GnRHR Lentiviral Activation Particles (h): sc-401783-LAC

Human GNRHR encodes gonadotropin-releasing hormone receptor (GnRHR), a class A G protein–coupled receptor that transduces hypothalamic GnRH signals in pituitary gonadotrophs to regulate luteinizing hormone and follicle-stimulating hormone synthesis and secretion. Upon ligand binding, GnRHR primarily couples to Gq/11 to activate PLCβ, generating IP3 and DAG, elevating intracellular Ca2+, and engaging PKC-dependent signaling with downstream MAPK/ERK pathway modulation. This signaling axis coordinates reproductive endocrine timing, steroidogenesis feedback loops, and gonadal development through tightly controlled transcriptional programs. Dysregulated GNRHR expression or signaling has been implicated in reproductive endocrine disorders, including hypogonadotropic hypogonadism and altered pubertal timing, and provides a mechanistic entry point for studying pituitary hormone regulation.

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

GnRHR Lentiviral Activation Particles (h) 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 GNRHR transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous GnRHR expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native GNRHR 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.