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Information on EC 3.6.5.2 - small monomeric GTPase and Organism(s) Mus musculus
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3.6.5.2 small monomeric GTPaseIUBMB Comments
A family of about 50 enzymes with a molecular mass of 21 kDa that are distantly related to the alpha-subunit of heterotrimeric G-protein GTPase (EC 3.6.5.1). They are involved in cell-growth regulation (Ras subfamily), membrane vesicle traffic and uncoating (Rab and ARF subfamilies), nuclear protein import (Ran subfamily) and organization of the cytoskeleton (Rho and Rac subfamilies).
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Word Map
- 3.6.5.2
- actin
- oncogene
- cytoskeleton
- endosomes
- colorectal
- pancreatic
- metastasis
- endothelial
- adenocarcinoma
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gtp-bound
- tumorigenesis
- carcinogenesis
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endocytic
- integrins
- gdp
-
gtpase-activating
-
dominant-negative
- phosphatidylinositol
- mapk
- vesicular
- erk
- microtubule
- synaptic
-
exocytosis
- filopodia
-
cargo
-
neurite
-
traffic
- myosin
- 3-kinase
- guanosine
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cell-cell
-
protrusion
-
cytokinesis
-
ruffle
- proto-oncogene
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farnesylation
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prenylation
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geranylgeranylation
-
rock
-
adhesions
- lamellipodia
-
adherens
-
pleckstrin
- raf
- aminoacyl-trnas
- melanosomes
-
farnesyltransferase
-
rho-associated
- actomyosin
- analysis
- drug development
- pharmacology
- medicine
The taxonomic range for the selected organisms is: Mus musculus
The enzyme appears in selected viruses and cellular organisms
The enzyme appears in selected viruses and cellular organisms
Synonyms
k-ras, cdc42, h-ras, small gtpase, ef-tu, rho gtpase, rab11, rab3a, rab27a, rap1a, 
more
topSYNONYM 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
Cdc42
GTP-phosphohydrolase
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-
-
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GTPase
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-
-
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guanine triphosphatase
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-
-
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guanosine 5'-triphosphatase
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-
-
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guanosine triphosphatase
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-
-
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Rac1
Rac2
Rap1
Rho1
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Rho1 is important for the localization of the Sec3 component of the exocyst complex
RhoA
RhoH
initially named translation three four, RhoH is a GTPase-deficient so-called atypical Rho GTPase, RhoH is only found in vertebrates
ribosomal GTPase
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-
-
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small GTPase
REACTION TYPE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
phosphorous acid anhydride hydrolysis
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-
-
-
SYSTEMATIC NAME
IUBMB Comments
GTP phosphohydrolase (cell-regulating)
A family of about 50 enzymes with a molecular mass of 21 kDa that are distantly related to the alpha-subunit of heterotrimeric G-protein GTPase (EC 3.6.5.1). They are involved in cell-growth regulation (Ras subfamily), membrane vesicle traffic and uncoating (Rab and ARF subfamilies), nuclear protein import (Ran subfamily) and organization of the cytoskeleton (Rho and Rac subfamilies).
CAS REGISTRY NUMBER
COMMENTARY
9059-32-9
-
SUBSTRATE
PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate)
(Substrate)
LITERATURE
(Substrate)
(Substrate)
COMMENTARY
(Product)
(Product)
LITERATURE
(Product)
(Product)
Reversibility
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
guanosine 5'-O-(3-thiotriphosphate) + H2O
guanosine 5'-O-diphosphate + thiophosphate
-
-
-
-
?
GTP + H2O
GDP + phosphate
-
-
-
-
?
GTP + H2O
GDP + phosphate
-
small nuclear GTPase Ran controls the directionality of macromolecular transport between the nucleus and the cytoplasm. Ran has important roles during mitosis, when the nucleus is reorganized to allow chromosome segregation. Ran directs the assembly of the mitotic spindle, nuclear-envelope dynamics and the timing of cell-cycle transitions
-
-
?
GTP + H2O
GDP + phosphate
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two conformational states of Ras GTPase exhibit differential GTP-binding kinetics
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-
?
additional information
?
-
-
Knock down of Rab21 impairs integrin-mediated cell adhesion and motility, its overexpression stimulates cell migration and cancer cell adhesion to collagen and human bone
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-
?
additional information
?
-
-
in 3T3-L1 adipocytes, stimulation of lipolysis increases the association of Rab18 with lipid droplets, suggesting that recruitment of Rab18 is regulated by the metabolic state of individual lipid droplets
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-
?
additional information
?
-
-
Rab and Ral GTPases function in exocyst assembly and vesicle-tethering processes, whereas the Rho family of GTPases functions in the local activation of the exocyst complex to facilitate downstream vesicle-fusion events
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-
?
additional information
?
-
-
Rac GTPases play an important role in enucleation of mammalian erythroblasts
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-
?
additional information
?
-
-
Rac1 and Cdc42 are not required for differentiation and migration of neural crest cells, but are essential for mitotic activity and cell-cycle control in neural crest cell target structures
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-
?
additional information
?
-
-
Rac1 is a central regulator of rapid encoding of novel spatial information in vivo, Rac1 mutants display deficits in working/episodic-like memory in the delayed matching-to-place
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-
?
additional information
?
-
-
Rac2 selectively controls phagosomal alkalinization and antigen crosspresentation in CD8+ dendritic cells, Rac2 determines the subcellular assembly of the NADPH oxidase complex to phagosomes in CD8+ cells whereas in CD8- cells Rac1 mediates the assembly of NOX2 at the plasma membrane
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-
?
additional information
?
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RalA is a critical component in biphasic insulin release from pancreatic beta cells
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-
?
additional information
?
-
-
Rap1 plays a critical role in the regulation of beta1-integrin affinity, adhesion, and migration in endothelial cells and in postnatal neovascularization
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-
?
additional information
?
-
RhoH inhibits IkappaB degradation and acts as a specific negative regulator for Rac and RhoA-induced p38 activity
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-
?
additional information
?
-
-
RhoH inhibits IkappaB degradation and acts as a specific negative regulator for Rac and RhoA-induced p38 activity
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-
?
additional information
?
-
-
the small GTPase RhoA is crucial for MC3T3-E1 osteoblastic cell survival
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-
?
additional information
?
-
the small GTPase RhoH is an atypical regulator of haematopoietic cells
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-
?
additional information
?
-
-
the small GTPase RhoH is an atypical regulator of haematopoietic cells
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-
?
additional information
?
-
Ras-related, small GTPases act as molecular switches that control a variety of cellular processes by cycling between alternative conformational states: in the active state, they are bound with GTP, and in the inactive state, they are bound with GDP. In their active state, GTPases recognize their target effector proteins and evoke responses until GTP hydrolysis returns the switch to the off position
-
-
?
additional information
?
