JMJD2C CRISPR Activation Plasmid (h): sc-403282-ACT

KDM4C (JMJD2C) encodes a Jumonji C (JmjC) domain–containing histone demethylase that primarily removes repressive methyl marks such as H3K9me3/me2, promoting chromatin opening and transcriptional competence. Through dynamic regulation of histone methylation, JMJD2C influences epigenetic control of gene expression programs linked to cell cycle progression, DNA damage responses, and lineage-specific transcriptional networks. Dysregulated KDM4C activity has been associated with aberrant chromatin states observed in multiple cancers, where altered enhancer and promoter accessibility can reinforce oncogenic transcriptional circuits. As a nuclear chromatin regulator, JMJD2C is frequently studied for its roles in transcription factor cooperation, chromatin remodeling, and maintenance of epigenetic plasticity in human cells.

JMJD2C CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KDM4C expression without altering the underlying DNA sequence.

JMJD2C CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KDM4C 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 KDM4C transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous JMJD2C expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KDM4C locus and enabling the study of JMJD2C-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of JMJD2C pathway restoration in tumor cells with silenced or reduced KDM4C expression.

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