
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GTSF1 CRISPR Activation Plasmid (m) | sc-428766-ACT | 20 µg | $397.00 |
Mouse Gtsf1 encodes GTSF1, a germline-enriched zinc-finger protein implicated in PIWI–piRNA pathway function and transposon silencing during spermatogenesis. GTSF1 supports maintenance of genome integrity by promoting repression of retrotransposons and coordinating small RNA–guided epigenetic regulation in developing germ cells. Disruption of Gtsf1-associated processes is linked to defects in male fertility and aberrant germ cell development, making it relevant to studies of meiosis, gametogenesis, and genome defense. As a node in small RNA and chromatin regulatory networks, GTSF1 is commonly investigated for its roles in transcriptional control and germline homeostasis.
GTSF1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Gtsf1 expression without altering the underlying DNA sequence.
GTSF1 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Gtsf1 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 Gtsf1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous GTSF1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Gtsf1 locus and enabling the study of GTSF1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of GTSF1 pathway restoration in tumor cells with silenced or reduced Gtsf1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.