
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Bcr CRISPR Activation Plasmid (h) | sc-401514-ACT | 20 µg | $397.00 | |||
Bcr CRISPR Activation Plasmid (h2) | sc-401514-ACT-2 | 20 µg | $397.00 |
Human BCR encodes the Bcr protein, a multifunctional cytoplasmic regulator with serine/threonine kinase activity and a RhoGEF domain that modulates small GTPase signaling. Through effects on RAC1/CDC42-dependent cytoskeletal dynamics, membrane trafficking, and stress-responsive signaling, Bcr contributes to control of cell adhesion, migration, and proliferation. BCR is widely studied in hematologic malignancy biology due to its involvement in oncogenic gene fusion events and downstream signaling rewiring. Altered BCR expression or regulation provides a tractable entry point for dissecting kinase- and GTPase-linked pathways relevant to transformation and lineage-specific signaling programs.
Bcr CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous BCR expression without altering the underlying DNA sequence.
Bcr CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the BCR 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 BCR transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Bcr expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native BCR locus and enabling the study of Bcr-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Bcr pathway restoration in tumor cells with silenced or reduced BCR expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.