MPZL1 CRISPR Activation Plasmid (h): sc-407478-ACT

MPZL1 (myelin protein zero-like 1), also known as PZR, encodes a transmembrane immunoglobulin superfamily protein that functions as a scaffold for tyrosine phosphatase signaling, most notably through SHP2 (PTPN11). Via its cytoplasmic ITIM motifs, MPZL1 modulates phosphorylation-dependent pathways controlling cell adhesion, spreading, migration, and cytoskeletal remodeling, integrating cues from receptor tyrosine kinases and extracellular matrix interactions. MPZL1-associated signaling has been linked to regulation of focal adhesion dynamics and MAPK/ERK pathway activity, influencing proliferative and motile phenotypes in diverse cellular contexts. Dysregulated MPZL1 expression or signaling has been reported in oncology-relevant processes such as invasion and metastasis-associated behavior, supporting its use in mechanistic studies of signaling networks and adhesion-driven phenotypes.

MPZL1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MPZL1 expression without altering the underlying DNA sequence.

MPZL1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MPZL1 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 MPZL1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MPZL1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MPZL1 locus and enabling the study of MPZL1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MPZL1 pathway restoration in tumor cells with silenced or reduced MPZL1 expression.

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