
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FMNL1 CRISPR Activation Plasmid (h) | sc-404817-ACT | 20 µg | $397.00 |
Formin-like protein 1 (FMNL1) is a Rho GTPase–regulated actin nucleation and elongation factor that supports dynamic remodeling of the cortical cytoskeleton. It contributes to filopodia formation, cell polarity, adhesion, and migration by coordinating actin filament assembly downstream of signaling pathways such as RhoA and Cdc42. FMNL1 is expressed prominently in hematopoietic lineages and is frequently studied in the context of immune cell trafficking, phagocytosis, and immune synapse organization. Dysregulated cytoskeletal control involving FMNL1 has been associated with altered leukocyte function and has been investigated across inflammatory and hematologic disease biology as a mechanism impacting cell motility and tissue infiltration.
FMNL1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FMNL1 expression without altering the underlying DNA sequence.
FMNL1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FMNL1 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 FMNL1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FMNL1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FMNL1 locus and enabling the study of FMNL1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FMNL1 pathway restoration in tumor cells with silenced or reduced FMNL1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.