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The protein encoded by MFN1 is a mediator of mitochondrial fusion. De plus, nous expédions Mitofusin 1 Anticorps (133) et Mitofusin 1 Kits (8) et beaucoup plus de produits pour cette protéine.
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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.
The results show that a metabolic shift from glycolysis in young to mitochondrial respiration in old normal human fibroblasts occurs during chronological lifespan, and MFN1 and OPA1 (Montrer OPA1 Protéines) regulate this process.
mitochondria elongation under hypoxic condition is regulated through SIRT1 (Montrer SIRT1 Protéines)-mediated MFN1 deacetylation and accumulation.
Regulation of Mfn1 by MGRN1 (Montrer MGRN1 Protéines) and the proteasome modulates mitochondrial fusion.
SLC25A46 (Montrer SLC25A46 Protéines) is a new component in mitochondrial dynamics that serves as a regulator for MFN1/2 oligomerization.
MFN1-positive expression could be seen mainly in ganglion cells after 1 week of minus lens intervention, and with time extension, more and more positive cells appeared in the rod-cone cell and bipolar cell layer, and this phenomenon could not be found in the normal control eyes.
crystal structures of engineered human MFN1 containing the GTPase (Montrer RACGAP1 Protéines) domain and a helical domain during different stages of GTP (Montrer AK3 Protéines) hydrolysis; mechanistic model for MFN1-mediated mitochondrial tethering is proposed; results shed light on the molecular basis of mitochondrial fusion and mitofusin (Montrer MFN2 Protéines)-related human neuromuscular disorders
These results suggest that MFN (Montrer TLL1 Protéines) tethers apposing membranes, likely through nucleotide-dependent dimerization.
Improper transcriptional (in)activation of mitofusin-1 and dynamin-related protein 1 (Montrer DNM1L Protéines) during early in vitro embryo development is associated with a decrease in mitochondrial membrane potential and with embryo fragmentation.
A fine balance of Mfn1 levels is maintained by MARCH5 (Montrer MARCH5 Protéines)-mediated quality control on acetylated Mfn1.
miR (Montrer MLXIP Protéines)-19b targets 3'UTR sequences of Mfn1 genes inhibit the expression of Mfn1
data posit MFN1-mediated mitochondrial dynamics in POMC (Montrer POMC Protéines) neurons as an intrinsic nutrient-sensing mechanism and unveil an unrecognized link between this subset of neurons and insulin (Montrer INS Protéines) release.
These results highlight the crucial role of MFN1 in maintaining the competency of the STING pathway.
Despite apparent mitochondrial dysfunction, hearts deficient in both Mfn1 and Mfn2 (Montrer MFN2 Protéines) are protected against acute myocardial infarction due to impaired mitochondria/sarcoplasmic reticulum tethering.
We found that mouse embryonic fibroblasts lacking Mfn2 (Montrer MFN2 Protéines) have altered lipid droplet morphology. However, triacylglycerol biosynthesis was not dependent on ER-mitochondrial tethering mediated by mitofusins. Lastly, Mfn2 (Montrer MFN2 Protéines) does not have a role in adipocyte differentiation.
MFN1 deficiency leads to defects in mitochondrial activity and male infertility.
Report exposes a novel role for Shh (Montrer SHH Protéines) 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 (Montrer MFF Protéines) knockout mice.
Data suggest that mitochondrial fusion and fission events are regulated by four GTPases: Mfn1, Mfn2 (Montrer MFN2 Protéines), OPA1 (optic atrophy 1 (Montrer OPA1 Protéines) protein), and Drp1 (dynamin 1-like protein (Montrer DNM1L Protéines)). [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 (Montrer HDAC6 Protéines).
These findings suggest that mitochondrial impairment is a very early event in Alzheimer disease pathogenesis and abnormal expression of Mfn1 and Mfn2 (Montrer MFN2 Protéines) caused by excessive intracellular Abeta (Montrer APP Protéines) is the possible molecular mechanism.
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