Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
C1q-C CRISPR Activation Plasmid (h): sc-403618-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- C1q-C CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- C1q-C CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by C1q-C CRISPR Activation Plasmid (h) and C1q-C CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the C1QC transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: C1q-C Antibody (A-12): sc-365301
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
C1q-C CRISPR Activation Plasmid (h) | sc-403618-ACT | 20 µg | $397.00 |
C1QC encodes the C chain of complement component C1q, an initiating recognition molecule of the classical complement pathway that binds immune complexes and altered self-structures to trigger downstream complement activation. Beyond complement proteolysis, C1q influences phagocytic clearance, apoptotic cell removal, and inflammatory signaling through interactions with cell-surface receptors on myeloid and tissue-resident immune cells. C1q biology is closely tied to innate immune surveillance and tissue homeostasis, and dysregulated complement activity has been associated with chronic inflammation and autoimmune-like phenotypes. Altered C1QC expression is also used as a marker of specific macrophage/microglia states relevant to neuroinflammation and fibrotic or tumor-associated immune microenvironments.
C1q-C CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous C1QC expression without altering the underlying DNA sequence.
C1q-C CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the C1QC 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 C1QC transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous C1q-C expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native C1QC locus and enabling the study of C1q-C-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of C1q-C pathway restoration in tumor cells with silenced or reduced C1QC expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.