Recombinant Mouse Mitofusin-2 (Mfn2)

1. The authors conclude that proper development of the lens and lens transparency depend on normal Mfn2 gene function. PMID:29367651
2. miR-497 promotes proliferation and inhibits apoptosis of cardiomyocytes by downregulating the expression of Mfn2 in a mouse model of myocardial I/R injury. PMID:29852387
3. This study explicitly demonstrated that mitofusin 2 could ameliorate Ischemia Reperfusion injury mainly through promoting autophagy. PMID:29734176
4. knockdown attenuates apoptosis in hypoxia PMID:29097872
5. 3D electron tomography shows that MFN2-deficient cardiac mitochondria are larger in volume, more elongated and have fewer mitochondria-sarcoplasmic reticulum contacts. PMID:28904083
6. These findings provide insights into potential mechanisms of Mfn2-mediated cellular alterations, which may have significant implications for oocyte maturation. PMID:27485634
7. findings indicate that down-regulation of Mfn2 may have an impact on the maturation and fertilization of immature oocytes in vitro by modulating meiosis and mitochondrial function. PMID:27469431
8. BAT (brown adipose tissue) adaptation to obesity is regulated by Mfn2 and with BAT-Mfn2 absent, BAT contribution to prevention of insulin resistance is independent and inversely correlated to whole-body cold-stimulated thermogenesis. PMID:28539390
9. Mfn2 stands as a bona fide endoplasmic-mitochondria tether whose ablation decreases interorganellar juxtaposition and communication. PMID:27647893
10. Mitofusin 2 - one of a few proteins involved in a maintenance of an appropriate mitochondrial architecture, and in the consequence in the regulation of mitochondrial metabolism and calcium signalling, the controlling of the mitochondrial DNA level, and the regulation of cell proliferation and differentiation is the focus. [REVIEW] PMID:28132466
11. Despite apparent mitochondrial dysfunction, hearts deficient in both Mfn1 and Mfn2 are protected against acute myocardial infarction due to impaired mitochondria/sarcoplasmic reticulum tethering. PMID:27228353
12. Presenilin 2 (PS2), mutations in which underlie familial Alzheimer's disease (FAD), promotes endoplasmic reticulum-mitochondria coupling only in the presence of mitofusin 2 (Mfn2). PMID:27239030
13. The data of this study suggest that post-translational modification of Mfn2 is associated with its dysregulation during a window of metabolic vulnerability that precedes glaucomatous degeneration. PMID:28684211
14. Study demonstrated that deregulation of mfn2 played a critical role in the mitochondrial disorder during the progression of Alzheimer's disease, and its decreased expression was regulated at least in part by miR-195. Therefore, upregulation of mfn2 expression by decreasing the level of miR-195 might be a potential new therapeutic strategy for treatment of Alzheimer's disease. PMID:27693395
15. Mfn2 downregulation or the exogenous expression of normal Parkin restored cytosolic Ca(2+) transients in fibroblasts from patients with PARK2 mutations, a catalytically inactive Parkinson's disease (PD)-related Parkin variant had no effect. Parkin is directly involved in regulating ER-mitochondria contacts and provide new insight into the role of the loss of Parkin function in PD development. PMID:27206984
16. Altogether, these results demonstrate that Mfn2 is a mediator of mitochondria to lipid droplet interactions, influencing lipolytic processes and whole-body energy homeostasis. PMID:28348166
17. we demonstrated that by modulating mitochondrial energy metabolism through Mfn2 and mitochondrial Ca2+, PPAR-b took an important role in neuronal differentiation induced by flavonoid compound 4a PMID:27315062
18. Furthermore, analysis of muscle Mfn2-deficient mice revealed that aging-induced Mfn2 decrease underlies the age-related alterations in metabolic homeostasis and sarcopenia. PMID:27334614
19. Mice hemizygous for a pathogenic Mfn2 allele exhibit hind limb/foot gait deficits and phenotypic perturbations in nerve and muscle. PMID:27907123
20. We found that mouse embryonic fibroblasts lacking Mfn2 have altered lipid droplet morphology. However, triacylglycerol biosynthesis was not dependent on ER-mitochondrial tethering mediated by mitofusins. Lastly, Mfn2 does not have a role in adipocyte differentiation. PMID:27404125
21. mitofusin 2 overexpression may attenuate hypoxia-induced apoptosis. PMID:26434502
22. Mitofusin 2, in addition to its role in mitochondrial fusion, is important for maintaining coenzyme Q levels and may be an integral player in the mevalonate synthesis pathway. PMID:27060252
23. low expression involved in mechanism of premature ovarian failure by affecting both mitochondria energy metabolism and apoptosis PMID:26327438
