SQSTM1 Knockout HEK293 Cell Line

The choice depends on whether you are studying p62's signaling functions or its scaffolding roles in NF-κB and Nrf2 pathway activation — applications where HEK293's high transfection efficiency provides advantages. The Knockout line is appropriate for biochemical studies of these signaling pathways and for reporter assay-based mechanism research. Overexpression is useful for testing condensation behavior, scaffolding capacity, and reporter readouts of NF-κB or ARE/Nrf2-driven gene expression. For p62 mechanistic research, the EDITGENE p62 Knockout in HEK293 is particularly suited to reporter-based and biochemical studies — HEK293 supports robust NF-κB-luc and ARE-luc reporters, and its transfection efficiency facilitates rapid structure-function screening. This product complements the parallel p62 Knockout in HeLa (preferred for imaging-based autophagy phenotypes). Rescue with wild-type or domain-mutant (PB1, ZZ, UBA, LIR, KIR) p62 enables systematic mapping of p62's multi-domain functions.

Primary applications: • NF-κB pathway: NF-κB reporter assays and target gene expression analysis to assess p62's scaffolding function in NF-κB activation. • Nrf2/Keap1 pathway: ARE-driven reporter assays (HMOX1, NQO1) and Keap1 sequestration analysis given p62's role in non-canonical Nrf2 activation. • mTORC1 regulation: phospho-S6K and phospho-4E-BP1 analysis to assess p62's contribution to amino acid-dependent mTORC1 activation. • Biochemical structure-function: HEK293's transfection efficiency enables systematic screening of p62 multi-domain (PB1, ZZ, UBA, LIR, KIR) mutant rescues. EDITGENE recommends this model for researchers investigating p62 signaling functions, particularly NF-κB and Nrf2 pathway studies and structure-function mechanism research.

Yes. p62 rescue in HEK293 is optimized for biochemical and signaling studies: • Construct design: use a codon-modified SQSTM1 sequence with a small tag (FLAG, HA). HEK293's high transfection efficiency supports rapid screening of p62 domain mutants. • Signaling pathway-specific rescue: KIR mutation (W347A, T350A) abolishes Keap1 binding for Nrf2 studies; ZZ domain mutations affect RIP1 binding for NF-κB studies; PB1 mutations affect aPKC/MEK5 interactions. • Reporter assay readouts: NF-κB-luc and ARE-luc reporters in HEK293 enable quantitative comparison of p62 domain mutant rescue effects on each signaling pathway. • Combined panel design: systematic rescue with single and combined domain mutants in HEK293 is the standard approach for mapping p62 multi-functional contributions. HEK293 transduces efficiently with lentivirus and has the highest transfection efficiency among p62 product cell lines, making it the preferred choice for biochemical structure-function studies.