In Stock Cell Lines
Homo sapiens (Human)
Lung
Adherent
The APOBEC3B Knockout HCC827 Cell Line is a CRISPR/Cas9-edited knockout model derived from the EGFR-mutant HCC827 lung adenocarcinoma cell line. This line enables targeted disruption of the APOBEC3B gene, which encodes a cytidine deaminase that generates C-to-T mutations, particularly in TCW motifs, contributing to cancer mutagenesis and genomic instability. APOBEC3B is regulated by type I interferon signaling and interacts with PCNA during DNA replication. Loss of APOBEC3B in this clinically relevant NSCLC model facilitates investigation of mutation signature formation, drug resistance mechanisms, and APOBEC-dependent tumor evolution, using assays such as targeted deep sequencing and DNA damage immunoblotting.
MYL6B Knockout SK-HEP-1 Polyclonal Cells
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ARHGDIA Knockout Raji Polyclonal Cells
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HMGN3 Knockout jurkat Polyclonal Cells
Cat. No. ARG34261
ASCC2 Knockout AGS Polyclonal Cells
Cat. No. ARG26667
ARMC9 Knockout AGS Polyclonal Cells
Cat. No. ARG26656
The APOBEC3B Knockout HCC827 Cell Line is a genetically engineered human cell line in which the APOBEC3B gene has been disrupted using CRISPR/Cas9 genome editing. Derived from the HCC827 parental line, this product offers a defined knockout model suitable for studying loss-of-function phenotypes associated with APOBEC3B. The cell line is supplied as a stable knockout population and is intended for use in advanced biomedical research, including cancer biology, DNA damage response, and drug discovery applications.
The HCC827 cell line is a widely characterized model of non-small cell lung cancer (NSCLC) harboring an activating deletion in EGFR exon 19 (E746-A750). Originally established from a lung adenocarcinoma of a 39-year-old Caucasian male, HCC827 cells retain key features of EGFR-mutant lung adenocarcinoma and are extensively used to investigate targeted therapy responses and resistance mechanisms. This genetic background provides a clinically relevant platform for assessing the functional impact of APOBEC3B disruption in EGFR-driven tumorigenesis.
APOBEC3B encodes a cytidine deaminase that targets single-stranded DNA during replication, interacting with PCNA to generate C-to-U lesions. Subsequent processing by uracil-DNA glycosylase (UNG) or replication bypass yields C-to-T transitions, preferentially at TCW motifs. Transcription of APOBEC3B is induced by type I interferons through JAK/STAT signaling, mediated by IRF1, IRF3, IRF7, and NF-??B. Persistent activity triggers a DNA damage response via ATM/ATR kinases and ??H2AX phosphorylation, contributing to genomic instability. APOBEC3B can also homodimerize or associate with other APOBEC3 family members.
In lung adenocarcinoma, APOBEC3B overexpression is linked to elevated mutational burden and the acquisition of APOBEC-signature mutations. The HCC827 knockout model enables direct examination of how APOBEC3B loss affects mutation rate, clonal evolution, and drug sensitivity in EGFR-mutant NSCLC. By eliminating the endogenous mutagenic enzyme, researchers can discern APOBEC3B-dependent from independent processes and evaluate whether its activity promotes resistance to EGFR inhibitors or other therapies.
This knockout line is suitable for a range of experimental approaches, including western blotting and Sanger sequencing to verify loss of APOBEC3B expression, targeted deep sequencing to monitor mutational signature dynamics, and supF shuttle vector assays to measure mutation frequency. Additional applications encompass immunofluorescence localization studies, drug sensitivity profiling with agents such as cisplatin or PARP inhibitors, and RNA-seq to characterize transcriptome-wide consequences of APOBEC3B disruption. The model also supports screens for small-molecule modulators of APOBEC3B activity. For further details or technical inquiries, please contact Ascent Research.
