serum reponse factor /SRF CRISPR Activation Plasmid (m): sc-423154-ACT

Mouse Srf encodes serum response factor (SRF), a MADS-box transcription factor that binds serum response elements and coordinates stimulus-dependent gene expression programs. SRF integrates RhoA–actin dynamics and MAPK/ERK signaling through cofactor partnerships with MRTFs and TCFs to regulate immediate-early gene induction, cytoskeletal remodeling, cell adhesion, migration, and myogenic and neuronal differentiation. By controlling transcriptional networks that shape cell identity and contractile function, SRF is widely studied in contexts such as cardiac and smooth muscle biology, angiogenesis, and synaptic plasticity. Dysregulated SRF activity has been linked to pathological remodeling and altered proliferation programs relevant to cardiovascular and neurodevelopmental research.

serum reponse factor /SRF CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Srf expression without altering the underlying DNA sequence.

serum reponse factor /SRF CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Srf locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.

Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the Srf transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous serum reponse factor /SRF expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Srf locus and enabling the study of serum reponse factor /SRF-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of serum reponse factor /SRF pathway restoration in tumor cells with silenced or reduced Srf expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.