
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Ect2 CRISPR Activation Plasmid (h) | sc-401538-ACT | 20 µg | $397.00 |
Human ECT2 encodes epithelial cell transforming 2 (Ect2), a Rho guanine nucleotide exchange factor that activates RhoA, Rac1, and Cdc42 to coordinate actin remodeling and cytokinesis. Ect2 is dynamically regulated during the cell cycle and localizes to the nucleus and mitotic structures to control cleavage furrow formation, spindle-associated signaling, and maintenance of epithelial polarity. Through Rho GTPase signaling, Ect2 influences processes including cell migration, adhesion, and proliferation that intersect with pathways governing genome stability and mitotic fidelity. Dysregulated ECT2 expression or activity has been associated with oncogenic transformation phenotypes and is frequently studied in the context of tumor cell invasion and aberrant cell division.
Ect2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ECT2 expression without altering the underlying DNA sequence.
Ect2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ECT2 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 ECT2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Ect2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ECT2 locus and enabling the study of Ect2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Ect2 pathway restoration in tumor cells with silenced or reduced ECT2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.