Inhibin α CRISPR Activation Plasmid (h): sc-402958-ACT

INHA encodes inhibin α, a secreted glycoprotein subunit that heterodimerizes with β subunits to form inhibin A and inhibin B, key endocrine regulators of pituitary FSH synthesis and reproductive axis homeostasis. Inhibin/activin signaling interfaces with TGF-β superfamily pathways to modulate SMAD-dependent transcriptional programs controlling gonadal development, steroidogenesis, and folliculogenesis. Altered INHA expression has been associated with dysregulated gonadotropin feedback, changes in granulosa and Sertoli cell function, and reproductive endocrine phenotypes. Because inhibin α influences cell proliferation and differentiation in reproductive tissues, it is frequently studied in the context of ovarian and testicular biology, hormone-responsive signaling networks, and tumor biology models.

Inhibin α CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous INHA expression without altering the underlying DNA sequence.

Inhibin α CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the INHA 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 INHA transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Inhibin α expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native INHA locus and enabling the study of Inhibin α-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Inhibin α pathway restoration in tumor cells with silenced or reduced INHA expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.