
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GCC2 Lentiviral Activation Particles (h) | sc-411304-LAC | 200 µl | $455.00 |
Human GCC2 encodes a coiled-coil Golgin family protein that localizes to the trans-Golgi network and contributes to Golgi organization, vesicle tethering, and cargo sorting within the secretory and endocytic trafficking system. By supporting membrane trafficking dynamics, GCC2 influences processes such as protein glycosylation, receptor recycling, and spatial coordination of signaling components. Perturbations in Golgi structure and trafficking pathways are broadly relevant to cellular stress responses and altered signaling behavior observed in diverse disease contexts, making GCC2 a useful node for studying organelle homeostasis. GCC2-associated mechanisms are therefore pertinent to investigating how trafficking defects remodel proteostasis and signal transduction in human cells.
GCC2 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 GCC2 upregulation across a broader range of human cell types.
GCC2 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 GCC2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous GCC2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native GCC2 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.