LCOR CRISPR Activation Plasmid (m): sc-431795-ACT

Lcor encodes ligand-dependent corepressor (LCOR), a nuclear transcriptional coregulator that associates with DNA-bound transcription factors and contributes to repression or modulation of gene expression through chromatin-dependent mechanisms. In mouse cells, LCOR is linked to signaling programs governed by nuclear receptors and other transcriptional regulators, shaping differentiation, cell-cycle control, and lineage-specific transcriptional states. By integrating corepressor activity with epigenetic remodeling, LCOR can influence pathways involved in developmental regulation and cellular identity maintenance. Dysregulated LCOR-associated transcriptional networks are relevant to disease biology where altered receptor signaling and chromatin control perturb gene expression programs.

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

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

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