SOCS-1 CRISPR Activation Plasmid (h): sc-400618-ACT

Human SOCS1 encodes SOCS-1, a key intracellular negative regulator of cytokine receptor signaling that constrains JAK/STAT pathway activity through SH2-mediated recognition of phosphotyrosine motifs and ubiquitin–proteasome targeting via its SOCS box. By attenuating signaling downstream of interferons, interleukins, and other inflammatory cues, SOCS-1 helps maintain immune homeostasis, modulates antigen-presenting cell function, and limits excessive inflammatory transcriptional programs. Dysregulated SOCS1 expression or activity has been associated with aberrant immune activation and oncogenic signaling contexts where persistent STAT activation contributes to altered proliferation and survival. These properties make SOCS-1 a useful node for studying feedback inhibition, cytokine responsiveness, and transcriptional adaptation in immune and cancer biology models.

SOCS-1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SOCS1 expression without altering the underlying DNA sequence.

SOCS-1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SOCS1 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 SOCS1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SOCS-1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SOCS1 locus and enabling the study of SOCS-1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SOCS-1 pathway restoration in tumor cells with silenced or reduced SOCS1 expression.

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