MALT1 CRISPR Activation Plasmid (h): sc-400791-ACT

Human MALT1 (mucosa-associated lymphoid tissue lymphoma translocation protein 1) is a paracaspase that functions as a central signaling node downstream of antigen receptors in lymphocytes, integrating signals from the CARD11–BCL10–MALT1 (CBM) complex to drive canonical NF-κB and MAPK pathway activation. Beyond scaffold activity, MALT1 protease cleaves select substrates to tune T cell and B cell activation, cytokine production, and survival programs. Dysregulated MALT1 signaling is linked to aberrant immune activation and is implicated in lymphoid malignancy biology through altered NF-κB-dependent transcriptional programs. Modulating MALT1 expression is therefore useful for dissecting signal-dependent transcription, immune receptor pathway wiring, and context-specific inflammatory gene regulation.

MALT1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MALT1 expression without altering the underlying DNA sequence.

MALT1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MALT1 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 MALT1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MALT1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MALT1 locus and enabling the study of MALT1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MALT1 pathway restoration in tumor cells with silenced or reduced MALT1 expression.

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