Rider M H, Crepin K M, De Cloedt M, Bertrand L, Hue L
Hormone and Metabolic Research Unit, International Institute of Cellular and Molecular Pathology, Brussels, Belgium.
Biochem J. 1994 May 15;300 ( Pt 1)(Pt 1):111-5. doi: 10.1042/bj3000111.
Asp-130 of the recombinant skeletal-muscle 6-phosphofructo-2-kinase (PFK-2)/fructose-2,6-bisphosphatase was mutated into Ala in order to study its role in catalysis and/or substrate binding. The D130A mutant displayed a 30- to 140-fold decreased 2-kinase Vmax, depending on the pH, and a 30- and 60-fold increase in Km for MgATP and Fru-6-P respectively at pH 8.5 compared with the wild-type. Mutagenesis of Asp-130 to Ala had no effect on the 2-phosphatase activity, and fluorescence measurements indicated that the changes in kinetic properties of PFK-2 in the D130A mutant were not due to instability. The role of Asp-130 in the 2-kinase reaction is discussed and compared with that of Asp-103 of 6-phosphofructo-1-kinase from Escherichia coli, which binds Mg2+.
为了研究重组骨骼肌6-磷酸果糖-2-激酶(PFK-2)/果糖-2,6-二磷酸酶中Asp-130在催化和/或底物结合中的作用,将其突变为丙氨酸。D130A突变体的2-激酶Vmax降低了30至140倍,具体取决于pH值,与野生型相比,在pH 8.5时,其对MgATP和Fru-6-P的Km分别增加了30倍和60倍。将Asp-130突变为丙氨酸对2-磷酸酶活性没有影响,荧光测量表明D130A突变体中PFK-2动力学性质的变化并非由于不稳定性。本文讨论了Asp-