ACSL5 Antibody / Long chain fatty acid CoA ligase 5

ACSL5 antibody detects Long chain fatty acid CoA ligase 5, an enzyme that activates long chain fatty acids for lipid metabolism, beta oxidation, and membrane synthesis. Encoded by the ACSL5 gene on chromosome 10q25.2, this enzyme belongs to the acyl CoA synthetase family, which catalyzes the conversion of free fatty acids to fatty acyl CoA thioesters using ATP and Coenzyme A. ACSL5 functions as a metabolic gatekeeper, determining whether lipids are directed toward energy production or anabolic pathways such as triglyceride and phospholipid synthesis.

Structurally, ACSL5 is an approximately 76 kilodalton enzyme localized to the outer mitochondrial membrane and the endoplasmic reticulum. It contains conserved AMP binding and acyl adenylate forming motifs required for catalysis of long chain fatty acids, typically those containing 12 to 20 carbon atoms. ACSL5 expression is highest in metabolically active tissues such as the small intestine, liver, and brown adipose tissue, where rapid fatty acid activation supports energy production during fasting, thermogenesis, and lipid absorption.

The ACSL5 antibody is widely used in metabolism, mitochondrial biology, and lipid biochemistry research to study fatty acid activation, transport, and oxidation. Western blot analysis detects a 76 kilodalton band corresponding to ACSL5, while immunofluorescence reveals perinuclear and mitochondrial membrane localization. This antibody provides a dependable tool for assessing lipid metabolic flux, energy homeostasis, and fatty acid utilization under physiological and pathological conditions.

Functionally, ACSL5 determines the metabolic fate of long chain fatty acids by channeling activated fatty acyl CoA into either mitochondrial beta oxidation for ATP production or endoplasmic reticulum based lipid synthesis. It interacts with key metabolic regulators such as carnitine palmitoyltransferase 1 (CPT1) and peroxisome proliferator activated receptor alpha (PPAR alpha), coordinating lipid oxidation and storage. Dysregulation of ACSL5 expression has been linked to obesity, insulin resistance, and nonalcoholic fatty liver disease, where altered fatty acid channeling contributes to lipid accumulation and oxidative stress. In intestinal epithelial cells, ACSL5 also plays a role in apoptosis regulation, reflecting its broader function in energy balance and cell survival.

Beyond energy metabolism, ACSL5 participates in mitochondrial dynamics and lipid signaling by influencing the composition of phospholipids that form mitochondrial membranes. Its activity affects membrane curvature and permeability, which can impact mitochondrial fission and fusion processes. Increased ACSL5 expression under stress conditions may enhance beta oxidation and reactive oxygen species production, whereas reduced expression limits fatty acid utilization and leads to metabolic inflexibility. The ACSL5 antibody allows detailed exploration of these adaptive responses and facilitates research into metabolic disorders, energy regulation, and mitochondrial health.