24. suggest a balance between negative metabolic consequences of mitofusin 2 deficiency and adaptive processes exemplified by increased level of PGC-1alpha and TFAM transcription factor which prevent an depletion of mtDNA and severe impairment of cell metabolism PMID:26230519
25. Our results indicate that HDAC6 is a critical regulator of MFN2 degradation by MARCH5, thus protecting mitochondrial connectivity from hypoxic stress. PMID:26210454
26. Mfn2 attenuates the blastocyst formation rate and cleavage speed in mouse zygotes and causes mitochondrial dysfunction, as confirmed by the ATP and mtDNA levels and mitochondrial membrane potential. PMID:25978725
27. Mfn2 is specifically required for the maintenance of hematopoietic stem cells (HSCs) with extensive lymphoid potential, but not, or less so, for the maintenance of myeloid-dominant HSCs PMID:26789249
28. confirm the hypothesis that the cellular consequences of mutations in the mitofusin 2 gene can mostly be manifested in the peripheral nervous system PMID:25574749
29. Data suggest that mitochondrial fusion and fission events are regulated by four GTPases: Mfn1, Mfn2, OPA1 (optic atrophy 1 protein), and Drp1 (dynamin 1-like protein). [REVIEW] PMID:26375863
30. Silencing Mfn2 results in amarked reduction in Ca2+uptake by mitochondria remaining asso-ciated with the triad junction and this reduction is due largely toa depolarization of the mitochondrial membrane potential PMID:25477138
31. a new model for ER-mitochondria juxtaposition in which Mfn2 works as a tethering antagonist preventing an excessive, potentially toxic, proximity between the two organelles. PMID:25870285
32. deficiency accelerates recovery of renal function and enhances animal survival after ischemic acute kidney injury PMID:25201884
33. These findings suggest that mitochondrial impairment is a very early event in Alzheimer disease pathogenesis and abnormal expression of Mfn1 and Mfn2 caused by excessive intracellular Abeta is the possible molecular mechanism. PMID:24710686
34. Overexpression of mitofusin 2 significantly inhibits the beta-amyloid-mediated cell death pathway. PMID:25359615
35. this study unravels an unexpected and novel role for MFN2 in maintenance of the terpenoid biosynthesis pathway, which is necessary for mitochondrial coenzyme Q biosynthesis. PMID:25688136
36. Calpain-mediated MFN2 degradation is a novel mechanism regulating mitochondrial fusion during glutamate excitotoxicity. PMID:25416777
37. Mice lacking mitofusin 2 (Mfn2) in hearts have impaired parkin-mediated mitophagy leading to accumulation of damaged ROS-producing organelles and progressive heart failure. PMID:24874428
38. MiR-106b targets Mfn2 and regulates skeletal muscle mitochondrial function and insulin sensitivity. PMID:23954742
39. Mitochondrial protein mitofusin 2 is required for NLRP3 inflammasome activation after RNA virus infection. PMID:24127597
40. Data establish MFN2 in pro-opiomelanocortin neurons as an essential regulator of systemic energy balance by fine-tuning the mitochondrial-endoplasmic reticulum axis homeostasis and function. PMID:24074867
41. Data unmask an important role for mitochondrial dynamics governed by Mfn1 and Mfn2 in Agrp neurons in central regulation of whole-body energy metabolism. PMID:24074868
42. Mfn2 is an upstream modulator of PERK.Mfn2 modulates the unfolded protein response and mitochondrial function via repression of PERK. PMID:23921556
43. Loss of Mfn2 results in progressive, retrograde degeneration of dopaminergic neurons in the nigrostriatal circuit. PMID:22859504
44. These results show that Mfn2, but not Mfn1, is required for axonal projections of DA neurons in vivo. PMID:22914740
45. Juxtaposition of endoplasmic reticulum and mitochondria was increased in Mitofusin-2-null embryonic fibroblasts. PMID:23029466
46. mfn2 mutations alter mitochondrial dynamics and induce retinal and cardiac pathology PMID:22957060
47. Mfn2 plays an important role in maintaining glucose and lipid homeostasis, and in the development of insulin resistance in vivo. PMID:20037808
48. Physical tethering of SR and mitochondria via Mfn2 is essential for normal interorganelle Ca(2+) signaling in the myocardium. PMID:22777004
49. Our findings establish that Mfn-1 and Mfn-2 are essential in mediating mitochondrial remodeling during postnatal cardiac development, a time of dramatic transitions in the bioenergetics and growth of the heart. PMID:22904094
50. Data indicate that eficiency of mitofusin 2 (MFN2) caused multiple molecular and functional defects that undermined cardiac reserve and gradually led to cardiac vulnerability and dysfunction. PMID:22619176

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UNIGENE: Mm.154312

KEGG: mmu:170731

STRING: 10090.ENSMUSP00000030884