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Human Monoclonal MFN2 Primary Antibody für 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 für 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
Mammalian Monoclonal MFN2 Primary Antibody für 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 Monoclonal MFN2 Primary Antibody für 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
Human Polyclonal MFN2 Primary Antibody für IHC, IHC (p) - ABIN4334778
Yang, Yang: Bit-by-bit autophagic removal of parkin-labelled mitochondria. in Nature communications 2013
Human Monoclonal MFN2 Primary Antibody für 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
Cow (Bovine) Polyclonal MFN2 Primary Antibody für 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
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Enhancing the profusion gene mitofusin/marf is beneficial in an in vivo model of TDP-43 (zeige TARDBP Antikörper) proteinopathies, serving as a potential therapeutic target.
activation of endoplasmic reticulum stress by defective mitochondria is neurotoxic in pink1 (zeige PINK1 Antikörper) and parkin (zeige PARK2 Antikörper) flies and that the reduction of this signalling is neuroprotective, independently of defective mitochondria.
Clu (zeige CLU Antikörper) is upstream of and binds to VCP (zeige vcp Antikörper) in vivo and promotes VCP (zeige vcp Antikörper)-dependent Marf degradation in vitro Marf accumulates in whole muscle lysates of clu (zeige CLU Antikörper)-deficient flies and is destabilized upon Clu (zeige CLU Antikörper) overexpression. Thus, Clu (zeige CLU Antikörper) is essential for mitochondrial homeostasis and functions in concert with Parkin (zeige PARK2 Antikörper) and VCP (zeige vcp Antikörper) for Marf degradation to promote damaged mitochondrial clearance.
lack of ChChd3 (zeige CHCHD3 Antikörper) leads to inactivation of Hippo activity under normal development, which is also dependent on the transcriptional coactivator Yorkie (Yki (zeige YAP1 Antikörper)). Furthermore, loss of ChChd3 (zeige CHCHD3 Antikörper) induces oxidative stress and activates the JNK (zeige MAPK8 Antikörper) pathway. In addition, depletion of other mitochondrial fusion components, Opa1 (zeige OPA1 Antikörper) 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 (zeige PARK2 Antikörper) 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 (zeige OPA1 Antikörper) control mitochondrial and cardiac function in Drosophila.
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.
These findings suggest that specific MFN2 mutations cause tissue-selective mitochondrial dysfunction with increased adipocyte proliferation and survival and confirm a novel form of excess adiposity with paradoxical suppression of leptin (zeige LEP Antikörper) expression.
This study identified a new mitochondria reprogramming pathway influencing breast cancer progression through SH3GL2 (zeige SH3G2 Antikörper) and MFN2. These proteins were frequently lost in breast cancer, which was traceable in the circulating exosomes.
MFN2 expression was lower in patients with heart failure with preserved ejection fraction compared to controls.
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]
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.
Mfn2 stands as a bona fide endoplasmic-mitochondria tether whose ablation decreases interorganellar juxtaposition and communication.
Despite apparent mitochondrial dysfunction, hearts deficient in both Mfn1 (zeige MFN1 Antikörper) and Mfn2 are protected against acute myocardial infarction due to impaired mitochondria/sarcoplasmic reticulum tethering.
Presenilin 2 (PS2 (zeige PSEN2 Antikörper)), mutations in which underlie familial Alzheimer's disease (FAD (zeige FANCD2 Antikörper)), 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 (zeige MLXIP Antikörper)-195. Therefore, upregulation of mfn2 expression by decreasing the level of miR (zeige MLXIP Antikörper)-195 might be a potential new therapeutic strategy for treatment of Alzheimer's disease.
Mfn2 downregulation or the exogenous expression of normal Parkin (zeige PARK2 Antikörper) restored cytosolic Ca(2 (zeige CA2 Antikörper)+) transients in fibroblasts from patients with PARK2 (zeige PARK2 Antikörper) mutations, a catalytically inactive Parkinson's disease (PD)-related Parkin (zeige PARK2 Antikörper) variant had no effect. Parkin (zeige PARK2 Antikörper) is directly involved in regulating ER-mitochondria contacts and provide new insight into the role of the loss of Parkin (zeige PARK2 Antikörper) 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 (zeige CA2 Antikörper)+, PPAR-b (zeige PPARD Antikörper) 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.
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 (zeige MFN1 Antikörper).
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