-
Ras-related, small GTPases act as molecular switches that control a variety of cellular processes by cycling between alternative conformational states: in the active state, they are bound with GTP, and in the inactive state, they are bound with GDP. In their active state, GTPases recognize their target effector proteins and evoke responses until GTP hydrolysis returns the switch to the off position
-
-
?
additional information
?
-
recombinant RhoA activity reduces Ba2+ currents through CaV2.1, CaV2.2 and CaV2.3 Ca2+ channels independently of CaVbeta subunit. This inhibition occurs independently of RGKs activity and without modification of biophysical properties and global level of expression of the channel subunit
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-
?
NATURAL SUBSTRATE
NATURAL PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate)
(Substrate)
LITERATURE
(Substrate)
(Substrate)
COMMENTARY
(Product)
(Product)
LITERATURE
(Product)
(Product)
REVERSIBILITY
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
GTP + H2O
GDP + phosphate
-
small nuclear GTPase Ran controls the directionality of macromolecular transport between the nucleus and the cytoplasm. Ran has important roles during mitosis, when the nucleus is reorganized to allow chromosome segregation. Ran directs the assembly of the mitotic spindle, nuclear-envelope dynamics and the timing of cell-cycle transitions
-
-
?
additional information
?
-
-
Knock down of Rab21 impairs integrin-mediated cell adhesion and motility, its overexpression stimulates cell migration and cancer cell adhesion to collagen and human bone
-
-
?
additional information
?
-
-
in 3T3-L1 adipocytes, stimulation of lipolysis increases the association of Rab18 with lipid droplets, suggesting that recruitment of Rab18 is regulated by the metabolic state of individual lipid droplets
-
-
?
additional information
?
-
-
Rab and Ral GTPases function in exocyst assembly and vesicle-tethering processes, whereas the Rho family of GTPases functions in the local activation of the exocyst complex to facilitate downstream vesicle-fusion events
-
-
?
additional information
?
-
-
Rac GTPases play an important role in enucleation of mammalian erythroblasts
-
-
?
additional information
?
-
-
Rac1 and Cdc42 are not required for differentiation and migration of neural crest cells, but are essential for mitotic activity and cell-cycle control in neural crest cell target structures
-
-
?
additional information
?
-
-
Rac1 is a central regulator of rapid encoding of novel spatial information in vivo, Rac1 mutants display deficits in working/episodic-like memory in the delayed matching-to-place
-
-
?
additional information
?
-
-
Rac2 selectively controls phagosomal alkalinization and antigen crosspresentation in CD8+ dendritic cells, Rac2 determines the subcellular assembly of the NADPH oxidase complex to phagosomes in CD8+ cells whereas in CD8- cells Rac1 mediates the assembly of NOX2 at the plasma membrane
-
-
?
additional information
?
-
-
RalA is a critical component in biphasic insulin release from pancreatic beta cells
-
-
?
additional information
?
-
-
Rap1 plays a critical role in the regulation of beta1-integrin affinity, adhesion, and migration in endothelial cells and in postnatal neovascularization
-
-
?
additional information
?
-
RhoH inhibits IkappaB degradation and acts as a specific negative regulator for Rac and RhoA-induced p38 activity
-
-
?
additional information
?
-
-
RhoH inhibits IkappaB degradation and acts as a specific negative regulator for Rac and RhoA-induced p38 activity
-
-
?
additional information
?
-
-
the small GTPase RhoA is crucial for MC3T3-E1 osteoblastic cell survival
-
-
?
additional information
?
-
the small GTPase RhoH is an atypical regulator of haematopoietic cells
-
-
?
additional information
?
-
-
the small GTPase RhoH is an atypical regulator of haematopoietic cells
-
-
?
additional information
?
-
Ras-related, small GTPases act as molecular switches that control a variety of cellular processes by cycling between alternative conformational states: in the active state, they are bound with GTP, and in the inactive state, they are bound with GDP. In their active state, GTPases recognize their target effector proteins and evoke responses until GTP hydrolysis returns the switch to the off position
-
-
?
additional information
?
-
Ras-related, small GTPases act as molecular switches that control a variety of cellular processes by cycling between alternative conformational states: in the active state, they are bound with GTP, and in the inactive state, they are bound with GDP. In their active state, GTPases recognize their target effector proteins and evoke responses until GTP hydrolysis returns the switch to the off position
-
-
?
METALS and IONS
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
INHIBITOR
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
additional information
-
RhoE downregulates the activity of RhoA by activating p190RhoGAP
-
additional information
RhoA- or ROCK-induced inhibitions are partially relieved upon incubation of the oocytes with the ROCK inhibitor Y27632
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ACTIVATING COMPOUND
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
ACAP3
aGTPase-activating protein (GAP) specific to small GTPase Arf6. ACAP3 is involved in neuronal migration in the developing cerebral cortex of mice, regulation mechanism, detailed overview. ACAP3 is abundantly expressed in the developing cerebral cortex. GAP activity of ACAP3 is required for neuronal migration. Knockdown of ACAP3 in the developing cortical neurons of mice in utero significantly abrogates neuronal migration in the cortical layer, which is restored by ectopic expression of wild-type ACAP3, but not by its GAP-inactive mutant
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cytotoxic necrotizing factor 1
activation of Rho proteins by the cytotoxic necrotizing factor 1 (CNF1) from Escherichia coli, while the isomeric cytotoxicnecrotizing factor from Yersinia pseudotuberculosis (CNFy) drives GTP-loading of basal RhoB but fails to cause activation of the rhoB promoter and thus its expression. CNF1 inhibits cytokinesis and induces the formation of bi-nucleated (tetraploid) cells. Cytotoxic-necrotizing factors encompass a class of auto-transporter toxins produced by Escherichia coli (CNF1-3) or Yersinia pseudotuberculosis (CNFy). CNF1 specifically deamidates RhoA. CNF1-induced RhoB response depends on the deamidation of Rho proteins
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geranylgeranyl transferase I
