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3.6.5.2: small monomeric GTPase

This is an abbreviated version!
For detailed information about small monomeric GTPase, go to the full flat file.

Word Map on EC 3.6.5.2

Reaction

GTP
+
H2O
=
GDP
 +
phosphate

Synonyms

ADP-ribosylation factor 6, ADP-ribosylation factor-like protein 2, Alp41, Alp41/Arl2, ARD1, Arf 1, Arf 1-6, Arf-like 3 small GTPase, Arf6, ARL2, Arl6, Arl6/BBS3, Arl9, AtRopGEF12, Cdc42, Cdc42Hs, Der, Der GTPase, double Era-like protein, EC 3.6.1.47, EF-Tu, EhRab11B, elF-2, EmRas, FgCdc42, FgRac1, FgRHO1, FgRHO2, FgRHO3, FgRHO4, GCC185, Gem, GhRac1 GTPase, Gsp1p, GTP-phosphohydrolase, GTPase, GTPase Alp41/Arl2, GTPase TcRho1, GTPase Toc33, GTPase Toc33/34, guanine triphosphatase, guanosine 5'-triphosphatase, guanosine triphosphatase, H-Ras, K-Ras, Kir, Krev-1, M-Ras, monomeric G protein, monomeric GTPase, More, non-canonical Ras-like G protein, OsRac1, p21 ras, Pc-Rac1, PfG, PRA, Pra2, Pra3, Rab GTPase, Rab GTPase protein 5, Rab11, Rab13, Rab15, Rab18, Rab1a, Rab1B, Rab21, Rab23, Rab27a, Rab27a GTPase, Rab27B, Rab2A, Rab2B, Rab30, Rab33A, Rab35, Rab36, Rab37, Rab38, Rab3A, Rab4a, Rab6A, Rab6B, Rab8, Rab8A, Rab9A, Rab9B, RabE, RabE1d, Rac, Rac GTPase, Rac-like GTP-binding protein 1, Rac1, Rac1 GTPase, Rac2, Rac3, Rac4, Rad, Rad GTPase, Ral GTPase, RalA, RalB, Ran, RAP, Rap GTPase, Rap1, Rap1 small GTPase, Rap1A, Rap1b, Rap2, Rap2 small GTPase, Rap2a, Rap2C, RAS, Ras GTPase, Ras homolog enriched in brain-like protein 1, Ras proximity 1, Ras related GTPase Rap, Ras-associated protein 1, Ras-like G-protein, Ras-like GTpase, Ras-related C3 botulinum toxin substrate 1, Ras-related protein rab-5, putative, Ras-related small GTPase, RAS1, RAS2, RasL10B, Rasl11a, Rem2, Rhb1, Rheb, Rheb GTPase, RHEBL1, Rho, Rho family small GTPase, Rho GTPase, RHO-1, Rho-GTPase, Rho-type GTPase, Rho-type small GTPase, Rho1, Rho1p, Rho3, Rho3p, RhoA, rhoA p21, RhoB, rhoB p20, RhoC, RhoGTPase, RhoH, ribosomal GTPase, ribosome-small-subunit-dependent GTPase A, RsgA, Ryh1, Ryh1 GTPase, Sar1, SdArf1, SdArf1-like, SdArf10, SdArf5, SdArf6, SdArl1, SdCdc42, SdK-Ras2, SdRab-like1, SdRab-like2, SdRab-like3, SdRab-like4, SdRab-like5, SdRab-like6, SdRab1-like, SdRab10, SdRab11, SdRab14, SdRab18, SdRab2, SdRab20-like, SdRab21, SdRab21-like, SdRab24, SdRab28, SdRab3, SdRab32, SdRab35, SdRab39, SdRab4, SdRab41/43, SdRab5, SdRab8, SdRac, SdRalA, SdRan, SdRap1, SdRap1-like, SdRheb, SdRho1, SdRho2, SdRho3, small G protein, small GTPase, small GTPase ARF6, small GTPase LIP1, small GTPase protein Rac-1, small GTPase Rab1, small GTPase Rab11b, small GTPase Rab2, small GTPase Rab21, small GTPase Rab27b, small GTPase Rac, small GTPase Rac-1, small GTPase Ral, small GTPase Ras, small GTPase Ras-related protein in brain 13, small GTPase Rho, small GTPase RhoA, small GTPase RhoV, small GTPase Rnd1, small GTPases Rab5, small GTPases Ral5, small nuclear GTPase Ran, small Rho GTPase, small Rho GTPase Rac1, small, monomeric G protein, small-GTPase, SmGTP, TbArl6, TcRABL4, vacuolar Rab GTPase, Wrch-1, YjeQ, Ypt1, Ypt1p, Ypt7, Ypt7p, YsxC

ECTree

     3 Hydrolases
         3.6 Acting on acid anhydrides
             3.6.5 Acting on GTP to facilitate cellular and subcellular movement
                3.6.5.2 small monomeric GTPase

