HDGF Lentiviral Activation Particles (h2): sc-402859-LAC-2

Human HDGF (hepatoma-derived growth factor) encodes a heparin-binding nuclear and secreted protein that can act as a mitogenic and pro-survival factor, with roles in cell-cycle progression, transcriptional regulation, and chromatin-associated processes. HDGF is linked to signaling networks that support proliferation, migration, and angiogenic programs, and it contributes to stress responses and tissue remodeling through context-dependent autocrine/paracrine activity. Dysregulated HDGF expression has been reported across multiple cancers and in fibrotic and vascular pathologies, where it is frequently associated with aggressive cellular phenotypes and altered tumor microenvironment interactions. Genetic perturbation of HDGF supports mechanistic studies of growth-factor biology, nuclear translocation motifs (e.g., PWWP domain–mediated chromatin binding), and downstream pathway mapping in models of oncogenesis, inflammation, and fibrosis.

HDGF 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 HDGF upregulation across a broader range of human cell types.

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