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RhoA is activated by geranylgeranylation, which promotes its membrane anchoring, the geranylgeranyl transferase I inhibitor GGTI-2166to is used to inhibit geranylgeranylation
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guanine nucleotide exchange factor Epac
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specifically increases Rap1 activity
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Insulin
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RalA is activated upon insulin stimulation in a dose-dependent manner
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lipopolysaccharide
Rap2a is activated by lipopolysaccharide in macrophages. In contrast to mRNA levels, Rap2a protein levels are increased after lipopolysaccharide treatments of macrophages
TGF-beta1
TGF-beta1 activates Rap1 through cAMP and Epac1/Epac2. 2',5-dideoxyadenosine is an inhibitor of adenlyate cyclase on Rap1 activity
-
additional information
-
growth factor receptor-induced activation of Cdc42 activates Rac, which in turn stimulates Rho activity
-
additional information
-
mDia2 is a downstream effector of the Rho GTPases Rac1 and Rac2, Rac1 and Rac2 bind to mDia2 GBD in a GTP-dependent manner
-
additional information
-
Rac is activated via stimulation of the G-protein-coupled seven-span transmembrane receptor CXCR4 by stromal derived factor-1, by adhesion via beta1 integrins, and via stimulation of c-kit by the stem cell factor
-
additional information
some of the amino acids that are crucial for GTPase activity are mutated in RhoH so that the protein is a GTPase-deficient, so-called atypical Rho GTPase. Other mechanisms of regulating RhoH activity include regulation at the mRNA level and tyrosine phosphorylation of the protein's unique ITAM-like motif. The C-terminal CaaX box of RhoH is mainly a target for farnesyl-transferase but can also be modified by geranylgeranyltransferase. Isoprenylation of RhoH and changes in subcellular localisation may be an additional factor to fine-tune signalling
-
additional information
-
some of the amino acids that are crucial for GTPase activity are mutated in RhoH so that the protein is a GTPase-deficient, so-called atypical Rho GTPase. Other mechanisms of regulating RhoH activity include regulation at the mRNA level and tyrosine phosphorylation of the protein's unique ITAM-like motif. The C-terminal CaaX box of RhoH is mainly a target for farnesyl-transferase but can also be modified by geranylgeranyltransferase. Isoprenylation of RhoH and changes in subcellular localisation may be an additional factor to fine-tune signalling
-
additional information
putative activator TLR-inducible Ras guanine exchange factor RasGEF1b is sufficient to induce, it is not fully required for Rap2a activation
-
pH OPTIMUM
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
TEMPERATURE OPTIMUM
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
ORGANISM
COMMENTARY
LITERATURE
UNIPROT
SEQUENCE DB
SOURCE
SOURCE TISSUE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
SOURCE
-
tumor-induced dysregulation of endocytic activity of dendritic cells is mediated by reduced activity of several members of the small Rho GTPase family
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tumor-induced dysregulation of endocytic activity of dendritic cells is mediated by reduced activity of several members of the small Rho GTPase family
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in the adult mouse brain, Rab23 is detected in betaIII tubulin positive neuronal cell bodies and are most prominent in cortex, hypothalamus and the cerebellum
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Ras is detected in medullary endothelial cells, medullary interstitial cells, cortical interstitial cells and glomerular endothelial cells. Ras plays a role in renal fibrosis
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ARF6 is an essential component in the signaling pathway coupling hepatocyte growth factor signaling to hepatic cord formation
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tumor-induced dysregulation of endocytic activity of dendritic cells is mediated by reduced activity of several members of the small Rho GTPase family
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Rac1 activity serves as a regulator of cell senescence through modulation of cellular ROS, genomic stability, and p53 activity
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tumor-induced dysregulation of endocytic activity of dendritic cells is mediated by reduced activity of several members of the small Rho GTPase family
RhoH is expressed strongest in T-lymphocytes and acts as a positive regulatory factor for thymocyte selection and T-cell receptor signalling
additional information
-
prepared from tumor-bearing mice ex vivo. Tumor-induced dysregulation of endocytic activity of dendritic cells is mediated by reduced activity of several members of the small Rho GTPase family
TLRs agonists induce changes in the expression of Rap2a in macrophages. In contrast to mRNA levels, Rap2a protein levels are increased after LPS treatments of macrophages
constitutively active RhoA in primary culture of spinal motoneurons
Rap1b is the predominant Rap1 isoform expressed in neutrophils
additional information
-
Rab23 is absent from glial fibrillary acidic protein positive astrocytes or CNPase positive oligodendrocytes
additional information
Rap1b is expressed in all tissues, including endothelial cells
LOCALIZATION
ORGANISM
UNIPROT
COMMENTARY
GeneOntology No.
LITERATURE
SOURCE
additional information
-
RalA localizes independently of intracellular insulin granules
-
only the membrane-localised form of RhoH is able to downregulate Rac1 efficiently
GENERAL INFORMATION
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
evolution
malfunction
metabolism
physiological function
additional information
-
activation of Rap1 by Epac1 leads to increased integrin activity and adhesion of endothelial progenitor cells, CD34+ hematopoietic progenitor cells and mesenchylmal stem cells, which show increased homing and neovascularization capabilities
evolution
Ras proximity 1 (Rap1) belongs to the Ras superfamily of GTPases that cycle between GTP-bound active and GDPbound inactive forms through GEFs and GAPs
evolution
the subfamily of Ras-like small GTPases contains numerous members including classical Ras (H-, K-, and N-Ras), R-Ras, TC21/R-Ras2, MRas/R-Ras3, DexRas1/RasD1, RalA/B, Rheb, Rit, Rin, Rap1 and Rap2, and atypical kappaB-Ras1 and kappaB-Ras2
malfunction
-
the loss of Rap1b leads to deficiencies both in B cell migration and in adhesion. Platelets from Rap1b null mice exhibit defective aggregation in response to integrin stimulation. These mice exhibit protection from arterial thrombosis and provide an independent role for this Rap1 isoform
