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RHOT2 encodes a member of the Rho family of GTPases. Additionally we are shipping Ras Homolog Gene Family, Member T2 Antibodies (38) and and many more products for this protein.
Showing 4 out of 7 products:
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.
Miro and Cenp-F (show CENPF Proteins) promote anterograde mitochondrial movement and proper mitochondrial distribution in daughter cells.
The Miro2-mediated mitochondrial transport in neurons and recently highlighted involvement of Miro2 proteins in mitochondrial turnover, emerging as a key process affected in neurodegeneration.
Study shows that both PINK1 (show PINK1 Proteins) and Parkin (show PARK2 Proteins) halt mitochondrial movement; PINK1 (show PINK1 Proteins) phosphorylates Miro (1 (show RHOT1 Proteins) and 2) and thereby initiates the rapid degradation of Miro through a Parkin (show PARK2 Proteins)- and proteasome-dependent pathway.
Moreover, we show that Miro interacts with the Kinesin-binding proteins, GRIF-1 and OIP106 (show TRAK1 Proteins), suggesting that the Miro GTPases form a link between the mitochondria and the trafficking apparatus of the microtubules.
Miro proteins serve as a [Ca(2 (show CA2 Proteins)+)](c)-sensitive switch and bifunctional regulator for both the motility and fusion-fission dynamics of the mitochondria.
both Miro proteins can act to coordinate microtubule-dependent and actin-dependent mitochondrial trafficking, Miro1 (show RHOT1 Proteins) preferentially acts to control microtubule-dependent trafficking through kinesin and dynein, while Miro2 plays a more prominent role in coordinating mitochondrial interactions with the actin cytoskeleton through a more efficient recruitment and stability of endogenous Myo19 (show MYO19 Proteins) in the mitochondrial membrane.
Using mouse knockout strategies, we demonstrate that Miro1 (show RHOT1 Proteins), as opposed to Miro2, is the primary regulator of mitochondrial transport in both axons and dendrites. Miro1 (show RHOT1 Proteins) 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 (show RHOT1 Proteins) in mature neurons causes a progressive loss
Armcx genes regulate mitochondrial trafficking in neurons and interact with Miro 1/2 and Trak2.
molecular cloning and characterization of a novel mouse cDNA encoding a putative atypical GTPase (show RACGAP1 Proteins) protein, Arht2
This gene encodes a member of the Rho family of GTPases. The encoded protein is localized to the outer mitochondrial membrane and plays a role in mitochondrial trafficking and fusion-fission dynamics.
ras homolog gene family, member T2
, mitochondrial Rho GTPase 2-like
, mitochondrial Rho (MIRO) GTPase 2
, mitochondrial Rho GTPase 2
, miro protein
, mitochondrial Rho 2
, ras homolog gene family member T2
, rho GTPase