B-Myb Lentiviral Activation Particles (h2): sc-401318-LAC-2

Human MYBL2 encodes the transcription factor B-Myb, a Myb family regulator that coordinates cell-cycle progression by controlling expression of genes required for G1/S transition, DNA replication, and mitotic entry. B-Myb functions within the DREAM–MMB regulatory axis and cooperates with E2F- and cyclin/CDK-driven signaling to modulate chromatin-associated transcriptional programs and genome stability. Dysregulated MYBL2 activity is frequently linked to proliferative phenotypes and has been associated with oncogenic transcriptional signatures across multiple tumor contexts, making it a useful molecular node for studying cell-cycle control and transcriptional rewiring. Gene editing of MYBL2 supports mechanistic interrogation of proliferation checkpoints, replication stress responses, and transcription factor dependency mapping in human cell models.

B-Myb 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 MYBL2 upregulation across a broader range of human cell types.

B-Myb 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 MYBL2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous B-Myb expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native MYBL2 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.