c-Fgr Lentiviral Activation Particles (m): sc-420347-LAC

Mouse Fgr encodes c-Fgr, a Src family non-receptor tyrosine kinase enriched in myeloid lineages that couples immunoreceptor and integrin signaling to downstream phosphorylation events. c-Fgr participates in pathways controlling leukocyte adhesion, chemotaxis, degranulation, and phagocytic responses, integrating cues from cytokines and pattern-recognition receptors to shape inflammatory programs. Through regulation of cytoskeletal dynamics and MAPK/PI3K-linked signaling nodes, Fgr influences innate immune cell activation and tissue infiltration. Dysregulated Src family kinase activity, including altered Fgr signaling, is implicated in inflammatory disease mechanisms and hematopoietic malignancy-relevant signaling networks, making Fgr a useful target for mechanistic immunology studies.

c-Fgr 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 Fgr upregulation across a broader range of human cell types.

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