FAM26F CRISPR Activation Plasmid (h): sc-405728-ACT

FAM26F encodes a small transmembrane protein implicated in immune cell biology and interferon-associated responses, with expression enriched in hematopoietic lineages and inducible under inflammatory cues. Reported functional links place FAM26F in processes that shape leukocyte activation, cell–cell communication, and immune signaling outputs that intersect with cytokine-driven pathways. Altered FAM26F expression has been observed in immune-related disease contexts and tumor-immune microenvironments, supporting its use as a marker and mechanistic node in studies of immunoregulation. As a result, FAM26F is of interest for dissecting how interferon-stimulated programs and membrane-associated signaling contribute to immune phenotypes and disease-associated transcriptional states.

FAM26F CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FAM26F expression without altering the underlying DNA sequence.

FAM26F CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FAM26F 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 FAM26F transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FAM26F expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FAM26F locus and enabling the study of FAM26F-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FAM26F pathway restoration in tumor cells with silenced or reduced FAM26F expression.

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