ETFA Antibodies

Structure of ETFA

The α subunit of the electron transfer flavoprotein encoded by the ETFA gene is a protein with a molecular weight of approximately 35 kDa. This molecular weight remains relatively stable across different species, reflecting its core conserved function in energy metabolism.

This protein is composed of approximately 300 amino acid residues and its tertiary structure forms a typical α/β sandwich fold. The core region is responsible for binding the flavin adenine dinucleotide (FAD) cofactor. This FAD binding domain is crucial for the electron transfer function, capable of reversibly accepting and releasing electrons. The protein surface contains specific charged residues and hydrophobic patches, which are essential for the correct assembly with the other subunit ETFB and the specific interaction with the downstream electron acceptor ETF-CoQ reductase (ETF-QO), thereby ensuring the efficient transfer of electrons in the metabolic pathway.

Fig. 1 ETFA Gene/Protein Structure and Mutational Bioinformatic Analysis.¹

Key structural properties of ETFA:

• Typical α/β sandwich folding structure
• Conservative FAD binding pockets, surrounded by hydrophobic residues
• Flavin adenine dinucleotide (FAD) cofactors serve as electron carriers

Functions of ETFA

The core function of the protein encoded by the ETFA gene is to act as an electron transfer carrier in the mitochondrial matrix. However, it also plays a role in various physiological and pathological processes, including the maintenance of cellular redox homeostasis and the regulation of metabolic diseases.

This protein acts as a soluble electron carrier and its mode of action is a linear single-electron transfer, which is completely different from the S-shaped curve of cooperative oxygen binding of hemoglobin. This reflects its characteristic of being an efficient and specific "transit station" in the metabolic network. Its dysfunction will immediately interrupt multiple metabolic pathways, highlighting its pivotal role in basic metabolism.

Applications of ETFA and ETFA Antibody in Literature

1. Chen, Wankun, et al. "RETRACTED: NBPF4 mitigates progression in colorectal cancer through the regulation of EZH2‐associated ETFA." Journal of cellular and molecular medicine 25.18 (2021): 9038-9050. https://doi.org/10.1111/jcmm.16867

The article indicates that NBPF4 is lowly expressed in colorectal cancer. It avoids being inhibited by miR-17-3p by binding to ZFP36, thereby down-regulating EZH2 and inhibiting the expression of ETFA, thus slowing down tumor development.

2. Chautard, Robin, et al. "A case report of a mild form of multiple acyl-CoA dehydrogenase deficiency due to compound heterozygous mutations in the ETFA gene." BMC medical genomics 13.1 (2020): 12. https://doi.org/10.1186/s12920-020-0665-6

This study reports for the first time two novel heterozygous mutations (c.354C>A and c.652G>A) in the ETFA gene, which lead to mild MADD with onset in childhood. After avoiding fasting and undergoing treatment with levocarnitine and riboflavin, the patient's development and academic performance returned to normal.

3. Guo, Jingjing, et al. "Hepatocyte-derived Igκ promotes HCC progression by stabilizing electron transfer flavoprotein subunit α to facilitate fatty acid β-oxidation." Journal of Experimental & Clinical Cancer Research 43.1 (2024): 280. https://doi.org/10.1186/s13046-024-03203-8

Research has found that the Vκ4-1/Jκ 3-type immunoglobulin κ chain (Igκ), which is highly expressed in liver cancer cells, can bind to ETFA protein, stabilize its expression, thereby interfering with fatty acid β -oxidation and promoting tumor development. Targeting this pathway may become a new strategy for the treatment of liver cancer.

4. Chen, Fuying, et al. "S1P defects cause a new entity of cataract, alopecia, oral mucosal disorder, and psoriasis‐like syndrome." EMBO Molecular Medicine 14.5 (2022): e14904. https://doi.org/10.15252/emmm.202114904

This study has for the first time discovered that mutations in the MBTPS1 gene lead to abnormal function of the S1P protease encoded by it, which cannot stabilize the ETFA/ETFB complex, thereby causing mitochondrial dysfunction and CAOP syndrome. Supplementation of riboflavin can restore the stability of ETFA/ETFB and improve symptoms.

5. Parvini, Farshid, Mobarakeh Ajam-Hosseini, and Marziyeh Shadpour. "First report of neonatal-onset glutaric aciduria type II in the Iranian population caused by a novel deleterious ETFA variant." Orphanet Journal of Rare Diseases 20.1 (2025): 590. https://doi.org/10.1186/s13023-025-04107-2

This study reports GA2 caused by a novel heterozygous deletion mutation (c.485_493del) of the ETFA gene for the first time in Iran. This discovery clarifies the importance of genetic diagnosis in the prognosis judgment and family counseling of rare metabolic diseases.

Creative Biolabs: ETFA Antibodies for Research

Creative Biolabs specializes in the production of high-quality ETFA antibodies for research and industrial applications. Our portfolio includes monoclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.

• Custom ETFA Antibody Development: Tailor-made solutions to meet specific research requirements.
• Bulk Production: Large-scale antibody manufacturing for industry partners.
• Technical Support: Expert consultation for protocol optimization and troubleshooting.
• Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.

For more details on our ETFA antibodies, custom preparations, or technical support, contact us at email.