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Mitochondrial GTPase involved in mitochondrial trafficking. Additionally we are shipping RHOT1 Antibodies (55) and RHOT1 Proteins (6) and many more products for this protein.
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Show that the C-terminal GTPase of the Parkin primary substrates Miro1 and Miro2 are necessary and sufficient for efficient ubiquitination. We present several new X-ray crystal structures of both Miro1 and Miro2 that reveal substrate recognition and ubiquitin transfer to be specific to particular protein domains and lysine residues.
Results provide evidence that ALS (show IGFALS ELISA Kits) mutant SOD1 (show SOD1 ELISA Kits) inhibits axonal transport of mitochondria by inducing PINK1 (show PINK1 ELISA Kits)/Parkin (show PARK2 ELISA Kits)-dependent Miro1 degradation.
Full-length APC (show APC ELISA Kits) promotes assembly of the Miro-1/Milton-2 complex.
Miro and Cenp-F (show CENPF ELISA Kits) promote anterograde mitochondrial movement and proper mitochondrial distribution in daughter cells.
Data indicate that outer mitochondrial membrane protein Miro1 can stabilize phospho-mutant versions of PARK2 (show PARK2 ELISA Kits) gene (encoding Parkin (show PARK2 ELISA Kits)) on the outer mitochondrial membrane (OMM).
Details of a robust association of DISC1 (show DISC1 ELISA Kits) with mitochondrial transport complexes containing TRAK1 and Miro1.
The Miro1-mediated mitochondrial transport in neurons and recently highlighted involvement of Miro1 proteins in mitochondrial turnover, emerging as a key process affected in neurodegeneration.
CXCL12 (show CXCL12 ELISA Kits)-dependent cell polarization and migration are reduced in Miro-1-silenced cells
results indicated that the low-expression levels of RhoT1 and Smad4 (show SMAD4 ELISA Kits) were significantly associated with LNM and shorter survival. RhoT1 may be considered as a potential novel marker for predicting the outcome in patients with pancreatic cancer
Study shows that both PINK1 (show PINK1 ELISA Kits) and Parkin (show PARK2 ELISA Kits) halt mitochondrial movement; PINK1 (show PINK1 ELISA Kits) phosphorylates Miro (1 and 2) and thereby initiates the rapid degradation of Miro through a Parkin (show PARK2 ELISA Kits)- and proteasome-dependent pathway.
Using mouse knockout strategies, we demonstrate that Miro1, as opposed to Miro2, is the primary regulator of mitochondrial transport in both axons and dendrites. Miro1 deletion leads to depletion of mitochondria from distal dendrites but not axons, accompanied by a marked reduction in dendritic complexity. Disrupting postnatal mitochondrial distribution in vivo by deleting Miro1 in mature neurons causes a progressive loss
Data establish that Miro1-mediated mitochondrial positioning at the leading edge provides localized energy production that promotes cell migration by supporting membrane protrusion and focal adhesion stability.
This study demonstrated that Miro1 regulates trafficking of mitochondria in the processes of astrocytes, as well as retention of mitochondria at sites that require energy production and Ca2 (show CA2 ELISA Kits)+-buffering such as the tripartite synapse
Neuron-specific loss of Miro1 causes depletion of mitochondria from corticospinal tract axons and progressive neurological deficits mirroring human upper motor neuron disease.
Miro1 overexpression leads to increased stem cell repair.
Armcx genes regulate mitochondrial trafficking in neurons and interact with Miro 1/2 and Trak2.
Mitochondrial GTPase involved in mitochondrial trafficking. Probably involved in control of anterograde transport of mitochondria and their subcellular distribution (By similarity).
, mitochondrial Rho GTPase 1-A
, ras homolog gene family member T1-A
, ras homolog gene family, member T1
, mitochondrial Rho GTPase 2
, ras homolog gene family, member T2
, mitochondrial Rho GTPase 1
, ras homolog gene family member T1
, mitochondrial Rho (MIRO) GTPase 1
, mitochondrial Rho 1
, rac-GTP binding protein-like protein
, rac-GTP-binding protein-like protein