The CARM1 Knockout HEK293T Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the CARM1 gene in the HEK293T human cell line. This loss-of-function model provides a heterogeneous mixture of cells with gene disruption, enabling robust functional studies without requiring single-cell cloning. It serves as an essential tool for dissecting CARM1-dependent signaling and transcriptional regulation, offering researchers a cost-effective knockout model with preserved cellular diversity.
HEK293T cells are a derivative of the human embryonic kidney HEK293 line, stably transformed with the SV40 large T antigen. This allows episomal replication of SV40 origin-containing plasmids, yielding high transient protein expression and efficient viral packaging. Widely used for recombinant protein production and functional genomics, HEK293T cells exhibit high transfection efficiency and robust growth, making them an optimal host for gene-editing experiments and subsequent mechanistic investigations.
CARM1 (PRMT4) catalyzes asymmetric dimethylation of arginine residues on histone H3 (R17, R26) and non-histone substrates such as BAF155 and RNA polymerase II CTD. It acts as a transcriptional coactivator recruited by p160/SRC proteins (NCOA1, NCOA2, NCOA3) and associates with p300/CBP to drive nuclear receptor-mediated gene activation. Its activity is regulated by E2F1, MYC, AKT1, and OGT, and it modulates pre-mRNA splicing through SRSF1 methylation, integrating hormone, NF-??B, p53, and Wnt pathways.
In the HEK293T background, CARM1 knockout disrupts its coactivator function, providing a clean platform to study signal-dependent transcription and chromatin regulation. The high transfection efficiency facilitates reconstitution with wild-type or mutant CARM1 and combinatorial manipulations with coactivators like p300. Researchers can measure epigenetic changes via ChIP for H3R17me2a, assess hormone receptor activity with luciferase reporters, and profile transcriptomes by RNA-seq, offering insights into CARM1??s role in cancers where it is deregulated.
This polyclonal knockout model supports drug target validation, epigenetic profiling, and functional genomics. In cancer research, it enables assessment of CARM1 dependence in proliferation, migration, and colony formation. Signaling studies can employ NF-??B or ??-catenin/TCF reporters to map pathway alterations. Co-immunoprecipitation and proteomics identify CARM1-associated complexes and substrates. It is also applicable to metabolic disease research, such as adipogenesis regulation. For more information or custom services, please contact Ascent Research.
