CD38 CRISPR Activation Plasmid (m): sc-419548-ACT

Mouse Cd38 encodes CD38, a multifunctional ectoenzyme that catalyzes NAD⁺ metabolism to generate second messengers such as cyclic ADP-ribose and NAADP, thereby regulating intracellular Ca²⁺ mobilization. CD38 activity shapes immune cell activation, differentiation, and adhesion, and contributes to metabolic and redox homeostasis through modulation of NAD⁺-dependent signaling. In hematopoietic and stromal compartments, CD38-linked pathways intersect with purinergic signaling, calcium-dependent transcriptional programs, and inflammatory cytokine networks. Altered CD38 expression or enzymatic function is widely used as a molecular correlate of immune dysregulation, metabolic remodeling, and age-associated changes in NAD⁺ turnover in mouse disease models.

CD38 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Cd38 expression without altering the underlying DNA sequence.

CD38 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Cd38 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 Cd38 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CD38 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Cd38 locus and enabling the study of CD38-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CD38 pathway restoration in tumor cells with silenced or reduced Cd38 expression.

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