Ikura M, Kay L E, Krinks M, Bax A
Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892.
Biochemistry. 1991 Jun 4;30(22):5498-504. doi: 10.1021/bi00236a024.
Heteronuclear 3D and 4D NMR experiments have been used to obtain 1H, 13C, and 15N backbone chemical shift assignments in Ca(2+)-loaded calmodulin complexed with a 26-residue synthetic peptide (M13) corresponding to the calmodulin-binding domain (residues 577-602) of rabbit skeletal muscle myosin light-chain kinase. Comparison of the chemical shift values with those observed in peptide-free calmodulin [Ikura, M., Kay, L. E., & Bax, A. (1990) Biochemistry 29, 4659-4667] shows that binding of M13 peptide induces substantial chemical shift changes that are not localized in one particular region of the protein. The largest changes are found in the first helix of the Ca(2+)-binding site I (E11-E14), the N-terminal portion of the central helix (M72-D78), and the second helix of the Ca(2+)-binding site IV (F141-M145). Analysis of backbone NOE connectivities indicates a change from alpha-helical to an extended conformation for residues 75-77 upon complexation with M13. This conformational change is supported by upfield changes in the C alpha and carbonyl chemical shifts of these residues relative to M13-free calmodulin and by hydrogen-exchange experiments that indicate that the amide protons of residues 75-82 are in fast exchange (kexch greater than 10 s-1 at pH 7, 35 degrees C) with the solvent. No changes in secondary structure are observed for the first helix of site I or the C-terminal helix of site IV. Upon complexation with M13, a significant decrease in the amide exchange rate is observed for residues T110, L112, G113, and E114 at the end of the second helix of site III.
异核三维和四维核磁共振实验已用于确定与一个26个残基的合成肽(M13)复合的钙离子负载钙调蛋白中1H、13C和15N主链化学位移归属,该合成肽对应于兔骨骼肌肌球蛋白轻链激酶的钙调蛋白结合结构域(残基577 - 602)。将化学位移值与在无肽钙调蛋白中观察到的值进行比较[池仓,M.,凯,L. E.,& 巴克斯,A.(1990)生物化学29,4659 - 4667]表明,M13肽的结合诱导了大量化学位移变化,这些变化并不局限于蛋白质的一个特定区域。最大的变化出现在钙离子结合位点I的第一个螺旋(E11 - E14)、中央螺旋的N端部分(M72 - D78)以及钙离子结合位点IV的第二个螺旋(F141 - M145)。主链核Overhauser效应(NOE)连接性分析表明,与M13复合时,残基75 - 77从α螺旋构象转变为伸展构象。相对于无M13的钙调蛋白,这些残基的Cα和羰基化学位移的高场变化以及氢交换实验支持了这种构象变化,氢交换实验表明残基75 - 82的酰胺质子与溶剂快速交换(在pH 7、35℃时交换速率常数kexch大于10 s-1)。位点I的第一个螺旋或位点IV的C端螺旋未观察到二级结构变化。与M13复合时,位点III第二个螺旋末端的残基T110、L112、G113和E114的酰胺交换速率显著降低。