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MFN2 encodes a mitochondrial membrane protein that participates in mitochondrial fusion and contributes to the maintenance and operation of the mitochondrial network. Additionally we are shipping Mitofusin 2 Proteins (10) and Mitofusin 2 Kits (6) and many more products for this protein.
Showing 10 out of 174 products:
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 7 references for ABIN564263
Human Monoclonal MFN2 Primary Antibody for ELISA, WB - ABIN523308
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
Chicken Polyclonal MFN2 Primary Antibody for WB - ABIN2775407
Chung, Cho, Hwang, Kim, Yoo, Kwon, Kim, Sunwoo, Züchner, Choi: Early-onset stroke associated with a mutation in mitofusin 2. in Neurology 2008
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
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
Human Polyclonal MFN2 Primary Antibody for IHC (p), WB - ABIN568087
Santel, Fuller: Control of mitochondrial morphology by a human mitofusin. in Journal of cell science 2001
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.
Dmfn-mRNA was widely expressed during embryogenesis accumulating in the mesoderm and endoderm during gut (show GUSB Antibodies) development, during oogenesis with transcripts maternally deposited into the early embryo and in the male germ line.
Low MFN2 expression in hepatocellular carcinoma indicated a worse overall survival.
Low expression of MFN2 is associated with lung adenocarcinoma.
Between 1999 and 2012, the genetic diagnosis of MFN2 mutation was made in 11 children who were treated in our department for different neurological symptoms. We found 5 different mutations in the MFN2 gene in 6 unrelated families
We report four novel mutations and four rare missense variants of MFN2 in Charcot-Marie-Tooth disease 2A families in mainland China
The results of this study suggested that the MFN2 gene should be considered in Polish hereditary motor-sensory neuropathiey II patients.
These results suggest that defects in Mfn2 could cause mitochondrial dysfunction and decrease trophoblastic cells' viability
This study demonstrated that Mfn2 gene polymorphisms were associated with essential hypertension in northern Han Chinese population, especially in male subjects
Report exposes a novel role for Shh (show SHH Antibodies) in regulating mitochondrial dynamics and rescue the metabolic profile of tumor cells through regulation of mitofusin 1 (show MFN1 Antibodies) and 2.
family study of early onset severe axonal Charcot-Marie-Tooth disease with dominant inheritance - SNP mutation in MFN2
Our findings provide new insight into the mechanism underlying Mitofusin-2 regulation and the potential role of miR (show MLXIP Antibodies)-761 in tocellular carcinoma, making it a potential candidate for use in HCC (show FAM126A Antibodies) therapy in the future
knockdown of Mfn2 in adipo and osteogenesis and the overexpression of a dominant negative form of Drp1 (show CRMP1 Antibodies) during chondrogenesis resulted in a loss of differentiation ability
SIRT1 (show SIRT1 Antibodies) overexpression substantially increased autophagy in wild-type cells, but not in MFN2-deficient cells.
mitofusin 2 overexpression may attenuate hypoxia-induced apoptosis.
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.
suggest a balance between negative metabolic consequences of mitofusin 2 deficiency and adaptive processes exemplified by increased level of PGC-1alpha (show PPARGC1A Antibodies) and TFAM (show TFAM Antibodies) transcription factor which prevent an depletion of mtDNA and severe impairment of cell metabolism
Our results indicate that HDAC6 (show HDAC6 Antibodies) is a critical regulator of MFN2 degradation by MARCH5 (show MARCH5 Antibodies), thus protecting mitochondrial connectivity from hypoxic stress.
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.
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
confirm the hypothesis that the cellular consequences of mutations in the mitofusin 2 gene can mostly be manifested in the peripheral nervous system
Data suggest that mitochondrial fusion and fission events are regulated by four GTPases: Mfn1 (show MFN1 Antibodies), Mfn2, OPA1 (optic atrophy 1 (show OPA1 Antibodies) protein), and Drp1 (dynamin 1-like protein (show DNM1L Antibodies)). [REVIEW]
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