RAC3 + GppNHp
RAC3 + GppNHp: Human ras-related C3 botulinum toxin substrate 3 (GTPase Rac3) in complex with GppNHp
PDB Code: 2IC5
Cells respond in many ways to environmental changes including altering gene expression, physically moving locations, changes to cell-cell interactions, differentiation and even altering their life spans. This is achieved through a signalling network that consists of several signalling pathways. The network receives multiple signals, interprets the signals, amplified and then transmits the signals. One of the best characterised signalling pathways involves the ras GTPase family. The importance of this family of small GTPases to human health was first recognised through the identification of the human H-Ras, N-Ras and K-Ras genes as being oncogenic.
The structure of this RAC3 crystal form has revealed the inactive-state conformation of the switch 1 loop of the bound GppNHp. Interestingly the main chain remained mostly unaltered when compared to the stucture of RAC3 in complex with GDP. These new structural features improve our understanding of the structural changes that occur as the GTPase changes from the active to inactive state.
Rac1, Rac2 and Rac3 are a subfamily within the Rho family of small GTPases. Rac1 is expressed in most cell tissues, Rac2 is specifically expressed in hematopietic cells whereas Rac3 is localised mostly to the adult brain and expression in the developing nervous system.
Rac3 has been shown to activate the JNK/stress activated kinase pathway. Up-regulation of this pathway and the p21-activated kinase by activated-GTP bound Rac3 occurs in breast cancer cells. Moreover, activated Rac3 is involved in the development of leukemia with the Rac3 knockout mice having a longer average survival rate. Hence, prevention of Rac3 activation by blocking binding of GTP would make Rac3 a potential therapeutic intervention point against certain leukemias and cancers.
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