
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CD37 CRISPR Activation Plasmid (m) | sc-419547-ACT | 20 µg | $397.00 |
Mouse Cd37 encodes CD37, a tetraspanin broadly expressed on B cells and other leukocyte subsets that organizes membrane microdomains and modulates receptor-mediated signaling. CD37 participates in regulation of B cell receptor signaling amplitude, immune synapse formation, and integrin-dependent adhesion and migration, influencing downstream pathways linked to cytokine responses and lymphocyte activation. Through its scaffolding functions, CD37 contributes to control of antigen presentation and cellular communication within lymphoid tissues. Dysregulated CD37 expression or signaling has been associated with altered humoral immune function and lymphocyte homeostasis, making Cd37 a useful target for mechanistic studies in immunology and hematologic disease models.
CD37 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Cd37 expression without altering the underlying DNA sequence.
CD37 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Cd37 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 Cd37 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CD37 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Cd37 locus and enabling the study of CD37-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CD37 pathway restoration in tumor cells with silenced or reduced Cd37 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.