SLC35F2 CRISPR Activation Plasmid (h): sc-406765-ACT

SLC35F2 (solute carrier family 35 member F2) is a human multi-pass membrane transporter implicated in cellular uptake and intracellular handling of small molecules, with reported roles in membrane trafficking and xenobiotic transport processes. As a member of the SLC35 family, it is studied in the context of transporter biology, cellular sensitivity to specific compounds, and determinants of intracellular exposure that influence stress response and survival pathways. Altered SLC35F2 expression has been associated with cancer-related phenotypes in transcriptomic datasets and is frequently evaluated as a functional modulator of drug response and metabolic vulnerability in tumor cell models. These features make SLC35F2 a useful target for mechanistic studies of transport-linked signaling, cellular fitness, and pathway rewiring under chemical or genetic perturbation.

SLC35F2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SLC35F2 expression without altering the underlying DNA sequence.

SLC35F2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SLC35F2 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 SLC35F2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SLC35F2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SLC35F2 locus and enabling the study of SLC35F2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SLC35F2 pathway restoration in tumor cells with silenced or reduced SLC35F2 expression.

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