This product consists of a CRISPR/Cas9-edited polyclonal knockout cell population of HT29 cells, in which the APOBEC3C gene has been disrupted to abolish its cytidine deaminase function. The knockout model is generated using CRISPR/Cas9-mediated gene disruption, resulting in loss of APOBEC3C expression.
The HT29 cell line is a widely used model of colorectal adenocarcinoma, originally derived from a primary tumor of a 44-year-old Caucasian female. These epithelial cells retain the ability to differentiate under appropriate conditions and are extensively employed in studies of intestinal epithelial biology, colorectal cancer progression, and drug transport mechanisms.
APOBEC3C is a member of the APOBEC3 cytidine deaminase family that restricts retroviruses and retrotransposons by inducing C-to-U mutations in single-stranded DNA and RNA. Its expression is strongly upregulated by type I and type II interferons (IFN-??, IFN-??, IFN-??) through the JAK-STAT signaling pathway, involving STAT1, STAT2, and IRF9, as well as through STING-TBK1-IRF3/IRF7 signaling. APOBEC3C interacts with HIV-1 Vif protein, hnRNP proteins, RPA, and other APOBEC3 family members such as APOBEC3B and APOBEC3G. Its primary downstream targets include viral genomes, retrotransposon RNA/DNA, and TCA/TCT motif-containing genomic DNA, leading to APOBEC signature mutagenesis.
In the context of HT29 colorectal cancer cells, APOBEC3C knockout provides a valuable platform to dissect its contributions to tumor-associated mutagenesis and innate immune responses. Loss of APOBEC3C deaminase activity impairs the restriction of endogenous retroelements and diminishes the formation of APOBEC-related mutation signatures commonly observed in colorectal, breast, and lung cancers. This model enables researchers to examine how interferon-mediated antiviral pathways intersect with DNA damage and repair processes in a well-characterized epithelial adenocarcinoma background.
This polyclonal knockout cell population is suitable for a range of applications, including investigation of APOBEC3C-mediated mutagenesis in colorectal cancer, innate immunity to retroviruses and hepadnaviruses, and retrotransposon control. Typical assays include western blotting and RT-qPCR for expression analysis, viral infectivity assays, mutation signature profiling by next-generation sequencing, co-immunoprecipitation for protein interactions, flow cytometry for cell cycle and apoptosis, and MTT assays for drug sensitivity. For more information, contact Ascent Research.
