Anti-ACSL3 antibody

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

The ACSL3 protein also known as Acyl-CoA synthetase long-chain family member 3 plays a central role in lipid metabolism. It is an enzyme with a mass of approximately 79 kDa that activates long-chain fatty acids by converting them into acyl-CoA thioesters. This process is critical for their subsequent use in metabolic pathways. ACSL3 expression occurs mainly in the liver adipose tissue and brain tissues involved in energy balance and storage. By catalyzing the initial step in the fatty acid metabolic pathway ACSL3 influences lipid biosynthesis and degradation.

Biological function summary

ACSL3 contributes to cellular processes involving lipid synthesis and energy production. It functions as part of a larger lipid metabolic framework where it facilitates the incorporation of fatty acids into complex lipids like phospholipids and triglycerides. Though not a member of a molecular complex in terms of protein structure its activity complements other enzymes involved in lipid metabolism indicating an indirect association with lipid-binding proteins and transport mechanisms. The metabolic activity of ACSL3 therefore plays a significant role in maintaining cell membrane integrity and energy balance.

Pathways

ACSL3 integrates into the peroxisome proliferator-activated receptor (PPAR) signaling and fatty acid metabolism pathways. These pathways coordinate the regulation and utilization of lipids for energy storage and consumption. The ACSL3 protein interacts with proteins such as PPARα and PPARγ which are transcription factors that regulate gene expression associated with lipid metabolism. Through these interactions ACSL3 affects lipid metabolism at a genomic level promoting the adaptive responses necessary for cellular energy requirements.

Associated diseases and disorders

ACSL3 association with metabolic conditions like obesity and non-alcoholic fatty liver disease (NAFLD) is evident. In obesity ACSL3 expression may alter lipid metabolism contributing to excess fat accumulation and energy imbalance. Additionally elevated ACSL3 levels in the liver could be linked to NAFLD enhancing lipid storage and steatosis. The protein interacts indirectly with other players in metabolic diseases such as SREBP-1c and AMPK which are critical regulators of lipid homeostasis and energy balance in cells. These connections suggest that ACSL3 is a potential target for therapeutic interventions in metabolic disorders.