TBL1XR1 CRISPR Activation Plasmid (h): sc-401998-ACT

TBL1XR1 (transducin beta-like 1 X-linked receptor 1) encodes a WD40 repeat–containing coregulator that participates in transcriptional control by bridging sequence-specific transcription factors with chromatin-modifying complexes. It functions in multiple signaling contexts, including nuclear receptor pathways and Wnt/β-catenin–associated transcription, and contributes to the dynamic exchange of co-repressor and co-activator assemblies to tune gene expression programs. Through these roles, TBL1XR1 influences cellular differentiation, proliferation, and stress-responsive transcriptional states. Dysregulation or altered activity of TBL1XR1 has been linked to aberrant transcriptional networks in cancer biology and neurodevelopmental phenotypes, making it a useful target for mechanistic studies of gene regulation.

TBL1XR1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TBL1XR1 expression without altering the underlying DNA sequence.

TBL1XR1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TBL1XR1 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 TBL1XR1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TBL1XR1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TBL1XR1 locus and enabling the study of TBL1XR1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TBL1XR1 pathway restoration in tumor cells with silenced or reduced TBL1XR1 expression.

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