CECR2 CRISPR Activation Plasmid (h): sc-405018-ACT

CECR2 encodes a chromatin-associated protein that functions as a transcriptional regulator through bromodomain-dependent recognition of acetylated histones, linking epigenetic state to gene expression programs. It is implicated in chromatin remodeling and coordination of developmental and differentiation pathways, with reported roles in neural tube development and control of transcriptional networks. Altered CECR2 activity has been associated with dysregulated epigenetic signaling in cancer-relevant processes, including invasion, inflammatory signaling, and cell state transitions. As a nuclear chromatin factor, CECR2 is studied for its contribution to lineage specification, transcriptional fidelity, and disease-associated epigenome remodeling.

CECR2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CECR2 expression without altering the underlying DNA sequence.

CECR2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CECR2 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 CECR2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CECR2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CECR2 locus and enabling the study of CECR2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CECR2 pathway restoration in tumor cells with silenced or reduced CECR2 expression.

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