HoxC10 CRISPR Activation Plasmid (m): sc-431637-ACT

Hoxc10 encodes the homeobox transcription factor HoxC10, a posterior HOX protein that controls embryonic patterning and positional identity by regulating developmental gene expression programs. In mouse, HoxC10 activity contributes to axial and limb morphogenesis and influences mesenchymal differentiation through transcriptional networks that intersect with WNT, BMP, and retinoic acid signaling. Dysregulated HOX gene expression is frequently associated with altered lineage specification, aberrant proliferation, and invasive phenotypes in disease-relevant contexts, making Hoxc10 a useful node for studying developmental mispatterning and oncogenic transcriptional reprogramming. HoxC10 also provides a tractable model for investigating epigenetic control of HOX clusters and chromatin state transitions during differentiation.

HoxC10 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Hoxc10 expression without altering the underlying DNA sequence.

HoxC10 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Hoxc10 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 Hoxc10 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous HoxC10 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Hoxc10 locus and enabling the study of HoxC10-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of HoxC10 pathway restoration in tumor cells with silenced or reduced Hoxc10 expression.

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