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Human MFN2 Protein expressed in HEK-293 Cells - ABIN2726078
Wang, Zhang, Li, Tang, Siedlak, Fujioka, Liu, Su, Pi, Wang: MFN2 couples glutamate excitotoxicity and mitochondrial dysfunction in motor neurons. in The Journal of biological chemistry 2015
Enhancing the profusion gene mitofusin/marf is beneficial in an in vivo model of TDP-43 (show TARDBP Proteins) proteinopathies, serving as a potential therapeutic target.
activation of endoplasmic reticulum stress by defective mitochondria is neurotoxic in pink1 (show PINK1 Proteins) and parkin (show PARK2 Proteins) flies and that the reduction of this signalling is neuroprotective, independently of defective mitochondria.
Clu (show CLU Proteins) is upstream of and binds to VCP (show vcp Proteins) in vivo and promotes VCP (show vcp Proteins)-dependent Marf degradation in vitro Marf accumulates in whole muscle lysates of clu (show CLU Proteins)-deficient flies and is destabilized upon Clu (show CLU Proteins) overexpression. Thus, Clu (show CLU Proteins) is essential for mitochondrial homeostasis and functions in concert with Parkin (show PARK2 Proteins) and VCP (show vcp Proteins) for Marf degradation to promote damaged mitochondrial clearance.
lack of ChChd3 (show CHCHD3 Proteins) leads to inactivation of Hippo activity under normal development, which is also dependent on the transcriptional coactivator Yorkie (Yki (show YAP1 Proteins)). Furthermore, loss of ChChd3 (show CHCHD3 Proteins) induces oxidative stress and activates the JNK (show MAPK8 Proteins) pathway. In addition, depletion of other mitochondrial fusion components, Opa1 (show OPA1 Proteins) or Marf, inactivates the Hippo pathway as well.
Marf is required for mitochondrial fusion and transport in long axons.
Expression of Mfn2 and endoplasmic reticulum (ER) stress reduction in flies lacking Marf corrected ER shape, attenuating the developmental and motor defects.
Parkin (show PARK2 Proteins) deficiency and resulting mitophagic disruption produces cardiomyopathy which can be contained by suppressing mitofusin.
mfn2 mutations alter mitochondrial dynamics and induce retinal and cardiac pathology
Data report here that Drosophila Reaper can induce mitochondrial fragmentation by binding to and inhibiting the pro-fusion protein MFN2 and its Drosophila counterpart dMFN/Marf.
MARF and Opa1 (show OPA1 Proteins) control mitochondrial and cardiac function in Drosophila.
a critical role of Mfn2 in CD4 (show CD4 Proteins)(+) T cell apoptosis in sepsis and the underlying mechanism of autophagy deficiency.
Loss of Yap (show YAP1 Proteins) reduced SIRT1 (show SIRT1 Proteins) expression and inhibited Mfn2-mediated mitophagy. Collectively, our results identified Hippo-Yap (show YAP1 Proteins) as a tumor promoter in gastric cancer that was mediated via activation of the SIRT1 (show SIRT1 Proteins)/Mfn2/mitophagy axis, with potential applications to gastric cancer therapy involving cancer survival and migration.
The overexpression of Mfn2 could trigger cervical tumour apoptosis in vitro and in vivo, which was related to the mitochondrial pathway, and may provide a new treatment target for cervical carcinoma.
Data suggest that mitofusin-2 (MFN2) may be involved in cervical cancer pathogenesis as an oncogene (show RAB1A Proteins) and might serve as a biomarker of cervical squamous cell carcinoma (SCC (show CYP11A1 Proteins)).
This study detected a compound heterozygous MFN2 mutation in a patient with a severe phenotype and the co-occurrence of MFN2 and PMP22 (show PMP22 Proteins) mutations in a patient with an uncommon phenotype.
The research findings indicate that the inhibition of microRNA-214 promotes the epithelial mesenchymal transition process and contributes to bladder wall fibrosis by up-regulating Mitofusin 2, thus leading to the occurrence of interstitial cystitis in postmenopausal women.
report of two patients with pure axonal peripheral neuropathy who are carrying novel compound heterozygous mutations in MFN2 gene
The heterozygous mutation c.2251C>T was identified in exon 19 of the MFN2 gene, presumably leading to the truncation of the MFN2 protein (p.Gln751Ter). The mutation co-segregated completely with the disease within the family
In this Chinese Han population a novel Charcot-Marie-Tooth disease-associated gene mutations including the MFN2 (c.497C>T) was discovered.
Mosaicism and missense mutation in MFN2 lead to severe Charcot-Marie-Tooth disease in a daughter, with minimal clinical features in the father.
This study explicitly demonstrated that mitofusin 2 could ameliorate Ischemia Reperfusion injury mainly through promoting autophagy.
3D electron tomography shows that MFN2-deficient cardiac mitochondria are larger in volume, more elongated and have fewer mitochondria-sarcoplasmic reticulum contacts.
These findings provide insights into potential mechanisms of Mfn2-mediated cellular alterations, which may have significant implications for oocyte maturation.
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.
BAT (show BAAT Proteins) (brown adipose tissue) adaptation to obesity is regulated by Mfn2 and with BAT (show BAAT Proteins)-Mfn2 absent, BAT (show BAAT Proteins) contribution to prevention of insulin (show INS Proteins) resistance is independent and inversely correlated to whole-body cold-stimulated thermogenesis.
Mfn2 stands as a bona fide endoplasmic-mitochondria tether whose ablation decreases interorganellar juxtaposition and communication.
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]
Despite apparent mitochondrial dysfunction, hearts deficient in both Mfn1 (show MFN1 Proteins) and Mfn2 are protected against acute myocardial infarction due to impaired mitochondria/sarcoplasmic reticulum tethering.
Presenilin 2 (PS2 (show PSEN2 Proteins)), mutations in which underlie familial Alzheimer's disease (FAD), promotes endoplasmic reticulum-mitochondria coupling only in the presence of mitofusin 2 (Mfn2).
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.
MFN2 mutation status should be investigated in patients presenting with early-onset recessively inherited axonal CMT
These results highlight the essential role of mitofusin 2 in the motor axon development and demonstrate the potential of zebrafish as a suitable and complementary platform for dissecting pathogenetic mechanisms of MFN2 mutations in vivo.
A highly unusual splicing defect, where an exonic single base exchange leads to the retention of the preceding intron, was identified in MFN2 (show MFN1 Proteins).
This gene encodes a mitochondrial membrane protein that participates in mitochondrial fusion and contributes to the maintenance and operation of the mitochondrial network. This protein is involved in the regulation of vascular smooth muscle cell proliferation, and it may play a role in the pathophysiology of obesity. Mutations in this gene cause Charcot-Marie-Tooth disease type 2A2, and hereditary motor and sensory neuropathy VI, which are both disorders of the peripheral nervous system. Defects in this gene have also been associated with early-onset stroke. Two transcript variants encoding the same protein have been identified.
, drosophila mitofusin
, mitochondrial assembly regulatory factor
, mitofusin 2
, hyperplasia suppressor
, transmembrane GTPase MFN2
, HSG protein
, hypertension related protein 1
, hypertension-related protein 1
, hypertension-related protein
, mitochondrial transmembrane GTPase FZO1A