
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Factor H CRISPR Activation Plasmid (h) | sc-401099-ACT | 20 µg | $397.00 |
Complement factor H (CFH) encodes factor H, a soluble regulator of the alternative pathway of complement that protects host surfaces by accelerating C3 convertase decay and serving as a cofactor for factor I–mediated C3b inactivation. By discriminating self from non-self through interactions with glycosaminoglycans and sialic acids, factor H helps restrain complement amplification, opsonization, and downstream inflammatory signaling. Perturbation of CFH expression or function is linked to dysregulated complement activity implicated in age-related macular degeneration, atypical hemolytic uremic syndrome, and glomerular inflammatory phenotypes. CFH is therefore widely studied in innate immunity, vascular and renal biology, and complement-driven tissue injury models.
Factor H CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CFH expression without altering the underlying DNA sequence.
Factor H CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CFH 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 CFH transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Factor H expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CFH locus and enabling the study of Factor H-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Factor H pathway restoration in tumor cells with silenced or reduced CFH expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.