hnRNP Q CRISPR Activation Plasmid (m): sc-425140-ACT

Mouse Syncrip encodes heterogeneous nuclear ribonucleoprotein Q (hnRNP Q), an RNA-binding protein that coordinates post-transcriptional gene regulation through control of pre-mRNA splicing, mRNA stability, subcellular localization, and translation. hnRNP Q participates in ribonucleoprotein complex assembly and helps shape gene expression programs linked to neuronal development, synaptic function, and cellular stress responses. Through interactions with transcript processing and transport machinery, Syncrip influences RNA metabolism pathways that are frequently perturbed in neurodegeneration, cancer-associated gene expression remodeling, and other disorders with dysregulated RNA homeostasis. Its broad transcriptome-wide binding profile makes it a useful node for studying RNA regulatory networks and pathway-level control of protein output.

hnRNP Q CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Syncrip expression without altering the underlying DNA sequence.

hnRNP Q CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Syncrip 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 Syncrip transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous hnRNP Q expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Syncrip locus and enabling the study of hnRNP Q-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of hnRNP Q pathway restoration in tumor cells with silenced or reduced Syncrip expression.

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