malfunction
-
deletion of Cdc42 in mature B cells results in an antibody response of reduced magnitude and lower affinity to soluble T cell-dependent antigen. B cells that lack Cdc42 remain dominant for 2 weeks postinduction with tamoxifen, following which Cdc42-sufficient B cells gradually dominate with very few Cdc42-deficient B cells being detected after 6 weeks. Deletion of Cdc42 in mature B cells alters their ability to activate T cells. B cells that lack Cdc42 fail to form long protrusions on Ab-coated surfaces. Reduced spreading and upregulation of CIP4 in Cdc42-deficient B cells. Deletion of Cdc42 in B cells leads to impaired humoral immune response, phenotype, overview
malfunction
expression of constitutively active RhoA in primary culture of spinal motoneurons also drastically reduces high-voltage-activated Ca2+ current amplitude
malfunction
Rap1b deficiency increases neutrophil transmigration, Rap1b loss promotes transendothelial migration via transcellular route. Rap1b-deficient mice exhibits enhanced neutrophil recruitment to inflamed lungs and enhanced susceptibility to endotoxin shock. Rap1b-/- neutrophils exhibit enhanced chemokinesis and chemotaxis. Rap1b deficiency promotes the transcellular route of diapedesis through endothelial cell. Increased transcellular migration of Rap1b-deficient neutrophils in vitro is selectively mediated by enhanced PI3K-Akt activation and invadopodia-like protrusions. Akt inhibition in vivo suppresses excessive Rap1b-deficient neutrophil migration and associated endotoxin shock. Pharmacological inhibition of Akt activation rescued Rap1b-/- neutrophil phenotype. Rap1a expression does not compensate for Rap1b loss in blood cells. Phenotype, overview
malfunction
upon long term treatment with CNF1, RhoB-/- mouse embryonic fibroblasts exhibit DNA fragmentation, phosphatidylserine exposure, and loss of membrane integrity, while RhoB+/- MEFs persist as bi-nucleated (tetraploid) cells without any signs of cell death
malfunction
ARF6Q67L promotes spontaneous metastasis from significantly smaller primary tumors than PTENNULL, implying an enhanced ability of ARF6-GTP to drive distant spread. ARF6Q67L tumors show upregulation of Pik3r1 expression, which encodes the p85 regulatory subunit of PI3K. Tumor cells expressing ARF6Q67L displays increased PI3K protein levels and activity, enhances PI3K distribution to cellular protrusions, and increases AKT activation in invadopodia. Aberrant ARF6 activation in human melanoma samples is associated with reduced survival
malfunction
both knockdown and overexpression of Rap2a small GTPase in macrophages result in impairment of NF-kappaB activity and inflammatory gene expression. Silencing of Rap2a impairs LPS-induced production of IL-6 cytokine and KC/Cxcl1 chemokine, and also NF-kappaB activity. Overexpression of Rap2a does also lead to marked inhibition of NF-kappaB activation induced by LPS, Pam3CSK4, and downstream TLR signaling molecules. Dysregulation of Rap2a expression in an inflammatory context may significantly alter the status of NF-kappaB activation
metabolism
high-voltage-activated Ca2+ channels are known regulators of synapse formation and transmission and play fundamental roles in neuronal pathophysiology. Small GTPases of Rho and RGK families, via their action on both cytoskeleton and Ca2+ channels are key molecules for these processes
metabolism
ACAP3, the GTPase-activating protein specific to the small GTPase Arf6, regulates neuronal migration in the developing cerebral cortex. ACAP3 is involved in neuronal migration in the developing cerebral cortex of mice. Knockdown of ACAP3 in the developing cortical neurons of mice in utero significantly abrogates neuronal migration in the cortical layer, which is restored by ectopic expression of wild-type ACAP3, but not by its GAP-inactive mutant
metabolism
Rap2a is activated by lipopolysaccharide in macrophages, and although putative activator TLR-inducible Ras guanine exchange factor RasGEF1b is sufficient to induce, it is not fully required for Rap2a activation. Dysregulation of Rap2a expression in an inflammatory context may significantly alter the status of NF-kappaB activation
physiological function
-
Rap1A and Rap1B have differing roles in the cardiovasculature. Activation of Rap1a and 1b in various cell types of the cardiovasculature lead to alterations in cell attachment, migration and cell junction formation. Rap1b is necessary for proper development, homing and T cell dependant immunity. Rap1b protein regulates the SERCA 3b-associated Ca2+ pool through its cAMP-dependent phosphorylation, and therefore plays a role in the transition between platelet activation and inhibition. Whereas Rap1a and 1b appear to be key regulators in differing cell types of the blood, neutrophils and platelets, both appear to contribute to the normal function of endothelial cells and to angiogenesis. In smooth muscle cells, Rap1 may elicit a protective response to maintain vessel wall integrity in response to cellular stress
physiological function
a pathway involving GTPase Rac1 positively regulates the activity of the rhoB promoter and RhoB expression. Critical role of transcriptional activation in CNF1-induced RhoB expression. Regulation of the rhoB promoter, overview. RhoB dependent suppression of CNF1-induced polyploidy and cell death
physiological function
RhoA inhibits HVA CaV2 Ca2+ channels in a CaVbeta subunit-independent manner, recombinant RhoA activity reduces Ba2+ currents through CaV2.1, CaV2.2 and CaV2.3 Ca2+ channels independently of CaVbeta subunit. This inhibition occurs independently of RGKs activity and without modification of biophysical properties and global level of expression of the channel subunit. High-voltage-activated Ca2+ channels regulation by RhoA might govern synaptic transmission during development and potentially contribute to pathophysiological processes when axon regeneration and growth cone kinetics are impaired. Effects of RhoA on CaV2 trafficking to the plasma membrane, regulation of Ca2+ channel expression and activity by small GTPases, overview
physiological function
-
role of intrinsic expression of Cdc42 by mature B cells in their activation and function, Cdc42 expression in B cells is essential for efficient IL-2 secretion of CD4+ T cells in cognate T-B cell interaction
physiological function
