mPRε Lentiviral Activation Particles (m2): sc-429117-LAC-2

Mouse Paqr9 encodes membrane progesterone receptor epsilon (mPRε), a PAQR family seven‑transmembrane protein implicated in rapid, non-genomic progesterone signaling at the plasma membrane. mPRε is thought to modulate GPCR-like second messenger cascades, including regulation of cAMP and intracellular calcium dynamics, thereby influencing cell signaling programs linked to steroid hormone responsiveness. Paqr9 expression has been associated with neuroendocrine and reproductive physiology, and altered progesterone-related signaling is relevant to studies of fertility, stress-axis regulation, and hormone-dependent tumor biology. Gene editing of Paqr9 in mouse models supports mechanistic dissection of membrane-initiated steroid pathways, receptor crosstalk with nuclear progesterone receptor signaling, and downstream transcriptional and metabolic adaptations in defined tissues or cell types.

mPRε Lentiviral Activation Particles (m2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Paqr9 upregulation across a broader range of human cell types.

mPRε Lentiviral Activation Particles (m2) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the Paqr9 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous mPRε expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Paqr9 genomic locus and regulatory architecture.

The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.

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