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Human Monoclonal MFN2 Primary Antibody for IHC (p), RNAi - ABIN564263
Holloway, Perry, Thrush, Heigenhauser, Dyck, Bonen, Spriet: PGC-1alpha's relationship with skeletal muscle palmitate oxidation is not present with obesity despite maintained PGC-1alpha and PGC-1beta protein. in American journal of physiology. Endocrinology and metabolism 2008
Show all 8 Pubmed References
Human Polyclonal MFN2 Primary Antibody for IF (p), IHC (p) - ABIN682528
Ku, Ji, Zhang, Li, Sang: PM2.5, SO2 and NO2 co-exposure impairs neurobehavior and induces mitochondrial injuries in the mouse brain. in Chemosphere 2016
Show all 2 Pubmed References
Human Monoclonal MFN2 Primary Antibody for IHC (p), WB - ABIN2475579
Minet, Gaster: The dynamic equilibrium between ATP synthesis and ATP consumption is lower in isolated mitochondria from myotubes established from type 2 diabetic subjects compared to lean control. in Biochemical and biophysical research communications 2011
Human Monoclonal MFN2 Primary Antibody for ELISA, WB - ABIN5326795
Sawyer, Cheuk-Him Ng, Innes, Wagner, Dyment, Tetreault, Majewski, Boycott, Screaton, Nicholson: Homozygous mutations in MFN2 cause multiple symmetric lipomatosis associated with neuropathy. in Human molecular genetics 2015
Human Monoclonal MFN2 Primary Antibody for IHC (p), ELISA - ABIN523306
Stacchiotti, Favero, Giugno, Lavazza, Reiter, Rodella, Rezzani: Mitochondrial and metabolic dysfunction in renal convoluted tubules of obese mice: protective role of melatonin. in PLoS ONE 2014
Mammalian Monoclonal MFN2 Primary Antibody for ISt, IHC - ABIN1304825
Hoppins, Edlich, Cleland, Banerjee, McCaffery, Youle, Nunnari: The soluble form of Bax regulates mitochondrial fusion via MFN2 homotypic complexes. in Molecular cell 2011
Human Polyclonal MFN2 Primary Antibody for IHC, IHC (p) - ABIN4334778
Yang, Yang: Bit-by-bit autophagic removal of parkin-labelled mitochondria. in Nature communications 2013
Cow (Bovine) Polyclonal MFN2 Primary Antibody for IHC, WB - ABIN2775408
Chung, Cho, Hwang, Kim, Yoo, Kwon, Kim, Sunwoo, Züchner, Choi: Early-onset stroke associated with a mutation in mitofusin 2. in Neurology 2008
Show all 2 Pubmed References
activation of endoplasmic reticulum stress by defective mitochondria is neurotoxic in pink1 (show PINK1 Antibodies) and parkin (show PARK2 Antibodies) flies and that the reduction of this signalling is neuroprotective, independently of defective mitochondria.
Clu (show CLU Antibodies) is upstream of and binds to VCP (show vcp Antibodies) in vivo and promotes VCP (show vcp Antibodies)-dependent Marf degradation in vitro Marf accumulates in whole muscle lysates of clu (show CLU Antibodies)-deficient flies and is destabilized upon Clu (show CLU Antibodies) overexpression. Thus, Clu (show CLU Antibodies) is essential for mitochondrial homeostasis and functions in concert with Parkin (show PARK2 Antibodies) and VCP (show vcp Antibodies) for Marf degradation to promote damaged mitochondrial clearance.
lack of ChChd3 (show CHCHD3 Antibodies) leads to inactivation of Hippo activity under normal development, which is also dependent on the transcriptional coactivator Yorkie (Yki (show YAP1 Antibodies)). Furthermore, loss of ChChd3 (show CHCHD3 Antibodies) induces oxidative stress and activates the JNK (show MAPK8 Antibodies) pathway. In addition, depletion of other mitochondrial fusion components, Opa1 (show OPA1 Antibodies) 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 Antibodies) 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 Antibodies) control mitochondrial and cardiac function in Drosophila.
The PINK1 (show PINK1 Antibodies)/Parkin (show PARK2 Antibodies) pathway affects mitochondrial fission/fusion as suggested by previous genetic interaction studies.
Our patient with MFN2-related CMT2 expands the clinical and mutational spectrum of individuals with autosomal recessive CMT2 and identifies a new clinical feature that warrants further observation.
