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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
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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
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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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
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.
This study detected a compound heterozygous MFN2 mutation in a patient with a severe phenotype and the co-occurrence of MFN2 and PMP22 (zeige PMP22 Antikörper) 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.
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]
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 (zeige BAAT Antikörper) (brown adipose tissue) adaptation to obesity is regulated by Mfn2 and with BAT (zeige BAAT Antikörper)-Mfn2 absent, BAT (zeige BAAT Antikörper) contribution to prevention of insulin (zeige INS Antikörper) 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.
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 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