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The protein encoded by MFN1 is a mediator of mitochondrial fusion. Additionally we are shipping Mitofusin 1 Proteins (9) and Mitofusin 1 Kits (4) and many more products for this protein.
Showing 10 out of 90 products:
Human Monoclonal MFN1 Primary Antibody for RNAi, ELISA - ABIN527615
Zanna, Ghelli, Porcelli, Karbowski, Youle, Schimpf, Wissinger, Pinti, Cossarizza, Vidoni, Valentino, Rugolo, Carelli: OPA1 mutations associated with dominant optic atrophy impair oxidative phosphorylation and mitochondrial fusion. in Brain : a journal of neurology 2008
Show all 13 references for ABIN527615
Human Polyclonal MFN1 Primary Antibody for WB - ABIN2787347
Bonala, McFarlane, Ang, Lim, Lee, Chua, Lokireddy, Sreekanth, Leow, Meng, Shyong, Lee, Gluckman, Sharma, Kambadur: Pid1 induces insulin resistance in both human and mouse skeletal muscle during obesity. in Molecular endocrinology (Baltimore, Md.) 2013
Show all 2 references for ABIN2787347
Human Polyclonal MFN1 Primary Antibody for IF (p), IHC (p) - ABIN670071
Lou, Guan, Liu, Liu, Zhang, Pan, Pei: The influence of chronic fluorosis on mitochondrial dynamics morphology and distribution in cortical neurons of the rat brain. in Archives of toxicology 2013
Show all 2 references for ABIN670071
Human Polyclonal MFN1 Primary Antibody for EIA, WB - ABIN953454
Perumalsamy, Nagala, Sarin: Notch-activated signaling cascade interacts with mitochondrial remodeling proteins to regulate cell survival. in Proceedings of the National Academy of Sciences of the United States of America 2010
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The results showed that high level of Mfn1 expression significantly improved the embryo development rates by increasing ATP level and Deltapsim, while reducing H(2)O(2) generation.
A fine balance of Mfn1 levels is maintained by MARCH5 (show MARCH5 Antibodies)-mediated quality control on acetylated Mfn1.
miR (show MLXIP Antibodies)-19b targets 3'UTR (show UTS2R Antibodies) sequences of Mfn1 genes inhibit the expression of Mfn1
In a amyotrophic lateral sclerosis transgenic mouse model, Mfn1 is significantly increased in spinal cord.
A novel role for the endoplasmic reticulum-associated Gp78 (show AMFR Antibodies) ubiquitin ligase and the Mfn1 mitochondrial fusion factor in mitophagy.
Knock-out of mitofusin (show MFN2 Antibodies) protein Mfn1 increased the frequency of mitochondrial fission with increased lifetime of unpaired events whereas deletion of both Mfn1 and Mfn2 (show MFN2 Antibodies) resulted in an instable dynamics.
These results collectively suggest a role for Mfn1 in regulating the activation of Bax (show BAX Antibodies) on the outer mitochondrial membrane in a GTPase (show RACGAP1 Antibodies)-dependent manner.
Patterned Purkinje cell degeneration (show AGTPBP1 Antibodies) is dependent on caspase (show CASP3 Antibodies) activation, leading to the marked decrease of mitofusion 1 in the transgeni (show AIFM1 Antibodies)c Harlequin cerebellum.
Our data supports a model whereby the translocation of parkin (show PARK2 Antibodies) to damaged mitochondria induces the degradation of mitofusin 1 leading to impaired mitochondrial fusion
The impact of mutations in endogenous PINK1 (show PINK1 Antibodies) and Parkin (show PARK2 Antibodies) on the ubiquitination of mitochondrial fusion and fission factors and the mitochondrial network structure, was investigated.
Gbeta2 also regulated the mobility of Mfn1 on the surface of the mitochondrial membrane and affected the mitochondrial fusion.
Ablating Mfn1 eliminates the cardiac-related lethality of Mff (show MFF Antibodies) knockout mice.
Data suggest that mitochondrial fusion and fission events are regulated by four GTPases: Mfn1, Mfn2 (show MFN2 Antibodies), OPA1 (optic atrophy 1 (show OPA1 Antibodies) protein), and Drp1 (dynamin 1-like protein (show DNM1L Antibodies)). [REVIEW]
Authors present evidence that metabolically challenged mitochondria undergo active fusion to suppress oxidative stress. In response to glucose starvation, mitofusin 1 (MFN1) becomes associated with the protein deacetylase HDAC6 (show HDAC6 Antibodies).
These findings suggest that mitochondrial impairment is a very early event in Alzheimer disease pathogenesis and abnormal expression of Mfn1 and Mfn2 (show MFN2 Antibodies) caused by excessive intracellular Abeta (show APP Antibodies) is the possible molecular mechanism.
Data identify MFN1 as an ERK (show EPHB2 Antibodies) target to modulate mitochondrial shape and apoptosis.
Mitochondrial shape governs BAX (show BAX Antibodies)-induced membrane permeabilization and apoptosis via Mfn1.
Data unmask an important role for mitochondrial dynamics governed by Mfn1 and Mfn2 (show MFN2 Antibodies) in Agrp (show AGRP Antibodies) neurons in central regulation of whole-body energy metabolism.
Our findings establish that Mfn-1 and Mfn-2 (show MFN2 Antibodies) are essential in mediating mitochondrial remodeling during postnatal cardiac development, a time of dramatic transitions in the bioenergetics and growth of the heart.
Data suggest that Mfn-1 deletion in cardiomyocytes confers protection against reactive oxygen species-induced mitochondrial dysfunction.
The protein encoded by this gene is a mediator of mitochondrial fusion. This protein and mitofusin 2 are homologs of the Drosophila protein fuzzy onion (Fzo). They are mitochondrial membrane proteins that interact with each other to facilitate mitochondrial targeting.
, mitofusin 2
, fzo homolog
, mitochondrial transmembrane GTPase FZO-2
, mitochondrial transmembrane GTPase Fzo-1
, putative transmembrane GTPase
, transmembrane GTPase MFN1
, mitochondrial transmembrane GTPase FZO1B