anti-Mitofusin 1 (MFN1) Antikörper

Cow (Bovine) Mitofusin 1 (MFN1) Interaktionspartner

1. 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.

Human Mitofusin 1 (MFN1) Interaktionspartner

1. Structural basis for how MFN1 mediates homotypic membrane fusion.

2. heptad repeat domain of Mitofusin proteins induces membrane fusion and possesses a conserved amphipathic helix that folds upon interaction with the lipid bilayer surface.

3. The mRNA upregulation of Mitofusin 1 and 2 provides first insight into the complex changes of mitochondrial dynamics in cardiomyocytes of patients with reversible heart failure due to tachycardiomyopathy.

4. The results lead to a revised understanding of Mfn 1 as single-spanning outer membrane proteins with an Nout-Cin orientation, providing functional insight into the IMS contribution to redox-regulated fusion events.

5. The results may suggest that TP53BP1 and MFN1 frameshift mutations and their intratumoral heterogeneity (ITH) could contribute to cancer development by inhibiting the TSG activities.

6. 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 regulate this process.

7. mitochondria elongation under hypoxic condition is regulated through SIRT1-mediated MFN1 deacetylation and accumulation.

8. Regulation of Mfn1 by MGRN1 and the proteasome modulates mitochondrial fusion.

9. SLC25A46 is a new component in mitochondrial dynamics that serves as a regulator for MFN1/2 oligomerization.

10. 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.

11. crystal structures of engineered human MFN1 containing the GTPase domain and a helical domain during different stages of GTP hydrolysis; mechanistic model for MFN1-mediated mitochondrial tethering is proposed; results shed light on the molecular basis of mitochondrial fusion and mitofusin-related human neuromuscular disorders

12. These results suggest that MFN tethers apposing membranes, likely through nucleotide-dependent dimerization.

13. Improper transcriptional (in)activation of mitofusin-1 and dynamin-related protein 1 during early in vitro embryo development is associated with a decrease in mitochondrial membrane potential and with embryo fragmentation.

14. A fine balance of Mfn1 levels is maintained by MARCH5-mediated quality control on acetylated Mfn1.

15. miR-19b targets 3'UTR sequences of Mfn1 genes inhibit the expression of Mfn1

16. In a amyotrophic lateral sclerosis transgenic mouse model, Mfn1 is significantly increased in spinal cord.

17. A novel role for the endoplasmic reticulum-associated Gp78 ubiquitin ligase and the Mfn1 mitochondrial fusion factor in mitophagy.

18. Knock-out of mitofusin protein Mfn1 increased the frequency of mitochondrial fission with increased lifetime of unpaired events whereas deletion of both Mfn1 and Mfn2 resulted in an instable dynamics.

19. These results collectively suggest a role for Mfn1 in regulating the activation of Bax on the outer mitochondrial membrane in a GTPase-dependent manner.

20. mitochondrial dynamics, particularly those mediated by the mitofusins, play a role in endothelial cell function and viability.

Mouse (Murine) Mitofusin 1 (MFN1) Interaktionspartner

1. EET enhances renal function in obese mice resulting in restoration of HO-1-Mfn1/2 signaling, and decrease in hypertension through inhibition of sodium chloride co-transporter.

2. data posit MFN1-mediated mitochondrial dynamics in POMC neurons as an intrinsic nutrient-sensing mechanism and unveil an unrecognized link between this subset of neurons and insulin release.

3. These results highlight the crucial role of MFN1 in maintaining the competency of the STING pathway.

4. Despite apparent mitochondrial dysfunction, hearts deficient in both Mfn1 and Mfn2 are protected against acute myocardial infarction due to impaired mitochondria/sarcoplasmic reticulum tethering.

5. We found that mouse embryonic fibroblasts lacking Mfn2 have altered lipid droplet morphology. However, triacylglycerol biosynthesis was not dependent on ER-mitochondrial tethering mediated by mitofusins. Lastly, Mfn2 does not have a role in adipocyte differentiation.

6. MFN1 deficiency leads to defects in mitochondrial activity and male infertility.

7. Report exposes a novel role for Shh in regulating mitochondrial dynamics and rescue the metabolic profile of tumor cells through regulation of mitofusin 1 and 2.

8. Ablating Mfn1 eliminates the cardiac-related lethality of Mff knockout mice.

9. Data suggest that mitochondrial fusion and fission events are regulated by four GTPases: Mfn1, Mfn2, OPA1 (optic atrophy 1 protein), and Drp1 (dynamin 1-like protein). [REVIEW]

10. 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.

11. These findings suggest that mitochondrial impairment is a very early event in Alzheimer disease pathogenesis and abnormal expression of Mfn1 and Mfn2 caused by excessive intracellular Abeta is the possible molecular mechanism.

12. Data identify MFN1 as an ERK target to modulate mitochondrial shape and apoptosis.

13. A fine balance of Mfn1 levels is maintained by MARCH5-mediated quality control on acetylated Mfn1.

14. Mitochondrial shape governs BAX-induced membrane permeabilization and apoptosis via Mfn1.

15. Data unmask an important role for mitochondrial dynamics governed by Mfn1 and Mfn2 in Agrp neurons in central regulation of whole-body energy metabolism.

16. Our findings establish that Mfn-1 and Mfn-2 are essential in mediating mitochondrial remodeling during postnatal cardiac development, a time of dramatic transitions in the bioenergetics and growth of the heart.

17. Data suggest that Mfn-1 deletion in cardiomyocytes confers protection against reactive oxygen species-induced mitochondrial dysfunction.

18. Patterned Purkinje cell degeneration is dependent on caspase activation, leading to the marked decrease of mitofusion 1 in the Harlequin cerebellum.

19. Double Mfn-null cells show neither outer nor inner membrane fusion, while mitochondria in OPA1-null cells contain multiple matrix compartments bounded together by a single outer membrane, consistent with uncoupling of outer versus inner membrane fusion.

20. results suggest that the heptad repeat region (HR2) of mfn1 functions as a mitochondrial tether before fusion