Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
The Rac-RhoGDI complex and the structural basis for the regulation of Rho proteins by RhoGDI.
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Crystal structure of LyGDI (ARHGDIB) with GDP-Rac2; the N-terminal arm contacts the switch regions and stabilizes Mg2+, explaining inhibition of nucleotide dissociation.
"The architecture of the complex interface suggests a mechanism for the inhibition of guanine nucleotide dissociation that is based on the stabilization of the magnesium (Mg2+) ion in the nucleotide binding pocket."
Cloning and characterization of bovine low molecular weight GTPases (Rac1 and Rac2) and rho GDP-dissociation inhibitor 2 (D4-GDI).
D4-GDI is cleaved by caspase-3 during daunorubicin-induced apoptosis in HL-60 cells.
RhoGDI2 is an invasion and metastasis suppressor gene in human cancer.
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Re-expression of RhoGDI2 suppresses invasion, motility and experimental lung metastasis of bladder cancer cells.
"When RhoGDI2 was transferred back into cells with metastatic ability that lacked its expression, it suppressed experimental lung metastasis but did not affect in vitro growth, colony formation, or in vivo tumorigenicity."
Proteomics of human umbilical vein endothelial cells applied to etoposide-induced apoptosis.
Large-scale proteomics and phosphoproteomics of urinary exosomes.
MHC class II-associated proteins in B-cell exosomes and potential functional implications for exosome biogenesis.
RhoGDI2 is expressed in human trophoblasts and involved in their migration by inhibiting the activation of RAC1.
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RhoGDI2 over-expression lowers and knockdown raises RAC1-GTP in trophoblast cells; RhoGDI2 inhibits trophoblast migration.
"In conclusion, RhoGDI2 inhibits trophoblast cell migration, and this function may involve suppression of RAC1 activation."
Interactome Mapping Provides a Network of Neurodegenerative Disease Proteins and Uncovers Widespread Protein Aggregation in Affected Brains.
Identification of a novel protein with GDP dissociation inhibitor activity for the ras-like proteins CDC42Hs and rac I.
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Recombinant human D4 (ARHGDIB) has GDI activity toward CDC42 and Rac1, with weaker binding than RhoGDI1.
"Functional studies with the human D4 protein demonstrate that D4 has GDI activity against the CDC42Hs and rac I proteins"
Identification of two human Rho GDP dissociation inhibitor proteins whose overexpression leads to disruption of the actin cytoskeleton.
Ly-GDI, a GDP-dissociation inhibitor of the RhoA GTP-binding protein, is expressed preferentially in lymphocytes.
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Ly-GDI binds RhoA and inhibits GDP dissociation; expression is restricted to hematopoietic tissues.
"Ly-GDI is expressed only in hematopoietic tissues and predominantly in B- and T-lymphocyte cell lines."
RhoGDIgamma: a GDP-dissociation inhibitor for Rho proteins with preferential expression in brain and pancreas.
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GFP-tagged GDI/D4 (ARHGDIB) is diffusely cytoplasmic; the vesicular perinuclear localization reported in this paper is for RhoGDIgamma (ARHGDIG).
"A similar construction with GFP tagged to the amino terminus of GDI/D4 or RhoGDI showed only a diffuse distribution in the cytoplasm without any of the perinuclear aggregates seen with RhoGDIγ (figure not shown)."
Immune responses in mice deficient in Ly-GDI, a lymphoid-specific regulator of Rho GTPases.
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Ly-GDI knockout mice have largely normal lymphoid development and immune responses, suggesting redundancy with other Rho regulators.
"These mice showed no striking abnormalities of lymphoid development or thymocyte selection."
GDIs block activation of RHOA
RAC1 GDIs block activation of RAC1
CDC42 GDIs block activation of CDC42
GDIs block activation of RHOG
UniProt record P52566 (ARHGDIB)