
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACCβ CRISPR Activation Plasmid (h) | sc-401903-ACT | 20 µg | $397.00 |
ACACB encodes acetyl-CoA carboxylase beta (ACCβ), a biotin-dependent mitochondrial-associated enzyme that catalyzes formation of malonyl-CoA, a key regulator of long-chain fatty acid oxidation. By modulating malonyl-CoA levels, ACCβ controls CPT1 activity and influences the balance between fatty acid synthesis and β-oxidation, linking lipid metabolism to cellular energy homeostasis. ACACB activity is integrated with nutrient-sensing pathways including AMPK signaling and is responsive to metabolic state in liver, muscle, and other oxidative tissues. Dysregulation of ACCβ-associated lipid flux has been connected to metabolic phenotypes relevant to insulin resistance, dyslipidemia, and hepatic steatosis, supporting mechanistic studies in metabolic disease biology.
ACCβ CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ACACB expression without altering the underlying DNA sequence.
ACCβ CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ACACB 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 ACACB transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ACCβ expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ACACB locus and enabling the study of ACCβ-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ACCβ pathway restoration in tumor cells with silenced or reduced ACACB expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.