
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Tec CRISPR Activation Plasmid (h) | sc-402051-ACT | 20 µg | $397.00 |
Human TEC encodes Tec, a non-receptor tyrosine kinase of the Tec family that transduces signals downstream of immune receptors, including the B cell receptor and Fc receptors. Tec integrates phosphorylation events that influence phospholipase C-γ activation, calcium flux, PI3K–AKT signaling, and MAPK pathways, thereby shaping lymphocyte activation, differentiation, and cytokine responses. Dysregulated TEC-linked signaling has been associated with aberrant immune cell function and inflammatory phenotypes, making TEC a useful node for studying receptor-proximal kinase networks. TEC is also leveraged as a pathway readout in systems-level analyses of immune signaling crosstalk and transcriptional remodeling.
Tec CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TEC expression without altering the underlying DNA sequence.
Tec CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TEC 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 TEC transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Tec expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TEC locus and enabling the study of Tec-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Tec pathway restoration in tumor cells with silenced or reduced TEC expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.