Bcl10 CRISPR Activation Plasmid (h): sc-400483-ACT

BCL10 encodes Bcl10, an adaptor protein that couples antigen receptor signaling to downstream transcriptional programs in immune cells. Bcl10 functions within the CARMA1–Bcl10–MALT1 (CBM) complex to promote canonical NF-κB activation, supporting lymphocyte activation, proliferation, and cytokine responses, and it can also influence MAPK signaling and apoptosis. Dysregulated BCL10 activity or localization has been linked to altered NF-κB pathway output and immune homeostasis, and is frequently studied in the context of lymphoid malignancy biology and inflammatory signaling networks. As a result, BCL10 is a common node for mechanistic studies of receptor-proximal signaling, transcriptional regulation, and pathway crosstalk.

Bcl10 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous BCL10 expression without altering the underlying DNA sequence.

Bcl10 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the BCL10 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 BCL10 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Bcl10 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native BCL10 locus and enabling the study of Bcl10-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Bcl10 pathway restoration in tumor cells with silenced or reduced BCL10 expression.

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