The APOL2 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the APOL2 gene has been disrupted in the HEK293T human embryonic kidney cell line. This pooled model provides a loss-of-function system for studying APOL2 without clonal selection, maintaining population-level heterogeneity. The cells are supplied as a polyclonal stock ready for expansion and downstream assays.
HEK293T is an immortalized epithelial cell line derived from human embryonic kidney, stably expressing the SV40 large T antigen for episomal plasmid replication. Widely used for protein expression and viral production, it offers high transfection efficiency and well-characterized signaling networks. This background supports robust functional genomics and genetic perturbation studies, making it a suitable host for investigating APOL2??s role in apoptosis and autophagy.
APOL2 encodes a lipid-binding protein that sensitizes cells to apoptosis by interacting with BCL2 family proteins BCL2L1, BAK1, and BCL2, promoting mitochondrial outer membrane permeabilization. It also regulates autophagy through binding BECN1 and modulating the ATG5?CMAP1LC3B conjugation system. APOL2 transcription is activated by TP53, TNF, IFNG, and NF-??B, and its downstream signaling involves BECN1, ATG5, and MAP1LC3B, with CASP3 executing apoptosis. This network integrates stress and immune signals to control cell death and survival.
In HEK293T cells, APOL2 knockout enables precise dissection of apoptosis?Cautophagy crosstalk, highlighting its relevance to cancer and neurodegenerative disorders. APOL2 is implicated in renal cell carcinoma and drug resistance, and genetic links to schizophrenia and bipolar disorder broaden the research scope. The polyclonal model avoids clonal artifacts, while HEK293T??s efficient transfection supports complementation assays and high-content mechanistic studies.
Research applications include Western blot and RT?qPCR for target validation, Annexin V/7?AAD apoptosis assays, LC3?I/II autophagy flux analysis, and co?immunoprecipitation of APOL2 with BCL2L1, BAK1, or BECN1. The cells are amenable to high?throughput screening for modulators of APOL2?mediated cell death pathways. For additional information, please contact Ascent Research.
