
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LHX1 Lentiviral Activation Particles (h) | sc-403100-LAC | 200 µl | $455.00 |
LHX1 (LIM homeobox 1) encodes a LIM-domain transcription factor that integrates DNA-binding with cofactor recruitment to control developmental gene regulatory networks. It contributes to cell fate specification and tissue patterning programs, including processes relevant to early embryogenesis and organogenesis, by coordinating transcriptional modules downstream of morphogen pathways such as WNT, BMP, and FGF signaling. In human biology, altered LHX1 regulation is linked to congenital developmental abnormalities and has been investigated in contexts where lineage identity and differentiation states become dysregulated. As a nuclear regulator of transcription, LHX1 is frequently used as a marker and functional node in studies of developmental signaling, transcriptional circuitry, and lineage reprogramming.
LHX1 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 LHX1 upregulation across a broader range of human cell types.
LHX1 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 LHX1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous LHX1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native LHX1 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.