Made-to-order (14-16 weeks)
Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
Value-added Deliverables
① 200ug * antigen (positive control); ② 1ml * Pre-immune serum (negative control);
Quality Guarantee
① Antibody purity can be guaranteed above 90% by SDS-PAGE detection; ② ELISA titer can be guaranteed 1: 64,000; ③ WB validation with antigen can be guaranteed positive;
Mitochondrial outer membrane GTPase that mediates mitochondrial clustering and fusion. Mitochondrial fusion is the physical merging of mitochondria that gives rise to mitochondrial networks, and this process is counterbalanced by mitochondrial fission which fragments networks. Promotes, but is not required for park recruitment to dysfunctional mitochondria.
Gene References into Functions
Enhancing the profusion gene mitofusin/marf is beneficial in an in vivo model of TDP-43 proteinopathies, serving as a potential therapeutic target.PMID:28324764
activation of endoplasmic reticulum stress by defective mitochondria is neurotoxic in pink1 and parkin flies and that the reduction of this signalling is neuroprotective, independently of defective mitochondria.PMID:27336715
Clu is upstream of and binds to VCP in vivo and promotes VCP-dependent Marf degradation in vitro Marf accumulates in whole muscle lysates of clu-deficient flies and is destabilized upon Clu overexpression. Thus, Clu is essential for mitochondrial homeostasis and functions in concert with Parkin and VCP for Marf degradation to promote damaged mitochondrial clearance.PMID:26931463
lack of ChChd3 leads to inactivation of Hippo activity under normal development, which is also dependent on the transcriptional coactivator Yorkie (Yki). Furthermore, loss of ChChd3 induces oxidative stress and activates the JNK pathway. In addition, depletion of other mitochondrial fusion components, Opa1 or Marf, inactivates the Hippo pathway as well.PMID:27317679
Marf is required for mitochondrial fusion and transport in long axons.PMID:25313867
Expression of Mfn2 and endoplasmic reticulum (ER) stress reduction in flies lacking Marf corrected ER shape, attenuating the developmental and motor defects.PMID:24469638
Parkin deficiency and resulting mitophagic disruption produces cardiomyopathy which can be contained by suppressing mitofusin.PMID:24192653
mfn2 mutations alter mitochondrial dynamics and induce retinal and cardiac pathologyPMID:22957060
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.PMID:21475305
MARF and Opa1 control mitochondrial and cardiac function in Drosophila.PMID:21148429
The PINK1/Parkin pathway affects mitochondrial fission/fusion as suggested by previous genetic interaction studies.PMID:20194754
Dmfn-mRNA was widely expressed during embryogenesis accumulating in the mesoderm and endoderm during gut development, during oogenesis with transcripts maternally deposited into the early embryo and in the male germ line.PMID:12128227
TRAFAC class dynamin-like GTPase superfamily, Dynamin/Fzo/YdjA family, Mitofusin subfamily
Tissue Specificity
Widely expressed in embryos, accumulating in the mesoderm and endoderm during gut development. In the male germ line, it is expressed in spermatogonia, spermatocytes and early spermatids.