
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BLC Lentiviral Activation Particles (m) | sc-424962-LAC | 200 µl | $455.00 |
Cxcl13 encodes BLC (B lymphocyte chemoattractant), a homeostatic CXC chemokine that binds CXCR5 to guide B cell and T follicular helper cell positioning within secondary lymphoid organs. In mouse immune tissues, the CXCL13–CXCR5 axis supports lymphoid follicle organization, germinal center dynamics, and coordinated leukocyte trafficking through chemokine-driven GPCR signaling and downstream cytoskeletal remodeling. Aberrant Cxcl13 expression is linked to ectopic lymphoid aggregate formation and sustained inflammatory microenvironments in autoimmune and chronic inflammatory settings, and it is also used as a marker of tertiary lymphoid structures in tumor immunology studies. These functions make Cxcl13 a useful node for dissecting immune cell migration, lymphoid stromal cell biology, and microenvironmental cues shaping humoral immunity.
BLC 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 Cxcl13 upregulation across a broader range of human cell types.
BLC 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 Cxcl13 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous BLC expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Cxcl13 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.