ANG I Lentiviral Activation Particles (h): sc-401766-LAC

Human ANG encodes angiogenin, a secreted ribonuclease (RNase A superfamily) that binds cell-surface receptors and extracellular matrix components to regulate endothelial cell biology, stromal interactions, and stress-adaptive RNA metabolism. ANG supports angiogenic programs by promoting migration and proliferation signals and can translocate to the nucleus to influence rRNA transcription and ribosome biogenesis. Under cellular stress, angiogenin-mediated cleavage of tRNAs generates tRNA-derived fragments that modulate translation and stress granule dynamics, linking ANG to integrated stress responses. Dysregulated ANG expression and activity have been associated with pathological neovascularization, inflammation, and tumor microenvironment remodeling, and ANG variants have been studied in neurodegeneration contexts including motor neuron vulnerability.

ANG I 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 ANG upregulation across a broader range of human cell types.

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