serum reponse factor /SRF Lentiviral Activation Particles (m): sc-423154-LAC

Mouse Srf encodes serum reponse factor /SRF, a MADS-box transcription factor that binds serum response elements to coordinate immediate-early gene expression with cytoskeletal dynamics. SRF integrates signals from RhoA–actin remodeling and MAPK/ERK pathways to regulate programs controlling proliferation, migration, differentiation, and stress responses. Through interactions with cofactors such as myocardin and MRTFs, SRF modulates smooth muscle and cardiac gene networks as well as neuronal activity-dependent transcription. Dysregulated SRF signaling has been associated with aberrant remodeling and growth phenotypes in cardiovascular and neuromuscular contexts, making it a useful node for mechanistic studies of transcriptional control in disease-relevant pathways.

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

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