CCNE1 Knockout Cell Line (HEK293)

The choice depends on whether you are studying CCNE1 (cyclin E1)'s role as the canonical G1/S cyclin or modeling CCNE1 amplification-driven cancer biology and CDK2 inhibitor sensitivity. The Knockout line is the standard tool for asking whether Cyclin E1 is required for these processes — CCNE1/Cyclin E1 partners with CDK2 at the G1/S boundary to drive DNA replication initiation; Cyclin E1 levels peak at G1/S and decline through SCF^FBXW7-mediated degradation; CCNE1 is amplified in ~10-20% of high-grade serous ovarian cancer, ~5-10% of breast cancer, and other malignancies, conferring sensitivity to CDK2 inhibitors. Overexpression is useful for studying CCNE1 amplification effects. For cancer biology research, the EDITGENE CCNE1 Knockout in HEK293 is uniquely valuable — CCNE1 is closely paired with CDK2 (the parallel CDK2 Knockout in HEK293 is also available), and CCNE1 amplification creates a therapeutic vulnerability targetable by CDK2-selective inhibitors. Rescue with wild-type or FBXW7-degradation-resistant CCNE1 enables cancer modeling. The knockout is a critical specificity tool for ⭐ tagtociclib (PF-07104091), BLU-222, INX-315 — CDK2-selective inhibitors in clinical development for CCNE1-amplified ovarian, breast, and endometrial cancer.

Primary applications: • Cyclin E1-CDK2 activity: in vitro and cellular CDK2 kinase activity in CCNE1-null cells given the Cyclin E1-CDK2 partnership. • S-phase entry: BrdU/EdU incorporation analysis given the Cyclin E1-CDK2 role in G1/S transition. • CCNE1 amplification rescue: rescue with wild-type or FBXW7-resistant (T62A, S384A) cyclin E1 for CCNE1 amplification cancer modeling. • CDK2 inhibitor sensitivity: combined CCNE1-CDK2 analysis using parallel CDK2 Knockout in HEK293 (also available) for systematic CDK2 inhibitor research in CCNE1-amplified cancers. EDITGENE recommends this model paired with CDK2 KO for emerging CDK2-selective drug development in CCNE1-amplified ovarian, breast, and endometrial cancers.

Yes. CCNE1 rescue experiments are well-established for cancer cell cycle research: • Construct design: use a codon-modified CCNE1 sequence with a small C-terminal tag (FLAG, HA). CCNE1 has N-terminal regulatory region with FBXW7 phosphodegron, cyclin-box domains, and C-terminal regions — preserve all elements. • FBXW7-resistant rescue: T62A and S384A mutations in the phosphodegron prevent SCF^FBXW7-mediated degradation, generating stable cyclin E1 — useful for studying CCNE1 amplification effects. • CDK2-binding-deficient rescue: cyclin-box mutations disrupt CDK2 partnership. • Functional readout: rescue should restore Cyclin E1-CDK2 kinase activity and CDK2 inhibitor sensitivity in CCNE1-amplified contexts. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation for systematic CCNE1-CDK2 axis research.