2F9Z
Complex between the chemotaxis deamidase CheD and the chemotaxis phosphatase CheC from Thermotoga maritima
2F9Z の概要
エントリーDOI | 10.2210/pdb2f9z/pdb |
分子名称 | chemotaxis protein CheC, PROTEIN (chemotaxis methylation protein) (3 entities in total) |
機能のキーワード | bacterial chemotaxis, signal transduction, receptor deamidase, aspartyl phosphatase, protein complex, reciprocal regulation, signaling protein |
由来する生物種 | Thermotoga maritima 詳細 |
タンパク質・核酸の鎖数 | 4 |
化学式量合計 | 78922.53 |
構造登録者 | |
主引用文献 | Chao, X.,Muff, T.J.,Park, S.Y.,Zhang, S.,Pollard, A.M.,Ordal, G.W.,Bilwes, A.M.,Crane, B.R. A receptor-modifying deamidase in complex with a signaling phosphatase reveals reciprocal regulation. Cell(Cambridge,Mass.), 124:561-571, 2006 Cited by PubMed Abstract: Signal transduction underlying bacterial chemotaxis involves excitatory phosphorylation and feedback control through deamidation and methylation of sensory receptors. The structure of a complex between the signal-terminating phosphatase, CheC, and the receptor-modifying deamidase, CheD, reveals how CheC mimics receptor substrates to inhibit CheD and how CheD stimulates CheC phosphatase activity. CheD resembles other cysteine deamidases from bacterial pathogens that inactivate host Rho-GTPases. CheD not only deamidates receptor glutamine residues contained within a conserved structural motif but also hydrolyzes glutamyl-methyl-esters at select regulatory positions. Substituting Gln into the receptor motif of CheC turns the inhibitor into a CheD substrate. Phospho-CheY, the intracellular signal and CheC target, stabilizes the CheC:CheD complex and reduces availability of CheD. A point mutation that dissociates CheC from CheD impairs chemotaxis in vivo. Thus, CheC incorporates an element of an upstream receptor to influence both its own effect on receptor output and that of its binding partner, CheD. PubMed: 16469702DOI: 10.1016/j.cell.2005.11.046 主引用文献が同じPDBエントリー |
実験手法 | X-RAY DIFFRACTION (2.4 Å) |
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