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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 (4) and many more products for this protein.
Showing 10 out of 140 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
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 (p), WB - ABIN568087
Santel, Fuller: Control of mitochondrial morphology by a human mitofusin. in Journal of cell science 2001
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
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.
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
HMGB1 (show HMGB1 Antibodies) can trigger apoptosis of T lymphocytes through mitochondrial death pathway associated with [Ca(2 (show CA2 Antibodies)+)]i elevation. Mfn2 plays a pivotal role in this process, and it might be a novel therapeutic target in T cell apoptosis related disorders.
Mutations in the gene encoding MFN2 are associated with Charcot-Marie-Tooth disease type 2A and MFN2 is involved in several intracellular pathways that interact to regulate the mitochondrial network within cells.
These findings show that homozygous mutations at p.R707W in MFN2 are a novel cause of multiple symmetrical lipomatosis.
A deletion of exons 7 and 8 is a founder mutation in MFN2 in the UK population.
increased expression of miR (show MLXIP Antibodies)-214 observed in a Huntington disease (show HTT Antibodies) cell model could target MFN2, altered mitochondrial morphology and deregulated cell cycle
Mitofusin-2 over-expression leads to dysregulation of cell cycle and cell invasion in lung adenocarcinoma.
MFN2 mutations caused about 6% of CMT in Korean families (22.5% of CMT2). Disease phenotypes were considerably varied with 42% severe, 18% moderate and 34% mild cases.
findings revealed the role of Mfn2 in regulating cell proliferation and mitochondrial metabolism, and shed new light on understanding the mechanisms of Mfn2 deficiency related diseases.
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]
Results suggest that Mfn2 and OPA1 (show MED12 Antibodies) are upregulated during bone marrow progenitor differentiation and promote the migration of immature dendritic cells by regulating the expression of CCR7 (show CCR7 Antibodies).
Silencing Mfn2 results in amarked reduction in Ca2 (show CA2 Antibodies)+uptake by mitochondria remaining asso-ciated with the triad junction and this reduction is due largely toa depolarization of the mitochondrial membrane potential
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