It has been shown that mitofusin-2 is modified with K6-linked polyubiquitin in a HUWE1-dependent manner.
Studied association of genetic variants of the MAVS, MITA and MFN2 genes with leprosy in Han Chinese from Southwest China; found no association between the variants and susceptibility to leprosy.
MFN2 gene polymorphisms (rs873457, rs2336384, rs1474868, rs4846085 and rs2236055) may be associated with acute liver failure and the rs873457 and rs4846085 polymorphisms are correlated with the risk and prognosis of acute liver failure.
SLC25A46 (show SLC25A46 Antibodies) is a new component in mitochondrial dynamics that serves as a regulator for MFN1 (show MFN1 Antibodies)/2 oligomerization.
Presenilin 2 (PS2 (show PSEN2 Antibodies)), mutations in which underlie familial Alzheimer's disease (FAD (show BRCA2 Antibodies)), promotes endoplasmic reticulum-mitochondria coupling only in the presence of mitofusin 2 (Mfn2).
PGC-1alpha (show PPARGC1A Antibodies) enhances Mfn2 transcription, but also leads to increased degradation of the Mfn2 protein, a key ubiquitylation target of Parkin (show PARK2 Antibodies) on mitochondria. In vivo, Parkin (show PARK2 Antibodies) has significant protective effects on the survival and function of nigral dopaminergic neurons in which the chronic expression of PGC-1alpha (show PPARGC1A Antibodies) is induced
Exome sequencing identified MFN2 SNVs in two of the individuals. Neuropathy-associated CNV outside of the PMP22 (show PMP22 Antibodies) locus is rare in Charcot-Marie-Tooth (CMT) disease . Nevertheless, there is potential clinical utility in testing for CNVs and exome sequencing in CMT cases negative for the CMT1A (show PMP22 Antibodies) duplication.
Smad2 (show SMAD2 Antibodies) is a key scaffold, allowing RIN1 (show RIN1 Antibodies) to act as a GTP (show AK3 Antibodies) exchange factor for MFN2-GTPase (show RACGAP1 Antibodies) activation to promote mitochondrial ATP synthesis and suppress superoxide production during mitochondrial fusion.
our results suggest that KAP1 (show CDKN3 Antibodies) Ser473 phosphorylation acts through MFN2 reduction to restrict mitochondrial hyperfusion, thereby contributing to cancer cell survival under conditions of sustained metabolic stress
Despite apparent mitochondrial dysfunction, hearts deficient in both Mfn1 (show MFN1 Antibodies) and Mfn2 are protected against acute myocardial infarction due to impaired mitochondria/sarcoplasmic reticulum tethering.
Presenilin 2 (PS2 (show PSEN2 Antibodies)), mutations in which underlie familial Alzheimer's disease (FAD (show FANCD2 Antibodies)), 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.
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 (show MLXIP Antibodies)-195. Therefore, upregulation of mfn2 expression by decreasing the level of miR (show MLXIP Antibodies)-195 might be a potential new therapeutic strategy for treatment of Alzheimer's disease.
Mfn2 downregulation or the exogenous expression of normal Parkin (show PARK2 Antibodies) restored cytosolic Ca(2 (show CA2 Antibodies)+) transients in fibroblasts from patients with PARK2 (show PARK2 Antibodies) mutations, a catalytically inactive Parkinson's disease (PD)-related Parkin (show PARK2 Antibodies) variant had no effect. Parkin (show PARK2 Antibodies) is directly involved in regulating ER-mitochondria contacts and provide new insight into the role of the loss of Parkin (show PARK2 Antibodies) function in PD development.
Altogether, these results demonstrate that Mfn2 is a mediator of mitochondria to lipid droplet interactions, influencing lipolytic processes and whole-body energy homeostasis.
we demonstrated that by modulating mitochondrial energy metabolism through Mfn2 and mitochondrial Ca2 (show CA2 Antibodies)+, PPAR-b (show PPARD Antibodies) took an important role in neuronal differentiation induced by flavonoid compound 4a
Furthermore, analysis of muscle Mfn2-deficient mice revealed that aging-induced Mfn2 decrease underlies the age-related alterations in metabolic homeostasis and sarcopenia.
Mice hemizygous for a pathogenic Mfn2 allele exhibit hind limb/foot gait deficits and phenotypic perturbations in nerve and muscle.
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.
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 Antibodies).
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