Alexa Fluor® 488 Anti-SUCLA2 antibody [EPR14924]

Supplementary information

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

SUCLA2 also known as succinate-CoA ligase (ADP-forming) subunit beta is an enzyme with a molecular mass of approximately 48 kDa. It plays an important role in the mitochondrial matrix where it participates in the citric acid cycle. The enzyme is found in various tissues with higher expression in muscle and brain tissues. SUCLA2 functions as part of the succinyl-CoA synthetase complex which catalyzes the reversible conversion of succinyl-CoA to succinate with the concurrent substrate-level phosphorylation of GDP to GTP or ADP to ATP depending on tissue type.

Biological function summary

The SUCLA2 subunit is essential for energy metabolism. It forms a component of the succinyl-CoA synthetase complex working with the alpha subunit SUCLG1. This complex supports the provision of energy by converting GDP to GTP in processes needing high energy levels critical for maintaining cellular homeostasis. Therefore it especially supports tissues with high energy demands. The action of SUCLA2 links energy production with the metabolic pathways involved in cellular respiration.

Pathways

SUCLA2 plays a critical role in the citric acid cycle also known as the Krebs cycle. Part of this cycle SUCLA2 contributes to cellular respiration and energy production. The SUCLA2 protein closely interacts with SUCLG1 to form the functional succinyl-CoA synthetase enzyme. Additionally it shows connections to the electron transport chain where the products of its catalysis are used in ATP generation. Defects in these pathways can have widespread effects on cellular energy states and mitochondrial function.

SUCLA2 mutations are linked to mitochondrial DNA depletion syndromes particularly myopathy and encephalopathy. These conditions lead to severe energy metabolism impairments due to faulty mitochondrial function. SUCLA2 has also been associated with Leigh syndrome a neurodegenerative disorder marked by compromised cellular respiration. Such disorders point towards deficient ATP synthesis highlighting the interconnected role of SUCLA2 with other mitochondrial proteins involved in cellular energy metabolism.