FAM171A2 CRISPR Activation Plasmid (h): sc-415352-ACT

FAM171A2 (family with sequence similarity 171 member A2) encodes a poorly characterized human protein predicted to be membrane associated, with emerging evidence linking the FAM171 family to cell–cell interactions and regulation of cellular morphology. Transcriptomic datasets suggest context-dependent expression in neural and epithelial lineages, implicating FAM171A2 in differentiation-associated programs and tissue-specific signaling states. Altered expression patterns have been reported in select cancer and neurobiology-focused studies, supporting investigation of FAM171A2 as a modifier of proliferation, migration, or lineage identity. Because mechanistic annotations remain limited, controlled perturbation of endogenous FAM171A2 is useful for mapping pathway connectivity and defining downstream transcriptional responses.

FAM171A2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FAM171A2 expression without altering the underlying DNA sequence.

FAM171A2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FAM171A2 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 FAM171A2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FAM171A2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FAM171A2 locus and enabling the study of FAM171A2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FAM171A2 pathway restoration in tumor cells with silenced or reduced FAM171A2 expression.

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