EGR1 Lentiviral Activation Particles (r): sc-437290-LAC

EGR1 (early growth response 1) is an immediate-early transcription factor rapidly induced by mitogenic and stress signals, functioning as a central regulator of stimulus-dependent gene expression programs in rat cells. It integrates upstream inputs from MAPK/ERK, PKC, calcium signaling, and growth factor pathways to control transcription linked to cell-cycle progression, differentiation, apoptosis, and synaptic plasticity. EGR1 modulates downstream networks involved in extracellular matrix remodeling, cytokine and chemokine signaling, and vascular and neuronal activity, making it broadly relevant to models of inflammation, fibrosis, and neuroadaptation. Dysregulated EGR1 activity has been associated with altered proliferative and stress-response phenotypes in diverse disease-relevant settings, supporting its utility as a mechanistic node for pathway interrogation.

EGR1 Lentiviral Activation Particles (r) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient upregulation across a broader range of human cell types.

EGR1 Lentiviral Activation Particles (r) 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 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous EGR1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native 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.