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RhoGDIbeta overexpression led to downregulation of miR-200c, whereas miR-200c was able directly to target 3'-UTR of jnk2mRNA and attenuated JNK2 protein translation, which resulted in attenuation of Sp1mRNA and protein expression in turn, inhibiting Sp1-dependent MMP-2 transcription.
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Binders to RhoGDI2 as a potential anti-cancer target have been first reported, and their weak interactions were depicted using NMR spectroscopy.
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Together, our results suggest a role for Ly-GDI in the localized regulation of Rho GTPases in platelets and hypothesize a link between the PKC and Rho GTPase signaling systems in platelet function.
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Delta19RhoGDIbeta has an apoptosisindependent role in the phorbol 12myristate 13acetate induced differentiation of THP1 cells to macrophages.
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The caspase-3-cleaved RhoGDIbeta is a possible determinant to promote cancer spreading.
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Our interpretation of these contradictions is that truncation and/or mutation of RhoGDI2 perturbs its conformation to expose a site that adventitiously binds FLNA and is not a bona-fide interaction.
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Results show that RhoGDI2 suppresses bladder cancer metastatic colonization via negative regulation of RhoC activity, providing a rationale for the development of therapeutics that target RhoC signaling.
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These findings indicate that RhoGDI2 repressed the activity of Rac1 and may be involved in the rearrangement of cytoskeleton in lung cancer cells.
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Short hairpin RNA-mediated knockdown of RhoGDI2 induces the invasion and migration of lung cancer due to cross-talk with the PI3K/Akt pathway and MMP-9.
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RhoGDI2 overexpression is associated with tumor growth, metastasis, and chemoresistance in gastric cancer.
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Depletion of RhoGDI2 expression inhibits the ability of invasion and migration in pancreatic carcinoma.
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RhoGDI2 inhibits trophoblast cell migration, and this function may involve suppression of RAC1 activation.
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14-3-3sigma is a RhoGDI2-regulated gene that appears to be important for suppressing the chemoresistance of gastric cancer cells.
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These results suggest that RhoGDIbeta has mitotic functions, including regulation of cytokinesis and bipolar spindle formation
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Rictor regulates cell migration by suppressing RhoGDI2.
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RhoGDI2 becomes rapidly phosphorylated at Ser31 in response to phorbol 12-myristate 13-acetate stimulation. Conventional type PKCalpha is responsible for this phosphorylation.
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Expression of ARHGDIB variants 6a, 6b, and 6c appears to be restricted to cancer cells and normal placental tissue, suggesting that these variants possess cancer-specific functions.
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The ARHGDIB is a lymphoid-specific intrinsic negative regulator of HIV-1 replication that acts by simultaneously inhibiting RhoA and Rac1 functions.
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Results suggest that D4-GDI may function as a biphasic regulator of breast cancer progression and metastasis.
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We delineate the mechanism by which RhoGDI2 promotes gastric cancer cell invasion and chemoresistance. In total, 47 differential protein spots were identified; 33 were upregulated, and 14 were downregulated by RhoGDI2 overexpression.
