CD79A CRISPR Activation Plasmid (h): sc-401827-ACT

CD79A encodes the Ig-α subunit of the B cell antigen receptor (BCR) complex, which pairs with CD79B to couple antigen recognition to intracellular signaling. Its immunoreceptor tyrosine-based activation motifs (ITAMs) become phosphorylated to initiate SYK-dependent cascades that engage PI3K–AKT, BTK, NF-κB, and MAPK pathways, shaping B cell activation, proliferation, and survival. CD79A expression is tightly linked to B cell lineage identity and influences antigen-driven selection during development and differentiation. Dysregulated BCR signaling and altered CD79A activity are implicated in B cell–derived immune dysfunction and hematologic disease biology, supporting its use as a mechanistic marker in immunology and oncology research.

CD79A CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CD79A expression without altering the underlying DNA sequence.

CD79A CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CD79A 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 CD79A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CD79A expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CD79A locus and enabling the study of CD79A-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CD79A pathway restoration in tumor cells with silenced or reduced CD79A expression.

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