Derived from cervical adenocarcinoma HeLa cells, the knockout line is ideal for autophagy flux assays, protein interaction studies, and cancer drug resistance research, offering insights into tumor suppression and neurodegenerative disease mechanisms.
MARVELD2 Knockout Hela Polyclonal Cells
Cat. No. ARG8258
C1orf174 Knockout HEK293T Polyclonal Cells
Cat. No. ARG25879
AMDHD2 Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG30316
KANK2 Knockout HGC-27 Polyclonal Cells
Cat. No. ARG30087
DLG1 Knockout 786-O Polyclonal Cells
Cat. No. ARG38870
METTL7B Knockout AGS Polyclonal Cells
Cat. No. ARG2301
The RB1CC Knockout HeLa Cell Line is a CRISPR/Cas9-edited human knockout cell line designed for targeted disruption of the RB1CC gene, which encodes the autophagy scaffold protein RB1CC (also known as RB1CC1/FIP200). This loss-of-function model is generated in the HeLa host cell background and provides a powerful tool for dissecting the roles of RB1CC in autophagy initiation, mTOR signaling, and cell cycle regulation. The line is suitable for a wide range of functional studies, including biochemical pathway analysis, protein interaction mapping, and cellular response assays under stress conditions.
HeLa cells, the first immortal human cell line, were derived from a cervical adenocarcinoma and are one of the most extensively characterized model systems in biomedical research. They exhibit robust proliferation, stable karyotype, and high transfection efficiency, making them a preferred platform for gene editing and cancer biology investigations. Their immortalized yet tumorigenic nature allows for long-term culture and reproducible results in studying oncogenic signaling, tumor metabolism, and drug sensitivity.
RB1CC1 acts as a critical scaffold that nucleates the ULK1 kinase complex??comprising ULK1, ATG13, ATG101, and itself??to initiate autophagosome formation upon nutrient deprivation or stress. This complex is negatively regulated by mTORC1 under nutrient-rich conditions and activated by AMPK during energy stress. RB1CC1 also directly binds RB1, contributing to cell cycle arrest through modulation of cyclin D/E expression, and interacts with p53 and TSC1, thereby integrating signals from tumor suppressive networks. Downstream events include the recruitment of the PI3K complex (VPS34/Beclin1/ATG14), LC3 lipidation, and selective autophagy receptor p62/SQSTM1 degradation.
In the HeLa background, where p53 function is compromised due to HPV E6-mediated degradation, the RB1CC knockout enables dissection of p53-independent autophagy mechanisms and tumor suppressor pathways. This model is particularly valuable for studying how RB1CC orchestrates ULK1 complex assembly and autophagic flux without the confounding influence of intact p53 signaling. Furthermore, it allows assessment of RB1CC’s role in cell cycle progression and proliferation in a context where RB1-mediated G1 arrest may be altered.
Key research applications include autophagic flux assays using bafilomycin A1 treatment combined with LC3-II and p62 Western blotting, immunofluorescence staining of LC3 puncta, co-immunoprecipitation of ULK1 complex components, cell cycle profiling by flow cytometry, and clonogenic survival assays to evaluate tumorigenic potential. This knockout line is also suitable for investigating resistance to chemotherapeutics and targeted agents in autophagy-dependent cancers, as well as for modeling neurodegenerative aspects in vitro. For additional information, please contact Ascent Research.
