Mitofusin1 (MFN1) is a key mitochondrial outer membrane protein involved in regulating mitochondrial fusion, a critical process for maintaining mitochondrial network integrity, cellular energy metabolism, and apoptosis. As a member of the dynamin-related GTPase family, MFN1 mediates the tethering and merging of adjacent mitochondria, working in concert with its homolog MFN2. Dysregulation of MFN1 is linked to mitochondrial dysfunction, which has been implicated in neurodegenerative disorders (e.g., Alzheimer’s and Parkinson’s diseases), cardiovascular conditions, metabolic syndromes, and cancer.
MFN1 antibodies are essential tools for studying the expression, localization, and functional roles of MFN1 in both physiological and pathological contexts. These antibodies are widely used in techniques such as Western blotting, immunofluorescence, and immunohistochemistry to visualize MFN1 distribution in cells or tissues. High-quality MFN1 antibodies exhibit specificity for their target, often validated through genetic knockout or siRNA-mediated knockdown experiments to confirm reduced signal in MFN1-deficient models. Researchers rely on these antibodies to explore how MFN1 mutations or altered expression contribute to disease mechanisms, such as impaired mitochondrial dynamics, oxidative stress, or defective mitophagy. Additionally, MFN1 antibodies aid in evaluating therapeutic strategies targeting mitochondrial fusion-fission balance. As mitochondrial health gains attention in aging and disease research, MFN1 antibodies remain pivotal for advancing our understanding of cellular bioenergetics and organelle homeostasis.