
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LATS1 CRISPR Activation Plasmid (h) | sc-401312-ACT | 20 µg | $397.00 |
LATS1 (large tumor suppressor kinase 1) is a core serine/threonine kinase in the Hippo signaling pathway that restrains cell proliferation and promotes apoptosis by phosphorylating key downstream effectors such as YAP/TAZ. Through integration of cell density cues, polarity, mechanical signaling, and GPCR inputs, LATS1 helps maintain tissue homeostasis by limiting transcriptional programs that drive growth and epithelial–mesenchymal transition. Dysregulated LATS1 activity or Hippo pathway impairment is frequently associated with altered contact inhibition, genomic instability, and oncogenic transcriptional states across multiple tumor contexts. In human cells, LATS1 function is also linked to cytoskeletal organization and cell cycle control, making it a useful node for dissecting signaling cross-talk that shapes proliferation and differentiation.
LATS1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous LATS1 expression without altering the underlying DNA sequence.
LATS1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the LATS1 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the LATS1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous LATS1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native LATS1 locus and enabling the study of LATS1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of LATS1 pathway restoration in tumor cells with silenced or reduced LATS1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.