Engineering

Engineering on EC 3.6.5.2 - small monomeric GTPase

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PROTEIN VARIANTS
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
Q74L
-
the mutant is preferentially GTP bound and therefore in an active state
S29N
-
the mutant is preferentially GDP bound and therefore in an inactive state
F37A
-
Cdc42Hs, fails to stimulate phospholipase C beta2 protein
Y40C
-
Cdc42Hs, fails to stimulate phospholipase C beta2 protein
G14V
-
constitutively active or gain of function
T19N
-
dominant negative mutation, phenotype
C192S
FgCDC42 cDNA is amplified from cDNA of PH-1 with a site mutation C192S to ensure that FgCdc42 protein cannot be prenylated and is soluble
C196S
FgRAC1 cDNA is amplified from cDNA of PH-1 with a site mutation C196S to ensure that FgRac1 protein cannot be prenylated and is soluble
G15V/D121A
constitutively active (G15V) and dominant negative mutations (D121A) are generated in the BD-FgCdc42 background
G17V/D123A
constitutively active (G17V) and dominant negative mutations (D123A) are generated in the BD-FgRac1 background
C192S
-
FgCDC42 cDNA is amplified from cDNA of PH-1 with a site mutation C192S to ensure that FgCdc42 protein cannot be prenylated and is soluble
-
C196S
-
FgRAC1 cDNA is amplified from cDNA of PH-1 with a site mutation C196S to ensure that FgRac1 protein cannot be prenylated and is soluble
-
G15V/D121A
-
constitutively active (G15V) and dominant negative mutations (D121A) are generated in the BD-FgCdc42 background
-
G17V/D123A
-
constitutively active (G17V) and dominant negative mutations (D123A) are generated in the BD-FgRac1 background
-
A152P
-
mutation dramatically affects both GTP and GDP nucleotide-binding activity of Rab27a, probably by disrupting protein folding
chimeras between RhoA/Cdc42
-
residues 85-122 contain specific binding determinants for guanosine nucleotide activating protein, p190
D60I
site-directed mutagenesis
D60K
site-directed mutagenesis
D90A
-
RhoA, significant decrease in p190-mediated stimulation of GTPase activity
F50A
site-directed mutagenesis, the mutation disrupts the interaction with TBCD, increased expression levels compared to wild-type
F50A/Q70L
site-directed mutagenesis, cells expressing mutant L3A/F50A show a reversal of the microtubule loss phenotype, with about 20% of transfected cells showing only intermediate loss in microtubule densities
G169A
-
the mutation causes the Bardet-Biedl syndrome, the mutant protein is destabilized probably due to the weak affinity to guanine nucleotides
H79G
-
a GTPase-defective Sar1 mutant. Overexpression of the GTPase-defective mutant Sar1 H79G, in its GTP-bound form, allows the development of ERES, but the transport to the Golgi apparatus is blocked because this mutant inhibits COPII coat dissociation, and its expression induces Golgi fragmentation as indicated by Rab6 dispersion and inhibits autophagosome formation
I6R
site-directed mutagenesis, the mutation disrupts the interaction with TBCD
I6R/Q70L
site-directed mutagenesis, the addition of the I6R mutation to Q70L does not reverse the effects of the dominant mutant on microtubule densities
L130P
-
mutation dramatically affects both GTP and GDP nucleotide-binding activity of Rab27a, probably by disrupting protein folding
L170W
-
the mutation causes the Bardet-Biedl syndrome, the mutant protein is destabilized probably due to the weak affinity to guanine nucleotides
L3A
site-directed mutagenesis, the mutation disrupts the interaction with TBCD
L3A/Q70L
site-directed mutagenesis, cells expressing mutant L3A/Q70L show a reversal of the microtubule loss phenotype, with about 10% of transfected cells showing only intermediate loss in microtubule densities
N-terminal truncation
-
Kir/Gem peptide, C-terminal calmodulin-binding domain, high affinity for dansyl-calmodulin
N121I
-
a dominant-negative GFP-tagged Rab1b mutant, inhibits autophagosome formation
Q67L
-
a GTPase-deficient Rab1b mutant, the distribution of Rab1b in the acidic compartments responds to inhibition of autophagy
Q70L
site-directed mutagenesis, ARL2 dominant activating mutation. Expression of ARL2 Q70L mutant causes the loss of polymerized microtubules in cultured cells
Q72L
-
the mutant decreases the GTP hydrolysis activity and stabilizes the active form of the protein
Q89L
site-directed mutagenesis, a GTP-bound active mutant
S88D
-
Cdc42, enhancement of GTP-hydrolysis
T30N
site-directed mutagenesis, ARL2 dominant inactivating mutation, shows decreased expression levels compared to wild-type
T31M
-
the mutation causes the Bardet-Biedl syndrome, the mutant protein is destabilized probably due to the weak affinity to guanine nucleotides
