
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Dlx-5 CRISPR Activation Plasmid (h) | sc-401825-ACT | 20 µg | $397.00 |
DLX5 encodes the homeobox transcription factor Dlx-5, a key regulator of embryonic patterning, osteogenic differentiation, and craniofacial and limb development. Dlx-5 integrates developmental signaling inputs, including BMP/TGF-β-associated transcriptional programs, to control lineage specification and extracellular matrix gene expression. In human cells, altered DLX5 expression or regulatory disruption has been linked to congenital malformations and dysregulated differentiation states, and aberrant activity has been reported in contexts of tumorigenesis and metastatic behavior. These features make DLX5 a useful node for studying transcriptional control of cell fate decisions, morphogenesis-related pathways, and disease-associated gene regulatory networks.
Dlx-5 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DLX5 expression without altering the underlying DNA sequence.
Dlx-5 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DLX5 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 DLX5 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Dlx-5 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DLX5 locus and enabling the study of Dlx-5-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Dlx-5 pathway restoration in tumor cells with silenced or reduced DLX5 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.