small GTPase Rap1 regulates cell migration through regulation of small GTPase RhoA activity in response to transforming growth factor-beta1. GTP-RhoA and GTP-Rap1 levels are reciprocally regulated in a time-dependent manner following TGF-beta1 stimulation. Ras-related, small GTPases act as molecular switches that control a variety of cellular processes by cycling between alternative conformational states. In the active state, they are bound with GTP, and in the inactive state, they are bound with GDP. In their active state, GTPases recognize their target effector proteins and evoke responses until GTP hydrolysis returns the switch to the off position. GTP-binding to small GTPases is catalyzed by guanine nucleotide exchange factors (GEFs), and hydrolysis of the bound GTP is accelerated by GTPase activating proteins (GAPs), Downstream effector proteins of Rap1, including RapL, AF6, and ARAP3 transmit the activated Rap1 signals within the cells. Rap1 regulates GTPase RhoA activity, but RhoA does not regulate the Rap1 activity
physiological function
small GTPase Rap1 regulates cell migration through regulation of small GTPase RhoA activity in response to transforming growth factor-beta1. GTP-RhoA and GTP-Rap1 levels are reciprocally regulated in a time-dependent manner following TGF-beta1 stimulation. Ras-related, small GTPases act as molecular switches that control a variety of cellular processes by cycling between alternative conformational states. In the active state, they are bound with GTP, and in the inactive state, they are bound with GDP. In their active state, GTPases recognize their target effector proteins and evoke responses until GTP hydrolysis returns the switch to the off position. GTP-binding to small GTPases is catalyzed by guanine nucleotide exchange factors (GEFs), and hydrolysis of the bound GTP is accelerated by GTPase activating proteins (GAPs). Downstream effector proteins of Rap1, including RapL, AF6, and ARAP3 transmit the activated Rap1 signals within the cells. Rap1 regulates GTPase RhoA activity, but RhoA does not regulate the Rap1 activity
physiological function
the cytoprotective RhoB response is not only evoked by bacterial protein toxins inactivatingRho/Ras proteins but also by the Rac1-activating toxin CNF
physiological function
the small GTPase Rap1b negatively regulates neutrophil chemotaxis and transcellular diapedesis by inhibiting Akt activation. The inhibitory action of Rap1b on PI3K signaling may be mediated by activation of phosphatase SHP-1. Role for Rap1b as a key suppressor of neutrophil migration and lung inflammation, which may represent an unappreciated regulatory pathway of neutrophil-related aberrant inflammatory responses. Rap1b inhibits Akt activation via CD11b outside-in signaling, Rap1b negatively regulates PI3K-Akt signaling via the phosphatase SHP-1
physiological function
Arf6 is a critical regulator of membrane dynamics-based cellular events such as reorganization of actin cytoskeleton and membrane trafficking. Like other small GTPases, Arf6 acts as a molecular switch by cycling between GDP-bound inactive and GTP-bound active forms in cellular signaling pathways. Arf6 is activated in response to agonist stimulation of the cell interacts with its downstream effectors to regulate their intracellular location and activity
physiological function
small Ras GTPases are key molecules that regulate a variety of cellular responses in different cell types. Rap2a. Rap2a can inhibit the LPS-induced phosphorylation of the NF-kappaB subunit p65 at serine 536. Rap2a is implicated in TLR-mediated responses by contributing to balanced NF-kappaB activity status in macrophages. Rap2a GTPase is involved in TLR signaling pathway to NF-kappaB. Rap2a exhibits a more potent inhibitory effect on Mal/TIRAP and TRAF6-induced NF-kappaB activation. In contrast, Rap2a fails to inhibit NF-kappaB activity induced directly by the monomer p65(RelA). Thus, Rap2a interferes in NF-kappaB activation by affecting upstream signaling events to p65(RelA)
physiological function
the small GTPase ARf6 activates PI3K in melanoma to induce a prometastatic state. Constitutive activation of the small GTPase ARF6 (ARF6Q67L) is sufficient to accelerate metastasis in mice with BRAFV600E/Cdkn2aNULL melanoma at a similar incidence and severity to Pten loss, a major driver of PI3K activation and melanoma metastasis. ARF6 activation increases lung colonization from circulating melanoma cells, suggesting that the prometastatic function of ARF6 extends to late steps in metastasis. ARF6 is necessary and sufficient for activation of both PI3K and AKT, and PI3K and AKT are necessary for ARF6-mediated invasion. Critical role for ARF6 in multiple steps of the metastatic cascade
UNIPROT
ENTRY NAME
ORGANISM
NO. OF AA
NO. OF TRANSM. HELICES
MOLECULAR WEIGHT[Da]
SOURCE
SEQUENCE
LOCALIZATION PREDICTION
The reliability class of the localization prediction ranges from 1 (very reliable) to 5 (not reliable).
The reliability class of the localization prediction ranges from 1 (very reliable) to 5 (not reliable). ARL8B_MOUSE
186
0
21539
Swiss-Prot
other Location (Reliability: 5)
RAB8A_MOUSE
207
0
23668
Swiss-Prot
other Location (Reliability: 5)
RALA_MOUSE
206
0
23553
Swiss-Prot
other Location (Reliability: 4)
RALB_MOUSE
206
0
23349
Swiss-Prot
Mitochondrion (Reliability: 5)
RB11A_MOUSE
216
0
24394
Swiss-Prot
other Location (Reliability: 1)
RAB1B_MOUSE
201
0
22187
Swiss-Prot
other Location (Reliability: 4)
RAB4A_MOUSE
218
0
24409
Swiss-Prot
other Location (Reliability: 3)
RASN_MOUSE
189
0
21199
Swiss-Prot
other Location (Reliability: 2)
ARF6_MOUSE
175
0
20082
Swiss-Prot
other Location (Reliability: 3)
RAB10_MOUSE
200
0
22541
Swiss-Prot
Secretory Pathway (Reliability: 3)
RAB7A_MOUSE
207
0
23490
Swiss-Prot
Secretory Pathway (Reliability: 5)
RAC3_MOUSE
192
0
21379
Swiss-Prot
other Location (Reliability: 2)
RASLC_MOUSE
266
0
29555
Swiss-Prot
Mitochondrion (Reliability: 4)
RASM_MOUSE
208
0
23901
Swiss-Prot
other Location (Reliability: 2)
RIT1_MOUSE
219
0
25169
Swiss-Prot
other Location (Reliability: 5)
RIT2_MOUSE
217
0
24802
Swiss-Prot
other Location (Reliability: 1)
RHOA_MOUSE
193
0
21782
Swiss-Prot
other Location (Reliability: 2)
RAC1_MOUSE
192
0
21450
Swiss-Prot
other Location (Reliability: 2)
RASH_MOUSE
189
0
21298
Swiss-Prot
other Location (Reliability: 3)
RASK_MOUSE
189
0
21656
Swiss-Prot
other Location (Reliability: 2)
RSLAA_MOUSE
203
0
22792
Swiss-Prot
Mitochondrion (Reliability: 4)
RSLAB_MOUSE
203
0
23229
Swiss-Prot
Mitochondrion (Reliability: 3)
CDC42_MOUSE
191
0
21259
Swiss-Prot
other Location (Reliability: 2)
RAP1A_MOUSE
184
0
20987
Swiss-Prot
other Location (Reliability: 3)
RAP2A_MOUSE
183
0
20642
Swiss-Prot
other Location (Reliability: 3)
RAP2B_MOUSE
183
0
20504
Swiss-Prot
other Location (Reliability: 3)
RAP2C_MOUSE
183
0
20745
Swiss-Prot
other Location (Reliability: 3)
RB11B_MOUSE
218
0
24489
Swiss-Prot
other Location (Reliability: 1)
RAB2A_MOUSE
212
0
23548
Swiss-Prot
