LATS2 Knockout HAP1 Cell Line

The choice depends on whether you are studying LATS2 (large tumor suppressor 2)'s role as a Hippo pathway tumor suppressor kinase or its functions in YAP/TAZ phosphorylation and inactivation. The Knockout line is the standard tool for asking whether LATS2 is required for these processes — LATS2 is the closest paralog of LATS1, both functioning as the terminal Hippo pathway kinases that phosphorylate YAP (S127) and TAZ (S89), promoting their cytoplasmic retention by 14-3-3 binding and proteasomal degradation. Overexpression is useful for studying LATS2 gain-of-function effects. Important consideration: LATS1 and LATS2 share substantial substrate scope — single LATS2 knockout in HAP1 may show modest phenotypes if LATS1 compensates. Rescue with wild-type or kinase-dead LATS2 is the standard specificity control. This product complements the parallel LATS1 Knockout in HAP1 (also available) for paralog-specific functional dissection — combined LATS1+LATS2 loss is required to fully de-repress YAP/TAZ. The knockout is valuable for studying Hippo pathway tumor suppression and YAP/TAZ-driven cancer biology.

Primary applications: • YAP/TAZ phosphorylation: phospho-YAP (S127) and phospho-TAZ (S89) Western blot to characterize LATS2 kinase activity. • Hippo pathway output: YAP/TAZ nuclear localization, CTGF/CYR61 target gene expression following Hippo pathway stimulation. • Combined LATS1+LATS2 studies: parallel analysis with LATS1 Knockout in HAP1 (also available) for paralog-specific dissection; combined loss is typically needed for full YAP/TAZ activation. • Hippo-modulating drug specificity: critical genetic control for emerging Hippo pathway-modulating compounds and YAP/TAZ-TEAD interaction inhibitors. EDITGENE recommends this model for researchers investigating Hippo pathway biology and YAP/TAZ-driven cancer mechanisms.

Yes. LATS2 rescue experiments require attention to AGC-family architecture: • Construct design: use a codon-modified LATS2 sequence with a small C-terminal tag (FLAG, HA). LATS2 has N-terminal regulatory region, central kinase domain, and C-terminal hydrophobic motif — preserve all elements. • Kinase-dead rescue: K697R mutation in the ATP-binding lysine abolishes catalytic activity. • MOB1-binding-deficient rescue: MOB1-binding region mutations disrupt LATS2-MOB1 heterodimer formation. • Combined LATS1+LATS2 considerations: full YAP/TAZ activation typically requires combined LATS1 and LATS2 loss — rescue interpretation considers LATS1 expression. • Functional readout: rescue should restore phospho-YAP (S127) and phospho-TAZ (S89) levels. HAP1-specific considerations: • Diploidization: HAP1 cells gradually diploidize during extended culture — confirm ploidy by flow cytometry at the time of phenotypic assay. • Integration site sensitivity: position effects on transgene expression are more pronounced in near-haploid backgrounds; generating multiple independent rescue clones is strongly recommended. • Transduction efficiency: HAP1 transduces with lentivirus at moderate efficiency — increase MOI compared to standard immortalized lines.