
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
5α-Reductase 2 CRISPR Activation Plasmid (h) | sc-402353-ACT | 20 µg | $397.00 |
SRD5A2 encodes human 5α-Reductase 2, an NADPH-dependent oxidoreductase that converts testosterone to the more potent androgen dihydrotestosterone (DHT), shaping androgen receptor signaling in androgen-responsive tissues. This enzymatic step is central to steroid hormone metabolism and influences transcriptional programs governing sexual differentiation, epithelial homeostasis, and reproductive biology. Altered SRD5A2 activity has been linked to disorders of androgen metabolism and genital development, and dysregulated androgen signaling is relevant to prostate biology and hormone-driven tissue remodeling. As a result, SRD5A2 is widely studied in endocrine regulation, steroidogenic pathway flux, and androgen-dependent cellular phenotypes.
5α-Reductase 2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SRD5A2 expression without altering the underlying DNA sequence.
5α-Reductase 2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SRD5A2 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 SRD5A2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous 5α-Reductase 2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SRD5A2 locus and enabling the study of 5α-Reductase 2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of 5α-Reductase 2 pathway restoration in tumor cells with silenced or reduced SRD5A2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.