CTNNBL1 CRISPR Activation Plasmid (h): sc-409293-ACT

CTNNBL1 (catenin beta like 1) encodes a nuclear armadillo-repeat protein that associates with spliceosomal components and has been implicated in regulation of pre-mRNA processing and RNA-binding protein networks. Functional studies link CTNNBL1 to coordination of gene expression programs that impact cell-cycle progression, DNA damage responses, and maintenance of nuclear organization. Perturbation of CTNNBL1 expression has been observed across cancer transcriptomic datasets and in genetic studies of immune-related phenotypes, supporting its relevance to dysregulated transcription–splicing coupling. As a result, CTNNBL1 is of interest for dissecting how nuclear protein complexes modulate RNA maturation and downstream signaling pathways in human cells.

CTNNBL1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CTNNBL1 expression without altering the underlying DNA sequence.

CTNNBL1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CTNNBL1 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 CTNNBL1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CTNNBL1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CTNNBL1 locus and enabling the study of CTNNBL1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CTNNBL1 pathway restoration in tumor cells with silenced or reduced CTNNBL1 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.