DOCK 2 CRISPR Activation Plasmid (m2): sc-430116-ACT-2

Mouse Dock2 encodes DOCK2, a hematopoietic-restricted guanine nucleotide exchange factor that activates Rac GTPases to control actin cytoskeleton remodeling and directional migration in lymphocytes, neutrophils, and other immune cells. DOCK2 functions downstream of chemokine receptors and antigen receptor signaling, coordinating integrin-dependent adhesion, immunological synapse formation, and trafficking through lymphoid tissues via pathways linking PI3K signaling to Rho-family GTPase regulation. Genetic and functional disruption of DOCK2 is associated with impaired innate and adaptive immune responses and has been implicated in inflammatory and autoimmune-like phenotypes, susceptibility to infection, and altered tumor immune surveillance in experimental systems. Dock2 mouse gene editing supports mechanistic studies of leukocyte motility, chemotaxis, and signaling network rewiring, enabling immune cell–intrinsic dissection in inflammation, host–pathogen interactions, and immuno-oncology research models.

DOCK 2 CRISPR Activation Plasmid (m2) provides a targeted, non-destructive approach to upregulating endogenous Dock2 expression without altering the underlying DNA sequence.

DOCK 2 CRISPR Activation Plasmid (m2) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Dock2 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 Dock2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DOCK 2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Dock2 locus and enabling the study of DOCK 2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DOCK 2 pathway restoration in tumor cells with silenced or reduced Dock2 expression.

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