BCMA CRISPR Activation Plasmid (h): sc-403058-ACT

TNFRSF17 encodes B-cell maturation antigen (BCMA), a TNF receptor superfamily member predominantly expressed on late-stage B cells and plasma cells. BCMA functions as a receptor for APRIL (TNFSF13) and BAFF (TNFSF13B), coupling ligand engagement to NF-κB and related survival signaling programs that support plasma cell differentiation, immunoglobulin production, and long-lived humoral immunity. Dysregulated BCMA signaling and expression are closely associated with aberrant plasma cell homeostasis and are frequently studied in the context of multiple myeloma and other B-lineage malignancies. As a lineage-restricted receptor, BCMA is also used as a molecular handle to interrogate plasma cell biology, immune regulation, and tumor–microenvironment interactions.

BCMA CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TNFRSF17 expression without altering the underlying DNA sequence.

BCMA CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TNFRSF17 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 TNFRSF17 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous BCMA expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TNFRSF17 locus and enabling the study of BCMA-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of BCMA pathway restoration in tumor cells with silenced or reduced TNFRSF17 expression.

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