Summary for 7AJK
Entry DOI | 10.2210/pdb7ajk/pdb |
Descriptor | Ras-related C3 botulinum toxin substrate 1, CYFIP-related Rac1 interactor B, MAGNESIUM ION, ... (5 entities in total) |
Functional Keywords | actin, cytoskeleton, rac1, gtpase, inhibitor, cytosolic protein |
Biological source | Homo sapiens (Human) More |
Total number of polymer chains | 2 |
Total formula weight | 57232.29 |
Authors | Yelland, T.,Anh, L.,Insall, R.,Machesky, L.,Ismail, S. (deposition date: 2020-09-29, release date: 2020-11-18, Last modification date: 2024-01-31) |
Primary citation | Yelland, T.,Le, A.H.,Nikolaou, S.,Insall, R.,Machesky, L.,Ismail, S. Structural Basis of CYRI-B Direct Competition with Scar/WAVE Complex for Rac1. Structure, 29:226-237.e4, 2021 Cited by PubMed Abstract: Rac1 is a major regulator of actin dynamics, with GTP-bound Rac1 promoting actin assembly via the Scar/WAVE complex. CYRI competes with Scar/WAVE for interaction with Rac1 in a feedback loop regulating actin dynamics. Here, we reveal the nature of the CYRI-Rac1 interaction, through crystal structures of CYRI-B lacking the N-terminal helix (CYRI-BΔN) and the CYRI-BΔN:Rac1Q61L complex, providing the molecular basis for CYRI-B regulation of the Scar/WAVE complex. We reveal CYRI-B as having two subdomains - an N-terminal Rac1 binding subdomain with a unique Rac1-effector interface and a C-terminal Ratchet subdomain that undergoes conformational changes induced by Rac1 binding. Finally, we show that the CYRI protein family, CYRI-A and CYRI-B can produce an autoinhibited hetero- or homodimers, adding an additional layer of regulation to Rac1 signaling. PubMed: 33217330DOI: 10.1016/j.str.2020.11.003 PDB entries with the same primary citation |
Experimental method | X-RAY DIFFRACTION (3.1 Å) |
Structure validation
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