TAB1 CRISPR Activation Plasmid (h): sc-402049-ACT

Human TAB1 (TAK1-binding protein 1) is an adaptor/regulatory factor that binds MAP3K7/TAK1 and facilitates signal propagation from pro-inflammatory and stress-responsive receptors to downstream kinase cascades. Through its role in activating TAK1, TAB1 contributes to NF-κB and MAPK signaling, influencing transcriptional programs that control cytokine production, innate immune responses, cell survival, and apoptosis. TAB1-dependent pathway tuning impacts cellular responses to TNF receptor and Toll/IL-1 receptor inputs, linking it to inflammation-associated processes and tissue stress responses. Dysregulated TAB1–TAK1 signaling has been studied in contexts of chronic inflammatory disease biology, tumor-associated inflammation, and other pathologies where NF-κB/MAPK activity is perturbed.

TAB1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TAB1 expression without altering the underlying DNA sequence.

TAB1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TAB1 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 TAB1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TAB1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TAB1 locus and enabling the study of TAB1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TAB1 pathway restoration in tumor cells with silenced or reduced TAB1 expression.

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