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The protein encoded by MFN1 is a mediator of mitochondrial fusion. Additionally we are shipping Mitofusin 1 Antibodies (131) and Mitofusin 1 Kits (4) and many more products for this protein.
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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 Proteins)-mediated quality control on acetylated Mfn1.
miR (show MLXIP Proteins)-19b targets 3'UTR 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 Proteins) ubiquitin ligase and the Mfn1 mitochondrial fusion factor in mitophagy.
Knock-out of mitofusin (show MFN2 Proteins) protein Mfn1 increased the frequency of mitochondrial fission with increased lifetime of unpaired events whereas deletion of both Mfn1 and Mfn2 (show MFN2 Proteins) resulted in an instable dynamics.
These results collectively suggest a role for Mfn1 in regulating the activation of Bax (show BAX Proteins) on the outer mitochondrial membrane in a GTPase (show RACGAP1 Proteins)-dependent manner.
Patterned Purkinje cell degeneration (show AGTPBP1 Proteins) is dependent on caspase (show CASP3 Proteins) activation, leading to the marked decrease of mitofusion 1 in the transgeni (show AIFM1 Proteins)c Harlequin cerebellum.
Our data supports a model whereby the translocation of parkin (show PARK2 Proteins) to damaged mitochondria induces the degradation of mitofusin 1 leading to impaired mitochondrial fusion
The impact of mutations in endogenous PINK1 (show PINK1 Proteins) and Parkin (show PARK2 Proteins) 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.
MFN1 deficiency leads to defects in mitochondrial activity and male infertility.
Report exposes a novel role for Shh (show SHH Proteins) in regulating mitochondrial dynamics and rescue the metabolic profile of tumor cells through regulation of mitofusin 1 and 2.
Ablating Mfn1 eliminates the cardiac-related lethality of Mff (show MFF Proteins) knockout mice.
Data suggest that mitochondrial fusion and fission events are regulated by four GTPases: Mfn1, Mfn2 (show MFN2 Proteins), OPA1 (optic atrophy 1 (show OPA1 Proteins) protein), and Drp1 (dynamin 1-like protein (show DNM1L Proteins)). [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 Proteins).
These findings suggest that mitochondrial impairment is a very early event in Alzheimer disease pathogenesis and abnormal expression of Mfn1 and Mfn2 (show MFN2 Proteins) caused by excessive intracellular Abeta (show APP Proteins) is the possible molecular mechanism.
Data identify MFN1 as an ERK (show EPHB2 Proteins) target to modulate mitochondrial shape and apoptosis.
Mitochondrial shape governs BAX (show BAX Proteins)-induced membrane permeabilization and apoptosis via Mfn1.
Data unmask an important role for mitochondrial dynamics governed by Mfn1 and Mfn2 (show MFN2 Proteins) in Agrp (show AGRP Proteins) neurons in central regulation of whole-body energy metabolism.
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