T31N
-
the guanine nucleotide-free Arl6 mutant protein is unstable and degraded in living cells
T31R
-
the mutation selectively abrogates the GTP-binding ability of Arl6 without affecting GDP-binding/dissociating properties
T33N
mutant enzyme is defective in GTP binding, cells expressing mutant Rab21 show defects in endocytosis of transferrin and epidermal growth factor and fail to effectively deliver the latter ligand to late endosomes and lysosomes for degradation, subcellular distribution
T35A
-
Rap1A, blocks abilitiy of Rap-GAP to stimulate GTP hydrolysis
T39N
-
a dominant-negative Sar1 mutant, expression induces Golgi fragmentation as indicated by Rab6 dispersion and inhibits autophagosome formation
T43N
site-directed mutagenesis, a GDP-bound inactive mutant
W269G
-
Kir/Gem peptide, abolish affinity for dansyl-calmodulin
W73G
-
mutant protein has GTP-binding activity but is inefficient in hydrolyzing GTP, in contrast to Q78L it neither interacts with the Rab27a effector melanophilin nor modifies melanosome distribution and cytotoxic granule exocytosis, mutation may increase switch flexibility and thus impair the dynamics of the conformational changes associated with each nucleotide binding
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
-
inactive
E78L/C123S/C188S
-
the mutant may modulate effector recognition by forming an intramolecular disulfide bridge
G12V
-
constitutively active Rac mutant
G23V
-
RalA mutant with higher affinity for GTP
N122I
-
mutant with nucleotide deficiency
S22N
-
mutant with constitutive GDP binding deficiency
T17N
-
dominant negative Rac mutant
C32S/Q68L
design OsRac1 mutants that display reduced binding to the NADPH oxidase OsRbohB. Tyr39 and Asp45 substitutions suppress ROS production in rice cells, these residues are critical for interaction with and activation of NADPH oxidase OsRbohB
G19V
the constitutively activated mutant of OsRac1 increases resistance to rice bacterial blight disease and subsequent cell death
G19V/D38A
site-directed mutagenesis, the Switch I mutant shows unaltered binding with OsRbohB(138-313) compared to the wild-type enzyme
G19V/D45A
site-directed mutagenesis, the Switch I mutant shows markedly attenuated binding with OsRbohB(138-313) compared to the wild-type enzyme
G19V/F35A
site-directed mutagenesis, the Switch I mutant shows markedly attenuated binding with OsRbohB(138-313) compared to the wild-type enzyme
G19V/F44A
site-directed mutagenesis, the Switch I mutant shows moderately reduced binding with OsRbohB(138-313) compared to the wild-type enzyme
G19V/I40A
site-directed mutagenesis, the Switch I mutant shows slightly attenuated binding with OsRbohB(138-313) compared to the wild-type enzyme
G19V/P36A
site-directed mutagenesis, the Switch I mutant shows almost unaltered binding with OsRbohB(138-313) compared to the wild-type enzyme
G19V/P41A
site-directed mutagenesis, the Switch I mutant shows slightly attenuated binding with OsRbohB(138-313) compared to the wild-type enzyme
G19V/T37A
site-directed mutagenesis, the Switch I mutant shows slightly attenuated binding with OsRbohB(138-313) compared to the wild-type enzyme
G19V/T42A
site-directed mutagenesis, the Switch I mutant shows markedly attenuated binding with OsRbohB(138-313) compared to the wild-type enzyme
G19V/V43A
site-directed mutagenesis, the Switch I mutant shows moderately reduced binding with OsRbohB(138-313) compared to the wild-type enzyme
G19V/Y39A
site-directed mutagenesis, the Switch I mutant shows markedly attenuated binding with OsRbohB(138-313) compared to the wild-type enzyme
T24N
a dominant-negative mutant of OsRac1 that decrease the resistance reaction to rice bacterial blight disease and subsequent cell death
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
G23V
-
RalA mutant with higher affinity for GTP
D124N
-
Ypt1, changed nucleotide specificity from guanine to xanthine, complete inhibition of guanosine nucleotide exchange factor-mediated nucleotide exchange
G80D
-
the Ypt1pG80D mutant protein has normal GTPase function and the ypt1-G80D mutant strain displays normal growth and nearly normal endoplasmic reticulum-to-Golgi vesicle trafficking at typical growth temperature (30°C), but experiences growth retardation at an elevated temperature (37°C). Ypt1pG80D does not undergo a heat-shock-induced structural change in vivo. Ypt1pG80D loses molecular chaperone activity. Sodium 4-phenylbutyric acid (PBA), a chemical chaperone, increases the thermotolerance of mutant ypt1-G80D cells, although it is not restored to the level seen for the wild-type YPT1 strain
R142G K143M K144I
-
triple mutation prevents interaction with Nsp1p nucleoporin
additional information