Product Specific References for Applications and Species
Immunocytochemistry: Human | ||
PMID | Dilution | Publication |
32315597 | 1:100 | Herkenne, S., et al. 2020. Developmental and Tumor Angiogenesis Requires the Mitochondria-Shaping Protein Opa1. Cell Metabolism, 987-1003. |
Western Blot: Human | ||
PMID | Dilution | Publication |
32315597 | 1:1000 | Herkenne, S., et al. 2020. Developmental and Tumor Angiogenesis Requires the Mitochondria-Shaping Protein Opa1. Cell Metabolism, 987-1003. |
Western Blot: Mouse | ||
PMID | Dilution | Publication |
35414122 | 1:500 | O’Connor, T.N., et al. 2022. Endurance exercise attenuates juvenile irradiation-induced skeletal muscle functional decline and mitochondrial stress. . Skeletal Muscle, 45306. |
30591411 | not listed | Moore, T.M., et al. 2019. The impact of exercise on mitochondrial dynamics and the role of Drp1 in exercise performance and training adaptations in skeletal muscle. Molecular Metabolism, 51-67. |
25497302 | not listed | Elezaby, A., et al. 2015. Mitochondrial remodeling in mice with cardiomyocyte-specific lipid overload.. Journal of Molecular and Cellular Cardiology, 275-283. |
24949970 | not listed | Soleimanpour, S.A., et al. 2014. The diabetes susceptibility gene Clec16a regulates mitophagy.. Cell, 1577-1590. |
23695218 | not listed | Dolinsky, V.W., et al. 2013. Both aerobic exercise and resveratrol supplementation attenuate doxorubicin-induced cardiac injury in mice.. American Journal of Physiology. Endocrinology and Metabolism, E243-253. |
23028113 | 1:1000 | Chao, L.C., et al. 2012. Skeletal muscle Nur77 expression enhances oxidative metabolism and substrate utilization.. The Journal of Lipid Research, 2610-2619. |
22511781 | 1:1000 | Ngoh, G.A., et al. 2012. Loss of mitofusin 2 promotes endoplasmic reticulum stress.. The Journal of Biological Chemistry, 20321-30332. |
22037195 | 1:1000 | Papanicolaou, K.N., et al. 2012. Cardiomyocyte deletion of mitofusin-1 leads to mitochondrial fragmentation and improves tolerance to ROS-induced mitochondrial dysfunction and cell death. American Journal of Physiology. Heart and Circulatory Physiology, H167-H179. |