
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ALKBH2 CRISPR Activation Plasmid (h) | sc-407363-ACT | 20 µg | $397.00 |
ALKBH2 (AlkB homolog 2) is a Fe(II)/2-oxoglutarate–dependent dioxygenase that repairs alkylation damage in DNA by directly reversing lesions such as 1-methyladenine and 3-methylcytosine. By restoring normal base pairing, ALKBH2 supports genome stability during DNA replication and coordinates with base excision repair and broader DNA damage response pathways. Its activity is relevant to cellular responses to endogenous and environmental alkylating agents, linking ALKBH2 expression to mutational burden and replication stress. Altered regulation of ALKBH2 has been studied in contexts of tumor biology and treatment-associated DNA damage tolerance, where changes in repair capacity can influence genomic integrity phenotypes.
ALKBH2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ALKBH2 expression without altering the underlying DNA sequence.
ALKBH2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ALKBH2 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 ALKBH2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ALKBH2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ALKBH2 locus and enabling the study of ALKBH2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ALKBH2 pathway restoration in tumor cells with silenced or reduced ALKBH2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.