TAB2 CRISPR Activation Plasmid (h): sc-401596-ACT

Human TAB2 (TAK1-binding protein 2) functions as an adaptor that links polyubiquitin-dependent signaling to activation of MAP3K7/TAK1, integrating cues from TNF receptor and Toll/IL-1 receptor pathways. Through interactions with ubiquitinated intermediates and TAB1/TAB3, TAB2 promotes downstream NF-κB and MAPK signaling, shaping inflammatory gene expression, stress responses, and cell survival decisions. TAB2 activity contributes to regulation of innate immune activation and cytokine-driven transcriptional programs. Dysregulated TAB2-associated signaling has been implicated in inflammatory phenotypes and cancer-related signaling contexts where aberrant NF-κB/MAPK pathway engagement supports pathogenic cellular states.

TAB2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TAB2 expression without altering the underlying DNA sequence.

TAB2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TAB2 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 TAB2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TAB2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TAB2 locus and enabling the study of TAB2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TAB2 pathway restoration in tumor cells with silenced or reduced TAB2 expression.

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