CD2AP CRISPR Activation Plasmid (h): sc-401218-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CD2AP CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- CD2AP 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 CD2AP CRISPR Activation Plasmid (h) and CD2AP CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the CD2AP 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: CD2AP Antibody (B-4): sc-25272
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CD2AP CRISPR Activation Plasmid (h) | sc-401218-ACT | 20 µg | $397.00 |
Human CD2AP encodes CD2-associated protein, an adaptor/scaffold that couples membrane receptors to the actin cytoskeleton and coordinates endocytosis, vesicle trafficking, and signal transduction. CD2AP participates in slit diaphragm and podocyte cytoskeletal organization, receptor internalization, and junctional stability through interactions with nephrin, c-Cbl, and actin-regulatory complexes, influencing PI3K/AKT and related pathways controlling cell survival and morphology. Altered CD2AP expression or function has been associated with glomerular filtration barrier defects, proteinuric kidney disease, and broader phenotypes linked to dysregulated cytoskeletal dynamics and immune cell signaling. This gene is therefore widely studied in models of podocyte biology, membrane trafficking, and receptor-driven signaling networks.
CD2AP CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CD2AP expression without altering the underlying DNA sequence.
CD2AP CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CD2AP 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 CD2AP transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CD2AP expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CD2AP locus and enabling the study of CD2AP-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CD2AP pathway restoration in tumor cells with silenced or reduced CD2AP expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.