other Location (Reliability: 3)
RAB2B_MOUSE
216
0
24198
Swiss-Prot
other Location (Reliability: 3)
RAB4B_MOUSE
213
0
23629
Swiss-Prot
other Location (Reliability: 5)
RAB5A_MOUSE
215
0
23599
Swiss-Prot
other Location (Reliability: 4)
RAB5B_MOUSE
215
0
23707
Swiss-Prot
Mitochondrion (Reliability: 5)
RASE_MOUSE
227
0
24321
Swiss-Prot
other Location (Reliability: 2)
RB27A_MOUSE
221
0
25017
Swiss-Prot
other Location (Reliability: 3)
RB27B_MOUSE
218
0
24560
Swiss-Prot
other Location (Reliability: 3)
RERG_MOUSE
199
0
22580
Swiss-Prot
other Location (Reliability: 5)
RSLBA_MOUSE
242
0
27067
Swiss-Prot
other Location (Reliability: 4)
RSLBB_MOUSE
247
0
27362
Swiss-Prot
other Location (Reliability: 2)
RAB1A_MOUSE
205
0
22678
Swiss-Prot
other Location (Reliability: 4)
RAB5C_MOUSE
216
0
23413
Swiss-Prot
other Location (Reliability: 4)
RAB6B_MOUSE
208
0
23462
Swiss-Prot
other Location (Reliability: 4)
RAP1B_MOUSE
184
0
20825
Swiss-Prot
other Location (Reliability: 3)
Q9CXY0_MOUSE
206
0
23597
TrEMBL
other Location (Reliability: 5)
Q3U0D7_MOUSE
175
0
20082
TrEMBL
other Location (Reliability: 3)
A0A1Y7VL93_MOUSE
137
0
15353
TrEMBL
other Location (Reliability: 4)
Q8CCG5_MOUSE
206
0
23349
TrEMBL
Mitochondrion (Reliability: 5)
Q544U7_MOUSE
221
0
25017
TrEMBL
other Location (Reliability: 3)
F6QC68_MOUSE
149
0
16795
TrEMBL
other Location (Reliability: 1)
Q4VA90_MOUSE
218
0
24590
TrEMBL
other Location (Reliability: 2)
Q549X4_MOUSE
218
0
24560
TrEMBL
other Location (Reliability: 3)
PDB
SCOP
CATH
UNIPROT
ORGANISM
POSTTRANSLATIONAL MODIFICATION
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
additional information
additional information
the CKIF motif in mouse RhoH is a target for the in vitro modification by farnesyl-transferase and geranylgeranyl-transferase
additional information
-
the CKIF motif in mouse RhoH is a target for the in vitro modification by farnesyl-transferase and geranylgeranyl-transferase
CRYSTALLIZATION (Commentary)
ORGANISM
UNIPROT
LITERATURE
crystallization of M-ras in the GDP-bound and guanosine 5'-(beta,gamma-imido)triphosphate-bound forms, hanging-drop vapour diffusion method at 20°C using the reservoir solution containing 20% w/v polyethylene glycol 8000 and 50 mM potassium phosphate at a protein concentration of 10 mg/ml
-
hanging drop vapour diffusion method, using 1.0 M sodium citrate trihydrate, 0.1 M sodium cacodylate, at pH 6.5
-
PROTEIN VARIANTS
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
AS28N
-
the mutant significantly inhibits KCl-induced insulin secretion but has no significant effect on glucose/carbachol-and glucose/KCl-induced insulin secretion despite an inhibitory trend
D57N
-
the dominant negative Rac GTPase mutation does not only inhibit Rac1, Rac2, and Rac3 activities, but may also inhibit Cdc42
E78L/C123S/C188S
-
the mutant may modulate effector recognition by forming an intramolecular disulfide bridge
Q67L
additional information
Q67L
ARF6Q67L promotes spontaneous metastasis from significantly smaller primary tumors than PTENNULL, implying an enhanced ability of ARF6-GTP to drive distant spread. In mice with metastases, there is a dramatic increase in metastatic volume in the ARF6Q67L cohort
additional information
-
the chocolate mutation is attributed to a G146T transversion in the conserved GTP/GDP-interacting domain of Rab38, recombinant Rab38chocolate proteins retain GTP-binding activity but fail to undergo prenyl modification, the genetic abnormality of Rab38 affects multiple lysosome-related organelles, resulting in lung disease in addition to oculocutaneous albinism
additional information
-
generation of Cdc42-deficient B cells, tamoxifen induction of Cdc42 excision
additional information
knockdown and overexpression of Rap2a small GTPase in macrophages resulting in impairment of NF-kappaB activity and inflammatory gene expression
PURIFICATION (Commentary)
ORGANISM
UNIPROT
LITERATURE
GppNHp-bound Rab27a in complex with the Rab27-binding domain of exophilin4/Slp2-a effector, glutathione Sepharose 4B resin chromatography and Superdex-75 gel filtration
-
CLONED (Commentary)
ORGANISM
UNIPROT
LITERATURE
expressed in Escherichia coli BL21(DE3) LysS cells. Three crystal structures of Rab27b-GDP were solved in three different space groups: P6522, C2 and P212121
-
heterologous expression of RhoA in Xenopus laevis oocytes. Expression of constitutively active RhoA in primary culture of spinal motoneurons also drastically reduces high-voltage-activated Ca2+ current amplitude
quantitative RT-PCR enzyme expression analysis, cotransfection of the NF-kappaB reporter with TLR2, TLR3, and TLR4, CD14, MD2 and Rap2a encoding plasmids into HEK-293 cells, and further treating the cells with the TLR ligands
EXPRESSION
ORGANISM
UNIPROT
LITERATURE
expression levels of Rap2a in macrophages might be tightly regulated to avoid unbalanced immune response
putative activator TLR-inducible Ras guanine exchange factor RasGEF1b is sufficient to induce, it is not fully required for Rap2a activation. In contrast to mRNA levels, Rap2a protein levels are increased after lipopolysaccharide treatments of macrophages
RhoB is the only member of the Rho subfamily of small GTPases, which is classified as an immediateearly gene product. RhoB is up-regulated in response to growth factors as well as cytotoxic and geno-toxic agents. Clostridial glucosylating toxins evoke pronounced RhoB expression, based on the inactivation of Rho/Ras proteins. Long lasting expression of RhoB in cultured cells upon activation of Rho proteins by the cytotoxic necrotizing factor 1 (CNF1) from Escherichia coli. CNF1-induced RhoB expression in primary and immortalized NIH3T3 fibroblasts. Deamidase-deficient CNF1-C866S fails to activate the rhoB promoter, CNF1-C866S only faintly induces expression of rhoB mRNA and RhoB protein. Critical role of Rac1 in CNF1-induced RhoB expression, overview
si-Rap1 augments GTP-RhoA levels and cell migration. si-RNAs of Epac1 and Epac2 reduced GTP-Rap1 levels leading to promotion of GTP-RhoA levels. si-RNA of ARAP3 (Rap-dependent RhoGAP) increased GTP-RhoA level and cell migration
APPLICATION
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
medicine
medicine
-
regulation of small Rho GTPases might serve as a new pharmacological tool for protection of dendridic cell vaccines from tumor-induced inhibition and functional failure
medicine
-
small Rho GTPases might serve as new targets for modulating functional activity of dendritic cell vaccines or endogenous dendritic cells in various immunotherapeutic or chemoimmunotherapeutic strategies
medicine
neither the overall survival nor the disease-free survival rate in diffuse large B-cell lymphoma can be linked to hypermutation of the RHOH gene
REF.
