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Promotes the exchange of GDP by GTP. Additionally we are shipping TRIO Antibodies (8) and and many more products for this protein.
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TRIO loss of function is associated with mild intellectual disability and affects dendritic branching and synapse function.
our data show the importance of spatio-temporal regulation of the actin cytoskeleton through Trio and Rac1 at VE-cadherin (show CDH5 Proteins)-based cell-cell junctions in the maintenance of the endothelial barrier.
Aberrant expression of TRIO might play an important role in hepatocellular carcinoma (HCC (show FAM126A Proteins)) through promoting cell proliferation and invasion, and TRIO may be a novel therapeutic target for the treatment of HCC (show FAM126A Proteins)
Strong statistical evidence for a causal role of TRIO in neurodevelopmental and neuropsychiatric disorders.
TRIO controls Rac1 activation in dividing cells which counteracts MgcRacGAP (show RACGAP1 Proteins) function in cytokinesis.
TRIO is an EB1 dependent MT plus end tracking protein, and forms a complex with NAV1 at growing MT ends, which regulates TRIO-mediated Rac1 activation and neurite outgrowth.
Describe here an invadopodia disassembly model, where a signalling axis involving TrioGEF, Rac1, Pak1 (show PAK1 Proteins), and phosphorylation of cortactin (show CTTN Proteins), causes invadopodia dissolution.
We conclude that Trio promotes leukocyte transendothelial migration by inducing endothelial docking structure formation in a filamin-dependent manner through the activation of Rac1 and RhoG.
Trio, is essential for activating Rho- and Rac (show AKT1 Proteins)-regulated signaling pathways acting on JNK (show MAPK8 Proteins) and p38 (show CRK Proteins).
GEF (show SLC2A4RG Proteins) Trio is responsible for lamellipodia formation through its N-terminal DH-PH domain in a Rac1-dependent manner during fibronectin (show FN1 Proteins)-mediated spreading and migration.
The Trio gene regulates the neuronal development of the hippocampus and that it affects the intelligence of adult mice.
Trio may serve as a a signal integrator decoding extrinsic signals to Rho GTPases for cytoskeleton organization
M-cadherin-dependent adhesion can activate Rac1 via the Rho-GEF (show ARHGEF2 Proteins) Trio at the time of myoblast fusion.
the results show a link between Trio activity,Rac1 activation,neuronal organization,and recruitment of Cadherin-11 receptor to form a complex with Trio in hindbrain embryology.
findings establish Trio as a guanine nucleotide exchange factor that mediates netrin-1 signaling in axon outgrowth and guidance through its ability to activate Rac1
Promotes the exchange of GDP by GTP. Together with leukocyte antigen-related (LAR) protein, it could play a role in coordinating cell-matrix and cytoskeletal rearrangements necessary for cell migration and cell growth.
, triple functional domain (PTPRF interacting)
, triple functional domain protein