CD79B CRISPR Activation Plasmid (h): sc-401760-ACT

CD79B encodes the Ig-β (B29) subunit of the B cell antigen receptor (BCR) complex, forming a signaling heterodimer with CD79A that is required for BCR surface expression and antigen-triggered signal transduction. Following antigen engagement, CD79B ITAM phosphorylation initiates downstream SYK activation and propagation through BTK, PI3K–AKT, and NF-κB/MAPK pathways to regulate B cell activation, survival, and differentiation. Altered CD79B expression or signaling competence can reshape BCR pathway output and immune receptor signaling dynamics. Dysregulation of BCR signaling components, including CD79B, is frequently studied in the context of B cell development, immune dysfunction, and B cell malignancy biology.

CD79B CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CD79B expression without altering the underlying DNA sequence.

CD79B CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CD79B 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 CD79B transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CD79B expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CD79B locus and enabling the study of CD79B-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CD79B pathway restoration in tumor cells with silenced or reduced CD79B expression.

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