MafB Lentiviral Activation Particles (h): sc-400554-LAC

Human MAFB encodes MafB, a basic leucine zipper transcription factor of the large Maf family that controls lineage specification and terminal differentiation programs. MafB regulates macrophage and monocyte identity, osteoclastogenesis, and tissue-resident immune functions by coordinating transcriptional networks involved in inflammatory signaling, phagocytosis, and extracellular matrix remodeling. In the kidney, MafB contributes to podocyte maturation and maintenance, linking its dysregulation to glomerular barrier defects and nephropathy-associated phenotypes. Altered MAFB activity has also been connected to oncogenic transcriptional states and aberrant differentiation in hematologic and solid tumor contexts, making it a useful node for pathway-focused mechanistic studies.

MafB 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 MAFB upregulation across a broader range of human cell types.

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