PEBP1 Knockout Cell Line (A549)

The choice depends on whether you are studying PEBP1 (RKIP, Raf kinase inhibitor protein)'s role as a metastasis suppressor in lung cancer or its functions inhibiting Raf-MEK-ERK and NF-κB pathways. The Knockout line is the standard tool for asking whether RKIP is required for these inhibitory functions — RKIP binds and inhibits Raf-1, MEK1, GRK2, and IKK, broadly attenuating proliferative and inflammatory signaling. Overexpression is useful for studying RKIP tumor suppressor functions in lung cancer contexts where RKIP downregulation is associated with metastatic progression. For lung cancer biology research, the EDITGENE PEBP1 Knockout in A-549 is highly relevant — A-549 is an NSCLC model and RKIP loss has been associated with NSCLC progression and metastasis. This product complements the parallel PEBP1 Knockout in HEK293 (also available); A-549 is preferred for lung cancer-relevant studies, HEK293 for biochemistry. Rescue with wild-type or phospho-RKIP-mimetic (S153D, which switches RKIP from Raf inhibition to GRK2 inhibition) enables comprehensive structure-function studies.

Primary applications: • Lung cancer metastasis biology: invasion, migration, and EMT marker analysis in NSCLC context — RKIP loss is associated with NSCLC progression. • Raf-MEK-ERK pathway hyperactivation: phospho-MEK and phospho-ERK analysis given RKIP's MAPK inhibitory function. • NF-κB pathway analysis: phospho-IKK, phospho-IκBα, and NF-κB target gene expression. • EGFR-driven lung cancer studies: RKIP attenuates RTK-driven signaling — assessment of EGFR-TKI sensitivity in RKIP-null lung cancer cells. EDITGENE recommends this A-549-based model for lung cancer metastasis research; the parallel PEBP1 Knockout in HEK293 (also available) is preferred for biochemical mechanism studies.

Yes. RKIP rescue experiments in A-549 are well-suited for lung cancer research: • Construct design: use a codon-modified PEBP1 sequence with a small C- or N-terminal tag (FLAG, HA). RKIP is small (~21 kDa). • Phospho-mimetic rescue: S153D mutation mimics PKC-phosphorylated RKIP, switching from Raf to GRK2 inhibition — invaluable for studying RKIP's dual regulation in lung cancer. • Metastasis-related rescue: assessment of migration/invasion phenotype restoration as functional readout of metastasis suppressor rescue. • Functional readout: rescue should restore Raf-MEK-ERK pathway attenuation, NF-κB inhibition, and lung cancer-relevant metastatic phenotype suppression. A-549 transduces efficiently with lentivirus and supports stable rescue line generation.