LATS1 Knockout HAP1 Cell Line

LATS1 Knockout HAP1 Cell Line
15% OFF
Cat.No.:

EDC08068

Species:

Human

Cell Name:

HAP1

Gene:

LATS1

Gene ID:

9113

Size:

1×10⁶cells

LATS1 Knockout HAP1 Cell Line is an exclusive upgraded CRISPR/Cas9 system-mediated gene knockout cell, with the advantages of Optimized Strategy Design, Efficient Cell Transfection, High-Performotion Cas9 Protein and Hassle-Free Cell Selection.
Cat.No. EDC08068
Product Name LATS1 Knockout HAP1 Cell Line
Species Human
Cell Line HAP1
Cellosaurus ID CVCL_0F62
Gene ID
Cell Line Synonyms Highly Aggressively Proliferating Immortalized
Gene LATS1
Summary
The protein encoded by this gene is a putative serine/threonine kinase that localizes to the mitotic apparatus and complexes with cell cycle controller CDC2 kinase in early mitosis. The protein is phosphorylated in a cell-cycle dependent manner, with late prophase phosphorylation remaining through metaphase. The N-terminal region of the protein binds CDC2 to form a complex showing reduced H1 histone kinase activity, indicating a role as a negative regulator of CDC2/cyclin A. In addition, the C-terminal kinase domain binds to its own N-terminal region, suggesting potential negative regulation through interference with complex formation via intramolecular binding. Biochemical and genetic data suggest a role as a tumor suppressor. This is supported by studies in knockout mice showing development of soft-tissue sarcomas, ovarian stromal cell tumors and a high sensitivity to carcinogenic treatments. [provided by RefSeq, Apr 2017]
Digestion Time 2 min
Morphology Adherent
Passage Ratio 1:8~1:10
Complete Culture Medium IMDM+10%FBS
Freezing Medium 90%FBS+10%DMSO
* For research use only. Not intended for use in humans or animals, including clinical, therapeutic, or diagnostic purposes.

FAQ

The choice depends on whether you are studying LATS1's role as the principal Hippo pathway tumor suppressor kinase or its functions distinct from LATS2. The Knockout line is the standard tool for asking whether LATS1 is required for YAP/TAZ phosphorylation — LATS1 partners with MOB1A/MOB1B to phosphorylate YAP (S127, S381) and TAZ (S89, S311), driving their cytoplasmic retention and degradation. Overexpression is useful for studying LATS1 gain-of-function effects. Important consideration: LATS1 and LATS2 share substantial substrate scope — combined LATS1+LATS2 loss is typically needed to fully de-repress YAP/TAZ. Rescue with wild-type or kinase-dead LATS1 is the standard specificity control. This product complements the parallel LATS2 Knockout in HAP1 (also available) for paralog-specific functional dissection. The knockout is a critical specificity tool for emerging Hippo pathway-modulating compounds and YAP/TAZ-targeted cancer therapeutics.
Primary applications: • YAP/TAZ phosphorylation: phospho-YAP and phospho-TAZ Western blot to characterize LATS1 kinase activity. • Hippo pathway output: YAP/TAZ subcellular localization and target gene expression analysis. • LATS family comparative studies: parallel analysis with LATS2 Knockout in HAP1 (also available) for paralog-specific characterization. • MOB1 partnership: MOB1A/MOB1B expression analysis given LATS1-MOB1 heterodimer dependence. EDITGENE recommends this model for researchers investigating Hippo pathway tumor suppressor biology and combined-LATS dependency studies.
Yes. LATS1 rescue experiments require attention to AGC-family architecture: • Construct design: use a codon-modified LATS1 sequence with a small C-terminal tag (FLAG, HA). LATS1 has the canonical AGC-family architecture similar to LATS2 — preserve all elements. • Kinase-dead rescue: ATP-binding lysine mutation abolishes catalytic activity. • Hydrophobic motif phospho-mimetic rescue: T1079D mutation mimics MST1/2-mediated activation loop phosphorylation. • Functional readout: rescue should restore phospho-YAP and phospho-TAZ levels and target gene attenuation. 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.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.

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