STRUCTURE AND FUNCTION OF PHOSPHOFRUCTOKINASE

磷酸果糖激酶的结构和功能

基本信息

批准号：
3150999
负责人：
KOSAKU UYEDA
金额：
$ 10.22万
依托单位：
UT SOUTHWESTERN MEDICAL CENTER
依托单位国家：
美国
项目类别：
财政年份：
1977
资助国家：
美国
起止时间：
1977-08-01 至 1987-07-31
项目状态：
已结题

项目摘要

The purpose of this project is to investigate the regulatory mechanisms of phosphofructokinase (PFK). Although regulation of this enzyme activity by various metabolites in vitro is well characterized, many in vivo observations are still not understood. We discovered an "activation factor" for PFK which is Beta-D-fructose-2,6-P2, and which appears to be the most important effector of PFK. The synthesis and degradaton of fructose-2,6-P2 and the control of its turnover will be investigated. Using isolated rat hepatocytes the effect of Alpha- and Beta-adrenergic agonists and antagonists on the level of fructose-2,6-P2 will be studied. We found an enzyme termed fructose-6-P,2-kinase which catalyzes the synthesis of fructose-2,6-P2, and this enzyme will be purified and characterized. We will search for an enzyme which is responsible for the degradation of this factor and if successful, this enzyme will be isolated and characterized. We will attempt to elucidate the control mechanisms of these enzymes. We will also determine the distribution of fructose-2,6-P2 in various tissues of rats as well as in diabetic rats. In order to elucidate the mechanism of action of fructose-2,6-P2 on purified muscle and liver PFKs, ligand binding to phospho and dephospho PFKs, conformational changes and its effect on association-dissociation reactions will be studied. In order to determine the physiological significance of the phosphorylation of muscle PFK in vivo, attempts will be made to correlate muscle contraction with phosphorylation using perfused rat muscle. If successful, we will study the biochemical mechanism of the reaction.

该项目的目的是研究磷酸果糖激酶（PFK）。尽管调节这种酶活性体外的各种代谢物的特征都很好，许多体内观察仍然尚不清楚。我们发现了一个“激活 PFK的因子是beta-d-fructose-2,6-p2，并且似乎是 PFK最重要的效应子。的合成和脱脂果糖2,6-P2及其周转率的控制将进行研究。使用孤立的大鼠肝细胞α-和β-肾上腺素能的作用将研究果糖2,6-P2水平的激动剂和拮抗剂。我们发现了一种称为果糖-6-P，2-激酶的酶，该酶催化催化果糖-2,6-P2的合成，该酶将被纯化，并且特征。我们将寻找一种负责的酶该因素的降解和如果成功的话，该酶将被隔离并描述了。我们将尝试阐明这些酶。我们还将确定果糖2,6-P2的分布在大鼠以及糖尿病大鼠的各种组织中。为了阐明果糖2,6-P2对纯化肌肉的作用机理和肝脏PFK，配体与磷酸和去磷PFK的结合，构象变化及其对关联分解反应的影响将是研究。为了确定生理意义体内肌肉PFK的磷酸化，将尝试与使用灌注大鼠肌肉的肌肉收缩与磷酸化。如果成功，我们将研究反应的生化机制。

项目成果

期刊论文数量（29）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

An activation factor of liver phosphofructokinase.

肝脏磷酸果糖激酶的激活因子。

DOI：
10.1073/pnas.77.10.5861
发表时间：
1980
期刊：
Proceedings of the National Academy of Sciences of the United States of America
影响因子：
11.1
作者：
Furuya,E;Uyeda,K
通讯作者：
Uyeda,K

The effect of natural and synthetic D-fructose 2,6-bisphosphate on the regulatory kinetic properties of liver and muscle phosphofructokinases.

DOI：
发表时间：
1981-08
期刊：
The Journal of biological chemistry
影响因子：
0
作者：
K. Uyeda;Eisuke Furuya;Lynne J. Luby
通讯作者：
K. Uyeda;Eisuke Furuya;Lynne J. Luby

An enzyme that catalyzes hydrolysis of fructose-2, 6-bisphosphate.

一种催化果糖-2, 6-二磷酸水解的酶。

DOI：
10.1016/s0006-291x(82)80040-5
发表时间：
1982
期刊：
Biochemical and biophysical research communications
影响因子：
3.1
作者：
Furuya,E;Yokoyama,M;Uyeda,K
通讯作者：
Uyeda,K

A novel enzyme catalyzes the synthesis of activation factor from ATP and D-fructose-6-P.

一种新型酶催化 ATP 和 D-果糖-6-P 合成活化因子。

DOI：
发表时间：
1981
期刊：
The Journal of biological chemistry
影响因子：
0
作者：
Furuya,E;Uyeda,K
通讯作者：
Uyeda,K

Regulation of fructose-6-phosphate 2-kinase by phosphorylation and dephosphorylation: possible mechanism for coordinated control of glycolysis and glycogenolysis.

通过磷酸化和去磷酸化调节果糖6-磷酸2-激酶：糖酵解和糖原分解协调控制的可能机制。

DOI：
10.1073/pnas.79.2.325
发表时间：
1982
期刊：
Proceedings of the National Academy of Sciences of the United States of America
影响因子：
11.1
作者：
Furuya,E;Yokoyama,M;Uyeda,K
通讯作者：
Uyeda,K