Date published: 2026-7-4

1-800-457-3801

SCBT Portrait Logo
Seach Input

CD163 Lentiviral Activation Particles (m): sc-429989-LAC

0.0(0)
Write a reviewAsk a question

Datasheets
  • Target species: mouse
  • 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
  • CD163 Lentiviral Activation Particles (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically and efficiently upregulate gene expression via lentiviral transduction of cells
  • CD163 Lentiviral Activation Particles (m) contain the following SAM Activation elements: a deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, an MS2-p65-HSF1 fusion protein and a target-specific 20 nt guide RNA. They also contain the blasticidin, hygromycin and puromycin resistance genes
  • Upon transduction, the SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
  • gRNAs encoded by CD163 Lentiviral Activation Plasmid (m) and CD163 Lentiviral Activation Plasmid (m2) target distinct regulatory regions of the Cd163 promoter. One or both designs may be available
  • Following transfection, gene activation efficiency can be assayed by WB, IF or IHC using antibody: CD163 Antibody (ED2): sc-58965
    Gene Editing Promo Banner

    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    CD163 Lentiviral Activation Particles (m)

    sc-429989-LAC
    200 µl
    $455.00

    Mouse Cd163 encodes CD163, a scavenger receptor predominantly expressed on monocytes and tissue macrophages that binds hemoglobin–haptoglobin complexes and supports their endocytic clearance. CD163 activity intersects with macrophage polarization programs and inflammatory signaling networks, including cytokine-driven pathways that shape antigen handling, oxidative stress responses, and resolution of inflammation. Through regulation of heme/iron handling and immunomodulatory ligand uptake, CD163 contributes to tissue homeostasis in settings of hemolysis, sterile injury, and pathogen exposure. Altered CD163 expression and macrophage distribution are frequently used as indicators of myeloid remodeling in models of chronic inflammation, metabolic dysregulation, fibrosis, and tumor-associated macrophage biology.

    CD163 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 Cd163 upregulation across a broader range of human cell types.

    CD163 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 Cd163 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CD163 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Cd163 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.