HoxB5 Lentiviral Activation Particles (m2): sc-420914-LAC-2

Mouse Hoxb5 encodes the homeobox transcription factor HOXB5, a sequence-specific DNA-binding regulator that helps establish anterior–posterior patterning and segment identity during embryogenesis. HOXB5 modulates gene expression programs controlling mesodermal and neural differentiation, coordinating developmental pathways involved in tissue morphogenesis, vascular and respiratory tract formation, and hematopoietic lineage specification. Dysregulated HOXB5 activity and altered HOX network balance are linked to developmental abnormalities and have been associated with oncogenic transcriptional states in hematologic malignancy models, making Hoxb5 a useful locus for probing differentiation, self-renewal, and lineage commitment. Gene editing of Hoxb5 in mouse systems supports mechanistic studies of cis-regulatory elements, transcriptional circuitry, and in vivo developmental phenotyping across organogenesis and stem/progenitor cell contexts.

HoxB5 Lentiviral Activation Particles (m2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Hoxb5 upregulation across a broader range of human cell types.

HoxB5 Lentiviral Activation Particles (m2) 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 Hoxb5 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous HoxB5 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Hoxb5 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.