AUTHORS
TITLE
JOURNAL
VOL.
PAGES
YEAR
ORGANISM (UNIPROT)
PUBMED ID
SOURCE
Ye, M.; Shima, F.; Muraoka, S.; Liao, J.; Okamoto, H.; Yamamoto, M.; Tamura, A.; Yagi, N.; Ueki, T.; Kataoka, T.
Crystal structure of M-Ras reveals a GTP-bound off state conformation of Ras family small GTPases
J. Biol. Chem.
280
31267-31275
2005
Mus musculus
Guo, A.; Wang, T.; Ng, E.L.; Aulia, S.; Chong, K.H.; Teng, F.Y.; Wang, Y.; Tang, B.L.
Open brain gene product Rab23: expression pattern in the adult mouse brain and functional characterization
J. Neurosci. Res.
83
1118-1127
2006
Mus musculus
Chavas, L.M.; Torii, S.; Kamikubo, H.; Kawasaki, M.; Ihara, K.; Kato, R.; Kataoka, M.; Izumi, T.; Wakatsuki, S.
Structure of the small GTPase Rab27b shows an unexpected swapped dimer
Acta Crystallogr. Sect. D
63
769-779
2007
Mus musculus
Liao, J.; Shima, F.; Araki, M.; Ye, M.; Muraoka, S.; Sugimoto, T.; Kawamura, M.; Yamamoto, N.; Tamura, A.; Kataoka, T.
Two conformational states of Ras GTPase exhibit differential GTP-binding kinetics
Biochem. Biophys. Res. Commun.
369
327-332
2008
Homo sapiens, Mus musculus, Suberites domuncula (A1XKQ5), Suberites domuncula (A1XKQ6), Suberites domuncula (A1XKQ7), Suberites domuncula (A1XKQ8), Suberites domuncula (A1XKQ9), Suberites domuncula (A1XKR0), Suberites domuncula (A1XKR1), Suberites domuncula (A1XKR2), Suberites domuncula (A1XKR3), Suberites domuncula (A1XKR5), Suberites domuncula (A1XKR6), Suberites domuncula (A1XKR7), Suberites domuncula (A1XKR8), Suberites domuncula (A1XKR9), Suberites domuncula (A1XKS0), Suberites domuncula (A1XKS1), Suberites domuncula (A1XKS2), Suberites domuncula (A1XKS3), Suberites domuncula (A1XKS4), Suberites domuncula (A1XKS5), Suberites domuncula (A1XKS6), Suberites domuncula (A1XKS7), Suberites domuncula (A1XKS8), Suberites domuncula (A1XKS9), Suberites domuncula (A1XKT0), Suberites domuncula (A1XKT1), Suberites domuncula (A1XKT2), Suberites domuncula (A1XKT3), Suberites domuncula (A1XKT4), Suberites domuncula (A1XKT5), Suberites domuncula (A1XKT6), Suberites domuncula (A1XKT7), Suberites domuncula (A1XKT8), Suberites domuncula (A1XKT9), Suberites domuncula (A1XKU0), Suberites domuncula (A1XKU1), Suberites domuncula (A1XKU2), Suberites domuncula (A1XKU3), Suberites domuncula (A1XKU4), Suberites domuncula (A1XKU5), Suberites domuncula (O97342), Suberites domuncula (Q4H115), Suberites domuncula (Q4H116)
Martinez-Salgado, C.; Rodriguez-Pena, A.B.; Lopez-Novoa, J.M.
Involvement of small Ras GTPases and their effectors in chronic renal disease
Cell. Mol. Life Sci.
65
477-492
2008
Homo sapiens, Mus musculus
Debidda, M.; Williams, D.A.; Zheng, Y.
Rac1 GTPase regulates cell genomic stability and senescence
J. Biol. Chem.
281
38519-38528
2006
Mus musculus
Pellinen, T.; Arjonen, A.; Vuoriluoto, K.; Kallio, K.; Fransen, J.A.; Ivaska, J.
Small GTPase Rab21 regulates cell adhesion and controls endosomal traffic of beta1-integrins
J. Cell Biol.
173
767-780
2006
Mus musculus
Tourkova, I.L.; Shurin, G.V.; Wei, S.; Shurin, M.R.
Small rho GTPases mediate tumor-induced inhibition of endocytic activity of dendritic cells
J. Immunol.
178
7787-7793
2007
Mus musculus
Shurin, G.V.; Tourkova, I.L.; Shurin, M.R.
Low-dose chemotherapeutic agents regulate small Rho GTPase activity in dendritic cells
J. Immunother.
31
491-499
2008
Mus musculus
Goldfinger, L.E.
Choose your own path: specificity in Ras GTPase signaling
Mol. Biosyst.
4
293-299
2008
Mus musculus
Suzuki, T.; Kanai, Y.; Hara, T.; Sasaki, J.; Sasaki, T.; Kohara, M.; Maehama, T.; Taya, C.; Shitara, H.; Yonekawa, H.; Frohman, M.A.; Yokozeki, T.; Kanaho, Y.
Crucial role of the small GTPase ARF6 in hepatic cord formation during liver development
Mol. Cell. Biol.
26
6149-6156
2006
Mus musculus
Clarke, P.R.; Zhang, C.
Spatial and temporal coordination of mitosis by Ran GTPase
Nat. Rev. Mol. Cell Biol.
9
464-477
2008
Homo sapiens, Mus musculus
Chavas, L.M.; Ihara, K.; Kawasaki, M.; Kato, R.; Izumi, T.; Wakatsuki, S.
Purification, crystallization and preliminary X-ray crystallographic analysis of Rab27a GTPase in complex with exophilin4/Slp2-a effector
Acta Crystallogr. Sect. F
64
599-601
2008
Mus musculus
Osanai, K.; Oikawa, R.; Higuchi, J.; Kobayashi, M.; Tsuchihara, K.; Iguchi, M.; Jongsu, H.; Toga, H.; Voelker, D.R.
A mutation in Rab38 small GTPase causes abnormal lung surfactant homeostasis and aberrant alveolar structure in mice
Am. J. Pathol.
173
1265-1274
2008
Mus musculus
Carmona, G.; Goettig, S.; Orlandi, A.; Scheele, J.; Baeuerle, T.; Jugold, M.; Kiessling, F.; Henschler, R.; Zeiher, A.M.; Dimmeler, S.; Chavakis, E.
Role of the small GTPase Rap1 for integrin activity regulation in endothelial cells and angiogenesis
Blood
113
488-497
2009
Homo sapiens, Mus musculus
Fueller, F.; Kubatzky, K.F.
