
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CD64 Lentiviral Activation Particles (m) | sc-420305-LAC | 200 µl | $455.00 |
Mouse Fcgr1 encodes CD64 (FcγRI), a high-affinity IgG Fc receptor predominantly expressed on monocytes, macrophages, dendritic cells, and activated neutrophils. CD64 couples immune complex recognition to FcR γ-chain signaling, promoting ITAM-dependent activation of Syk and downstream pathways such as PI3K–AKT, MAPK, and NF-κB that regulate phagocytosis, respiratory burst, cytokine production, and antigen presentation. Through these processes, Fcgr1 influences innate immune sensing, myeloid cell polarization, and crosstalk with adaptive immunity. Dysregulated CD64 activity or expression is frequently used as a marker and mechanistic node in studies of inflammation, infection, and autoimmune-like immune complex pathology in mouse models.
CD64 Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Fcgr1 upregulation across a broader range of human cell types.
CD64 Lentiviral Activation Particles (m) 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 Fcgr1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CD64 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Fcgr1 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.