B-ATF Lentiviral Activation Particles (h2): sc-401553-LAC-2

Human BATF encodes B-ATF, a basic leucine zipper transcription factor of the AP-1 network that heterodimerizes with JUN proteins and modulates DNA binding at AP-1–like and composite AICE/IRF elements to shape context-specific gene expression programs. BATF is a central regulator of immune cell differentiation and effector function, influencing T helper and T follicular helper lineage specification, germinal center responses, and cytokine-driven signaling downstream of pathways such as TCR activation and IL-21/STAT-dependent transcriptional control. Dysregulated BATF activity and associated transcriptional circuits have been linked to immune-mediated inflammation, autoimmunity, and oncogenic transcriptional states in hematologic malignancies, making it a useful target for mechanistic studies of immune regulation. Gene editing of BATF supports functional genomics applications including perturbation of AP-1/IRF cooperativity, mapping enhancer usage and chromatin remodeling, and dissecting immune signaling networks in engineered human cell models.

B-ATF Lentiviral Activation Particles (h2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient BATF upregulation across a broader range of human cell types.

B-ATF Lentiviral Activation Particles (h2) 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 BATF transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous B-ATF expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native BATF 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.