Laminet A A, Kumamoto C A, Plückthun A
Genzentrum der Universität München, Max-Planck-Institut für Biochemie, D-8033 Martinsried, Germany.Departments of Physiology, and Molecular Biology and Microbiology. Tufts University School of Medicine, 136 Harrison Avenue, Boston. Massachusetts 02111. USA.
Mol Microbiol. 1991 Jan;5(1):117-122. doi: 10.1111/j.1365-2958.1991.tb01832.x.
The rate of folding of the precursor of β-lactamase is not influenced by the presence of SecB under conditions in which GroEL/ES retards the folding. Wild-type β-lactamase and several mutants in the signal or the mature protein, affecting either transport or enzyme kinetics and probably folding, were examined for total expression, total enzymatic activity, and transported β-lactamase (in vivo resistance) in secB and secB strains. We conclude that there is no indication of any relevant interaction between SecB and pre-β-lactamase in vitro, nor did the secB mutation affect the transport of wild-type β-lactamase or any of the mutants in vivo. Thus, putative Escherichia coli'folding modulators'must be of limited specificity.
在GroEL/ES延缓折叠的条件下，β-内酰胺酶前体的折叠速率不受SecB存在的影响。我们检测了野生型β-内酰胺酶以及信号肽或成熟蛋白中的几个突变体（这些突变体影响转运、酶动力学，可能还影响折叠）在secB⁺和secB⁻菌株中的总表达量、总酶活性以及转运的β-内酰胺酶（体内抗性）。我们得出结论，体外没有迹象表明SecB与前β-内酰胺酶之间存在任何相关相互作用，secB突变在体内也不影响野生型β-内酰胺酶或任何突变体的转运。因此，假定的大肠杆菌“折叠调节剂”的特异性一定有限。
