ITX3 emerges as a specific and non-toxic inhibitor of TrioN, the N-terminal GEF domain of the multi-domain Trio protein, displaying an IC50 value of 76 μM. This inhibitor is noted for its potential in research applications[1].[2].
体外研究
ITX3 demonstrates its inhibitory effect on TrioN signaling across various concentrations (5, 10, 25, 50, and 100 μM) over 24 hours. At 100 μM for 36 hours, ITX3 impedes nerve growth factor-induced neurite outgrowth in PC12 cells[1].
Moreover, ITX3, at concentrations of 1, 10, and 100 μM, restricts Rac1 activity and dose-dependently elevates the levels of E-cadherin protein and phospho-p38 signal in Tara-KD cells[2].
ITX3 细胞实验
Cell Line
Concentration
Treated Time
Description
References
MDCK cells
100 µM
ITX3 inhibits the Rac1-GEF activity of Trio RhoGEF, reverses Rac1 activation in Tara-KD cells, and up-regulates E-cadherin protein levels
J Cell Biol. 2011 Apr 18;193(2):319-32.
MRC5 cells
100 μM
30 min
Inhibition of Trio expression significantly reduced RhoG activation, decreased the number of cells forming CDRs, and reduced the average area of CDRs.
Mol Biol Cell. 2017 Jul 1;28(13):1768-1781.
A7r5 cells
100 μM
30 min
Inhibition of Trio expression significantly reduced RhoG activation, decreased the number of cells forming CDRs, and reduced the average area of CDRs.
Mol Biol Cell. 2017 Jul 1;28(13):1768-1781.
human pulmonary artery ECs (HPA ECs)
50 µM
30 min
Inhibited the interaction of Trio with Rac1, reducing VE-cadherin adhesion area at junctions
J Cell Biol. 2019 Jan 7;218(1):299-316.
hippocampal neurons
100 nM
45 min
Inhibition of Trio GEF1 activity, significantly decreased Rac activity, and promoted growth cone collapse
Sci Signal. 2011 Dec 6;4(202):ra82.
Human umbilical vein endothelial cells (HUVECs)
75 µM
2 h
To inhibit TrioGEF1 activity and study its effect on flow-induced endothelial cell alignment. Results showed that ITX3-treated cells aligned normally under long-term flow conditions, indicating that TrioGEF1 activity is not required for flow-induced EC alignment.
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