AKT1 and AKT2 Knockout A-549 Cell Line

AKT (Protein Kinase B) is a family of three paralogous serine/threonine kinases (AKT1/PKBα, AKT2/PKBβ, AKT3/PKBγ) that are activated downstream of PI3K signaling — PI3K generates PIP3, which recruits AKT to the plasma membrane via its PH domain; AKT is then phosphorylated at T308 (activation loop, by PDK1) and S473 (hydrophobic motif, by mTORC2) for full activation. AKT family members share substantial substrate scope but have distinct tissue expression and functions: AKT1 is broadly expressed and important in cell survival/growth; AKT2 is enriched in insulin-sensitive tissues (liver, muscle, adipose) and central to insulin signaling; AKT3 is enriched in brain and testis with roles in neural development. Substantial paralog redundancy means that single-isoform knockouts often show modest phenotypes — paired and combination knockouts are essential for systematic functional dissection. This AKT1 & AKT2 Double Knockout in A-549 is uniquely valuable for asking which functions are AKT1/AKT2-dependent versus AKT3-dependent — combined loss of AKT1 and AKT2 leaves only AKT3 as the functional AKT isoform; AKT3 is principally expressed in brain and testis, making AKT3-only cells particularly suited to neural-relevant signaling research. Single-isoform rescue (AKT1 alone or AKT2 alone) in the double knockout enables paralog-specific functional dissection. For systematic AKT family research, this product is part of EDITGENE's complete AKT paralog dissection toolkit. The AKT1&AKT2 double KO removes the two principal AKT isoforms (~95% of total AKT signaling in most non-neural contexts), enabling clean AKT3-only signaling analysis. The knockout is uniquely valuable for studying brain-relevant AKT3 functions in heterologous A-549 background.

Primary applications: • AKT3-only signaling: pure AKT3-mediated PI3K signaling analysis given AKT1/2 loss — ideal for studying brain-relevant AKT3 functions in heterologous expression contexts. • Maximal AKT signaling loss: AKT1+AKT2 represent the principal AKT isoforms in most non-neural tissues — this double KO removes ~95% of total AKT activity. • Single-isoform rescue: AKT1 alone or AKT2 alone re-introduction enables paralog-specific dissection. • AKT paralog matrix dissection: complete AKT paralog dissection toolkit analysis. EDITGENE recommends this double KO for studying brain-relevant AKT3 biology and maximal AKT loss phenotypes.

Yes, and rescue experiments are uniquely powerful in this AKT1&2 double knockout: • Single-isoform rescue: re-introduction of AKT1 alone or AKT2 alone enables paralog-specific dissection. • AKT3-only signaling: this double KO is the cleanest model for AKT3-specific functions (brain-relevant). • Construct design: same considerations as AKT family rescues. • Functional readout: rescue should restore PI3K-AKT signaling. A-549-specific considerations: • A-549 is a human non-small cell lung carcinoma (NSCLC) cell line widely used for lung cancer drug development. • Lentiviral transduction is supported with moderate efficiency. • A-549's PI3K-AKT pathway activity makes it a relevant context for systematic AKT paralog research.