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. 2019 Jul 21;8(7):759. doi: 10.3390/cells8070759

Table 1.

A. Cdc42 and Rac1 variants used in the study. B. Inhibitors used in the study.

A. Cdc42 and Rac1 variants used in the study
Small GTPase Mutant Phenotype
Cdc42 Q61L GTPase defective
G12V GTPase defective
T17N Dominant negative (nucleotide binding-defective)
F28L Fast-cycling (increased GDP/GTP exchange)
D118N Elevated GDP/GTP exchange
R66A RhoGDI binding-defective
T35A Effector loop mutant
F37A Effector loop mutant
Y40C Effector loop mutant
Δins Insert domain mutant
SAAX CAAX box mutant
Rac1 Q61L GTPase defective
T17N Dominant negative (nucleotide binding- defective)
F28L Fast-cycling (increased GDP/GTP exchange)
P29S Fast-cycling (increased GDP/GTP exchange). Cancer mutation
Rac1B Fast-cycling (increased GDP/GTP exchange). Cancer mutation
B. Inhibitors used in the study
Inhibitor Concentration Used Targeted Pathway
GGTI298 10 μM Inhibitor of geranylgeranylation
FFT277 10 μM Inhibitor of farnesylation
2-bromopalmitate (2-BP) 100 μM Inhibitor of palmitoylation
SU6656 2 μM Inhibitor of Src family kinases
LY294002 10 μM Inhibitor of PI3 kinases
Y27632 10 μM Inhibitor of Rho kinase (ROCK)
NSC23766 30 μM Inhibitor of Rac
ML-141 10 μM Inhibitor of Cdc42
SMIFH2 30 μM Inhibitor of formins
CK-666 100 μM Inhibitor of Arp2/3