The small GTPase RhoH is an atypical regulator of haematopoietic cells
Cell Commun. Signal.
6
6-6
2008
Homo sapiens (Q15669), Homo sapiens, Mus musculus (Q9D3G9), Mus musculus
Fuchs, S.; Herzog, D.; Sumara, G.; Buechmann-Moller, S.; Civenni, G.; Wu, X.; Chrostek-Grashoff, A.; Suter, U.; Ricci, R.; Relvas, J.B.; Brakebusch, C.; Sommer, L.
Stage-specific control of neural crest stem cell proliferation by the small Rho GTPases Cdc42 and Rac1
Cell Stem cell
4
236-247
2009
Mus musculus
Savina, A.; Peres, A.; Cebrian, I.; Carmo, N.; Moita, C.; Hacohen, N.; Moita, L.F.; Amigorena, S.
The small GTPase Rac2 controls phagosomal alkalinization and antigen crosspresentation selectively in CD8+ dendritic cells
Immunity
30
544-555
2009
Mus musculus
Lopez, J.A.; Kwan, E.P.; Xie, L.; He, Y.; James, D.E.; Gaisano, H.Y.
The RalA GTPase is a central regulator of insulin exocytosis from pancreatic islet beta cells
J. Biol. Chem.
283
17939-17945
2008
Mus musculus, Rattus norvegicus
Yoshida, T.; Clark, M.F.; Stern, P.H.
The small GTPase RhoA is crucial for MC3T3-E1 osteoblastic cell survival
J. Cell. Biochem.
106
896-902
2009
Mus musculus
Martin, S.; Parton, R.G.
Characterization of Rab18, a lipid droplet-associated small GTPase
Methods Enzymol.
438
109-129
2008
Mus musculus
Williams, D.A.; Zheng, Y.; Cancelas, J.A.
Rho GTPases and regulation of hematopoietic stem cell localization
Methods Enzymol.
439
365-393
2008
Mus musculus
Haditsch, U.; Leone, D.P.; Farinelli, M.; Chrostek-Grashoff, A.; Brakebusch, C.; Mansuy, I.M.; McConnell, S.K.; Palmer, T.D.
A central role for the small GTPase Rac1 in hippocampal plasticity and spatial learning and memory
Mol. Cell. Neurosci.
41
409-419
2009
Mus musculus
Ji, P.; Jayapal, S.R.; Lodish, H.F.
Enucleation of cultured mouse fetal erythroblasts requires Rac GTPases and mDia2
Nat. Cell Biol.
10
314-321
2008
Mus musculus
Wu, H.; Rossi, G.; Brennwald, P.
The ghost in the machine: small GTPases as spatial regulators of exocytosis
Trends Cell Biol.
18
397-404
2008
Mus musculus
Jeyaraj, S.C.; Unger, N.T.; Chotani, M.A.
Rap1 GTPases: an emerging role in the cardiovasculature
Life Sci.
88
645-652
2011
Homo sapiens, Mus musculus
Huelsenbeck, S.C.; Roggenkamp, D.; May, M.; Huelsenbeck, J.; Brakebusch, C.; Rottner, K.; Ladwein, M.; Just, I.; Fritz, G.; Schmidt, G.; Genth, H.
Expression and cytoprotective activity of the small GTPase RhoB induced by the Escherichia coli cytotoxic necrotizing factor 1
Int. J. Biochem. Cell Biol.
45
1767-1775
2013
Homo sapiens (P62745), Mus musculus (P62746), Mus musculus
Moon, M.Y.; Kim, H.J.; Kim, J.G.; Lee, J.Y.; Kim, J.; Kim, S.C.; Choi, I.G.; Kim, P.H.; Park, J.B.
Small GTPase Rap1 regulates cell migration through regulation of small GTPase RhoA activity in response to transforming growth factor-beta1
J. Cell. Physiol.
228
2119-2126
2013
Mus musculus (Q91VL8), Mus musculus (Q9QUI0), Mus musculus C57BL/6 (Q91VL8), Mus musculus C57BL/6 (Q9QUI0)
Kumar, S.; Xu, J.; Kumar, R.S.; Lakshmikanthan, S.; Kapur, R.; Kofron, M.; Chrzanowska-Wodnicka, M.; Filippi, M.D.
The small GTPase Rap1b negatively regulates neutrophil chemotaxis and transcellular diapedesis by inhibiting Akt activation
J. Exp. Med.
211
1741-1758
2014
Mus musculus (Q99JI6), Mus musculus C57BL/6 (Q99JI6)
Gerasimcik, N.; Dahlberg, C.I.; Baptista, M.A.; Massaad, M.J.; Geha, R.S.; Westerberg, L.S.; Severinson, E.
The Rho GTPase Cdc42 is essential for the activation and function of mature B cells
J. Immunol.
194
4750-4758
2015
Mus musculus, Mus musculus C57BL/6
Rousset, M.; Cens, T.; Menard, C.; Bowerman, M.; Bellis, M.; Bruses, J.; Raoul, C.; Scamps, F.; Charnet, P.
Regulation of neuronal high-voltage activated CaV2 Ca2+ channels by the small GTPase RhoA
Neuropharmacology
97
201-209
2015
Mus musculus (Q9QUI0)
Miura, Y.; Kanaho, Y.
ACAP3, the GTPase-activating protein specific to the small GTPase Arf6, regulates neuronal migration in the developing cerebral cortex
Biochem. Biophys. Res. Commun.
493
1089-1094
2017
Mus musculus (P62331), Mus musculus C57BL/6J (P62331)
Yoo, J.; Brady, S.; Acosta-Alvarez, L.; Rogers, A.; Peng, J.; Sorensen, L.; Wolff, R.; Mleynek, T.; Shin, D.; Rich, C.; Kircher, D.; Bild, A.; Odelberg, S.; Li, D.; Holmen, S.; Grossmann, A.
The small GTPase ARf6 activates PI3K in melanoma to induce a prometastatic state
Cancer Res.
79
2892-2908
2019
Homo sapiens (P62330), Homo sapiens, Mus musculus (P62331)
Carvalho, B.C.; Oliveira, L.C.; Rocha, C.D.; Fernandes, H.B.; Oliveira, I.M.; Leao, F.B.; Valverde, T.M.; Rego, I.M.G.; Ghosh, S.; Silva, A.M.
Both knock-down and overexpression of Rap2a small GTPase in macrophages result in impairment of NF-kappaB activity and inflammatory gene expression
Mol. Immunol.
109
27-37
2019
Mus musculus (Q80ZJ1)
EXTERNAL LINKS (specific for EC-Number 3.6.5.2)
Transporter Classification Database (TCDB): 8.A.92.1.15, 9.A.3.1.1
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