CREM CRISPR Activation Plasmid (m): sc-419799-ACT

Mouse CREM (cAMP responsive element modulator) is a bZIP transcription factor in the CREB/ATF family that binds cAMP response elements to regulate stimulus-dependent gene expression programs. Through integration of cAMP/PKA signaling, calcium-dependent inputs, and MAPK-linked phosphorylation events, CREM influences transcriptional dynamics that shape neuronal plasticity, endocrine outputs, and immune cell activation states. CREM isoform diversity, including inducible activators and repressors such as ICER, enables context-specific control of immediate-early and metabolic gene networks. Dysregulated CREM activity has been associated with altered reproductive physiology, stress-responsive signaling, and immune-mediated pathology in experimental models, supporting its utility in mechanistic studies of transcriptional control in disease-relevant pathways.

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

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

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