
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MARCKSL1 CRISPR Activation Plasmid (h) | sc-403985-ACT | 20 µg | $397.00 |
MARCKSL1 (MARCKS-like 1) encodes an actin-binding, membrane-associated protein that regulates cytoskeletal remodeling, cell polarity, and motility through phosphorylation-dependent interactions with phospholipids and F-actin. As a downstream effector of PKC signaling, MARCKSL1 participates in pathways that coordinate neurite outgrowth, lamellipodia dynamics, and vesicle trafficking, linking extracellular cues to changes in cell shape. Altered MARCKSL1 expression has been associated with invasive phenotypes and metastatic progression in multiple tumor contexts, consistent with its role in migration and adhesion. These properties make MARCKSL1 a useful target for studying cytoskeleton-driven mechanisms underlying development, wound-like responses, and cancer cell dissemination.
MARCKSL1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MARCKSL1 expression without altering the underlying DNA sequence.
MARCKSL1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MARCKSL1 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 MARCKSL1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MARCKSL1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MARCKSL1 locus and enabling the study of MARCKSL1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MARCKSL1 pathway restoration in tumor cells with silenced or reduced MARCKSL1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.