Author/Authors :
Ming Lei، نويسنده , , Wange Lu، نويسنده , , Wuyi Meng، نويسنده , , Maria-Carla Parrini، نويسنده , , Michael J Eck، نويسنده , , Bruce J Mayer، نويسنده , , Stephen C Harrison، نويسنده ,
Abstract :
The p21-activated kinases (PAKs), stimulated by binding with GTP-liganded forms of Cdc42 or Rac, modulate cytoskeletal actin assembly and activate MAP-kinase pathways. The 2.3 Å resolution crystal structure of a complex between the N-terminal autoregulatory fragment and the C-terminal kinase domain of PAK1 shows that GTPase binding will trigger a series of conformational changes, beginning with disruption of a PAK1 dimer and ending with rearrangement of the kinase active site into a catalytically competent state. An inhibitory switch (IS) domain, which overlaps the GTPase binding region of PAK1, positions a polypeptide segment across the kinase cleft. GTPase binding will refold part of the IS domain and unfold the rest. A related switch has been seen in the Wiskott-Aldrich syndrome protein (WASP).