
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
APC1 CRISPR Activation Plasmid (h) | sc-405103-ACT | 20 µg | $397.00 |
Human ANAPC1 encodes APC1, a core scaffold subunit of the anaphase-promoting complex/cyclosome (APC/C), an essential E3 ubiquitin ligase that coordinates ordered proteolysis during mitosis and G1. Through APC/C interactions with co-activators such as CDC20 and CDH1, APC1 supports ubiquitination and degradation of key cell-cycle regulators, thereby enforcing spindle checkpoint control, mitotic exit, and genome stability. Dysregulation of APC/C activity and related ubiquitin–proteasome pathways is linked to chromosomal instability and altered proliferative signaling, making ANAPC1 a relevant node for studies of cell-cycle control and cancer-associated phenotypes.
APC1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ANAPC1 expression without altering the underlying DNA sequence.
APC1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ANAPC1 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 ANAPC1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous APC1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ANAPC1 locus and enabling the study of APC1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of APC1 pathway restoration in tumor cells with silenced or reduced ANAPC1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.