
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GTSF1L CRISPR Activation Plasmid (h) | sc-410333-ACT | 20 µg | $397.00 |
GTSF1L (gametocyte-specific factor 1-like) encodes a small, germline-enriched RNA-binding protein thought to participate in post-transcriptional gene regulation. Based on homology to GTSF family proteins, GTSF1L is linked to piRNA-associated pathways that help regulate transposable elements and support genome integrity during germ cell development. These processes intersect with RNA silencing, chromatin regulation, and maintenance of epigenetic stability in reproductive tissues. Dysregulation of germline genome-defense programs and aberrant expression of germline factors in somatic contexts are frequently studied as contributors to genomic instability and cancer/testis antigen–like expression patterns.
GTSF1L CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous GTSF1L expression without altering the underlying DNA sequence.
GTSF1L CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the GTSF1L 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 GTSF1L transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous GTSF1L expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native GTSF1L locus and enabling the study of GTSF1L-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of GTSF1L pathway restoration in tumor cells with silenced or reduced GTSF1L expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.