
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CHMP4B CRISPR Activation Plasmid (h) | sc-401802-ACT | 20 µg | $397.00 |
Human CHMP4B encodes a core component of the ESCRT-III complex that polymerizes on endosomal membranes to drive membrane constriction and scission during multivesicular body biogenesis. Through ESCRT-dependent trafficking, CHMP4B helps regulate receptor downregulation, lysosomal targeting, and turnover of signaling complexes, influencing pathways linked to growth factor signaling and cellular homeostasis. ESCRT-III activity also supports late stages of cytokinetic abscission and contributes to nuclear envelope reformation and plasma membrane repair. Dysregulation of ESCRT components, including CHMP4B, has been associated with altered endolysosomal dynamics and is relevant to research on neurodegeneration, cancer cell signaling, and virus budding mechanisms.
CHMP4B CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CHMP4B expression without altering the underlying DNA sequence.
CHMP4B CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CHMP4B 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 CHMP4B transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CHMP4B expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CHMP4B locus and enabling the study of CHMP4B-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CHMP4B pathway restoration in tumor cells with silenced or reduced CHMP4B expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.