FCRLM1 CRISPR Activation Plasmid (h): sc-417336-ACT

FCRLA encodes Fc receptor–like A, an intracellular FcR-family protein predominantly expressed in B-lineage cells and associated with endoplasmic reticulum and immunoglobulin-containing compartments. It is implicated in B-cell differentiation and immune homeostasis by influencing immunoglobulin assembly/trafficking and signaling networks that shape antigen-dependent responses. Altered expression patterns of Fc receptor–like genes, including FCRLA, have been reported across B-cell malignancies and autoimmune-associated immune states, supporting its value as a marker and mechanistic node in B-cell biology. Studying FCRLA regulation helps define pathways controlling B-cell activation, antibody production, and stress responses linked to dysregulated humoral immunity.

FCRLM1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FCRLA expression without altering the underlying DNA sequence.

FCRLM1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FCRLA 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 FCRLA transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FCRLM1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FCRLA locus and enabling the study of FCRLM1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FCRLM1 pathway restoration in tumor cells with silenced or reduced FCRLA expression.

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