CDK4 Knockout Cell Line (HEK 293)

The choice depends on whether you are studying CDK4's role as the canonical G1/S CDK or modeling CDK4/6 inhibitor pharmacology and breast cancer biology. The Knockout line is the standard tool for asking whether CDK4 is required for these processes — CDK4 partners with D-type cyclins to phosphorylate RB1; CDK4 is the principal CDK4/6 family member in many epithelial contexts, with critical roles in breast, pancreatic, and other cancers. Overexpression is useful for studying CDK4 gain-of-function effects. Important consideration: CDK4 and CDK6 paralog dissection is essential — combined CDK4+CDK6 loss is typically required to fully arrest in G1. This product complements the parallel CDK6 Knockout in HEK293 (also available) for systematic CDK4/6 paralog studies. Rescue with wild-type or kinase-dead CDK4 is the standard specificity control. The knockout is a critical specificity tool for ⭐⭐⭐ palbociclib, ribociclib, abemaciclib FDA-approved breast cancer drugs, the new CDK4-selective inhibitor PF-07220060 (in development), and emerging CDK4-targeted approaches.

Primary applications: • RB phosphorylation: phospho-RB1 Western blot to characterize CDK4 kinase activity. • Combined CDK4+CDK6 dissection: parallel analysis with CDK6 Knockout in HEK293 (also available) — combined CDK4/6 loss is typically required for full G1 arrest. • Palbociclib/ribociclib/abemaciclib specificity: critical genetic control for FDA-approved CDK4/6 inhibitors. • CDK4-selective inhibitor specificity: PF-07220060 and other CDK4-selective compounds. EDITGENE recommends this model for systematic CDK4/6 inhibitor pharmacology and breast cancer drug development.

Yes. CDK4 rescue experiments are well-established for breast cancer drug research: • Construct design: use a codon-modified CDK4 sequence with a small C-terminal tag (FLAG, HA). CDK4 has the canonical CDK architecture — preserve all elements. • Kinase-dead rescue: K35R mutation in the ATP-binding lysine abolishes catalytic activity. • CDK4/6 inhibitor-resistant rescue: gatekeeper mutations can confer palbociclib/ribociclib/abemaciclib resistance for on-target validation. • Functional readout: rescue should restore Cyclin D-CDK4 kinase activity and phospho-RB1. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation.