
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
JMJD1B CRISPR Activation Plasmid (h) | sc-404249-ACT | 20 µg | $397.00 |
KDM3B (JMJD1B) encodes a JmjC-domain histone demethylase that primarily removes repressive H3K9 methylation marks to promote chromatin accessibility and transcriptional activation. By reshaping epigenetic landscapes, JMJD1B influences lineage-specific gene programs, cellular differentiation, and context-dependent control of proliferation and stress responses. Its activity integrates with broader chromatin regulatory networks and can modulate signaling-dependent transcription, linking metabolic and developmental cues to gene expression outputs. Dysregulation of KDM3B has been reported across multiple disease contexts, making it a useful target for mechanistic studies of epigenetic control and aberrant transcriptional states in human cells.
JMJD1B CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KDM3B expression without altering the underlying DNA sequence.
JMJD1B CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KDM3B 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 KDM3B transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous JMJD1B expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KDM3B locus and enabling the study of JMJD1B-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of JMJD1B pathway restoration in tumor cells with silenced or reduced KDM3B expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.