2μg (R: reducing condition, N: non-reducing condition).
Product Details
Product Details
Product Specification
| Species | Human |
| Synonyms | ACSL5, ACS5, FACL5 |
| Accession | Q9ULC5 |
| Amino Acid Sequence | Met1-Asp683 with GST Tag at the N-Terminus |
| Expression System | HEK293 |
| Molecular Weight | 70-100kDa (Reducing) |
| Purity | >90% by SDS-PAGE |
| Conjugation | Unconjugated |
| Tag | GST Tag |
| Physical Appearance | Liquid |
| Storage Buffer | 50mM Tris, 150mM NaCl, pH7.5, 1mM DTT, 10%Glycerol |
| Stability & Storage | Stable for 12 months upon stored at -80℃ from the date of receipt. And avoid repeated freeze-thaws cycles. |
| Reference | 1. Wang, Y., et al. (2021). ACSL5 is a Biomarker for Ferroptosis and a Potential Therapeutic Target in Gastric Cancer. Frontiers in Oncology, 11, 675944. |
Background
ACSL5 (Acyl-CoA Synthetase Long-Chain Family Member 5) is a key enzyme located in the outer mitochondrial membrane and endoplasmic reticulum. It belongs to the acyl-CoA synthetase family, which catalyzes the essential activation step of long-chain fatty acids (typically C16-C20) by converting them into their corresponding acyl-CoA esters. This reaction, dependent on ATP and Coenzyme A, is the first and committed step in fatty acid metabolism, preparing fatty acids for subsequent processes such as β-oxidation (for energy production), phospholipid synthesis (for membrane biogenesis), or triglyceride storage.
ACSL5 expression and activity are implicated in several diseases. Its dysregulation is associated with metabolic disorders (e.g., insulin resistance, non-alcoholic fatty liver disease), where altered lipid partitioning plays a key role. In cancer, ACSL5 exhibits context-dependent roles, acting as a tumor suppressor in colorectal and gastric cancers, possibly by modulating cell death pathways, while potentially supporting tumor growth in other contexts by fueling lipid anabolism. This dual nature makes it a complex but interesting target for metabolic and cancer research.
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