OPA1 Antibodies

Structure of OPA1

The mitochondrial dynamin-like GTPase encoded by the OPA1 gene is a large protein with a molecular weight of approximately 112 kDa. This molecular weight may fluctuate slightly due to various isomers produced by differential splicing of transcripts.

This protein contains an N-terminal GTPase domain, a central kinetoprotein domain and a C-terminal transmembrane domain, which together form the functional structural basis of it. Its core function relies on the synergistic effect of soluble long L-OPA1 and the membrane-anchored short S-OPA1 after proteolysis. The two jointly complete the teaming and fusion of the mitochondrial inner membrane through trans-interaction. The dysregulation of this process directly disrupts the morphology of mitochondrial crists, leading to the release of cytochrome c and triggering apoptosis, which constitutes the core pathological mechanism of autosomal dominant optic atrophy caused by OPA1 gene mutations.

Fig. 1 Domain organization of OPA1.¹

Key structural properties of OPA1:

• Modular multi-domain architecture
• Central coiled-coil domains that mediate membrane tethering
• The N-terminal GTPase domain drives conformational change and energy supply
• Proteolytic sensitive sites regulate the functional balance of long and short isomers

Functions of OPA1

The core function of the OPA1 protein is to regulate mitochondrial inner membrane fusion and maintain crest morphology. In addition, it is also involved in a variety of cellular physiological processes, including energy metabolism regulation and apoptosis inhibition.

The functional activity of OPA1 is precisely regulated by proteolysis. The synergistic effect of its long and short isomers constitutes the core mechanism of mitochondrial quality control, and the disruption of this mechanism is the direct cause of hereditary optic neuropathy.

Applications of OPA1 and OPA1 Antibody in Literature

1. Zanfardino, Paola, et al. "The balance of MFN2 and OPA1 in mitochondrial dynamics, cellular homeostasis, and disease." Biomolecules 15.3 (2025): 433. https://doi.org/10.3390/biom15030433

The article indicates that OPA1 mediates mitochondrial fusion, and its mutations can lead to neurodegenerative diseases such as ADOA, affecting energy metabolism and autophagy. Therapies targeting mTOR and others to restore mitochondrial function hold great promise.

2. Herkenne, Stephanie, and Luca Scorrano. "OPA1, a new mitochondrial target in cancer therapy." Aging (Albany NY) 12.21 (2020): 20931. https://doi.org/10.18632/aging.104207

The article indicates that in addressing the challenges of drug resistance and metastasis in cancer, research has found that the mitochondrial protein OPA1 is the key. Inhibiting OPA1 can effectively block tumor angiogenesis, inhibit metastasis and reverse drug resistance, opening up a new path for the development of novel anti-cancer therapies.

3. Yang, Wenbo, et al. "Empagliflozin improves renal ischemia–reperfusion injury by reducing inflammation and enhancing mitochondrial fusion through AMPK–OPA1 pathway promotion." Cellular & Molecular Biology Letters 28.1 (2023): 42. https://doi.org/10.1186/s11658-023-00457-6

Research has found that mutations in the OPA1 gene not only disrupt the structure of mitochondria but also lead to abnormal distribution of genetic material (mtDNA nucleoli) within them, with a large number of mitochondria or even complete absence of nucleoli. This provides a new mechanism for revealing the etiology of hereditary optic atrophy.

4. Weng, Jiali, et al. "TRPA1-PI3K/Akt-OPA1-ferroptosis axis in ozone-induced bronchial epithelial cell and lung injury." Science of the Total Environment 918 (2024): 170668. https://doi.org/10.1016/j.scitotenv.2024.170668

Research has revealed that ozone activates the TRPA1 receptor and inhibits the mitochondrial fusion protein OPA1 through the PI3K/Akt pathway, thereby inducing mitochondrial dysfunction and ferroptosis, leading to lung injury. Blocking TRPA1 has a protective effect.

5. Chen, Jiaqi, et al. "OPA1, a molecular regulator of dilated cardiomyopathy." Journal of Cellular and Molecular Medicine 27.20 (2023): 3017-3025. https://doi.org/10.1111/jcmm.17918

Research reveals that in dilated cardiomyopathy, the p53 gene affects the key protein OPA1 by activating Bak/Bax and OMA1, thereby leading to apoptosis, mitochondrial dynamic imbalance and ridge structure changes. OPA1 is the core mediator of this process.

Creative Biolabs: OPA1 Antibodies for Research

Creative Biolabs specializes in the production of high-quality OPA1 antibodies for research and industrial applications. Our portfolio includes monoclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.

• Custom OPA1 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 OPA1 antibodies, custom preparations, or technical support, contact us at email.