SOCS-6 CRISPR Activation Plasmid (h): sc-402344-ACT

Human SOCS6 (suppressor of cytokine signaling 6) encodes SOCS-6, an SH2 domain–containing adaptor and E3 ubiquitin ligase component that attenuates receptor tyrosine kinase and cytokine receptor signaling. Through its SOCS box, SOCS-6 can couple activated signaling complexes to the elongin B/C–cullin ubiquitination machinery, influencing protein turnover and downstream MAPK/ERK, PI3K–AKT, and JAK/STAT pathway dynamics. SOCS6 activity contributes to regulation of cell proliferation, survival, and differentiation by shaping feedback control of growth factor–driven signaling. Dysregulated SOCS6 expression or function has been associated with altered oncogenic signaling and tumor suppressive networks in multiple cancer contexts, supporting its value in mechanistic pathway studies.

SOCS-6 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SOCS6 expression without altering the underlying DNA sequence.

SOCS-6 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SOCS6 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 SOCS6 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SOCS-6 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SOCS6 locus and enabling the study of SOCS-6-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SOCS-6 pathway restoration in tumor cells with silenced or reduced SOCS6 expression.

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