
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
L-Plastin CRISPR Activation Plasmid (h) | sc-402131-ACT | 20 µg | $397.00 |
LCP1 encodes L-plastin, an actin-bundling protein predominantly expressed in hematopoietic cells that stabilizes filamentous actin and supports dynamic remodeling of the cytoskeleton. Through regulation of lamellipodia formation, integrin-dependent adhesion, and immune synapse architecture, L-plastin influences leukocyte activation, chemotaxis, and phagocytic functions. Its activity intersects with signaling pathways that coordinate motility and adhesion, including downstream effectors of PI3K and small GTPases that couple receptor cues to actin organization. Dysregulated LCP1 expression or phosphorylation has been associated with altered immune cell behavior and has been reported in contexts of inflammation and cancer cell invasiveness, making it relevant for mechanistic studies of migration and tissue infiltration.
L-Plastin CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous LCP1 expression without altering the underlying DNA sequence.
L-Plastin CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the LCP1 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 LCP1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous L-Plastin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native LCP1 locus and enabling the study of L-Plastin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of L-Plastin pathway restoration in tumor cells with silenced or reduced LCP1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.