Literature DB >> 3511972

Studies on the specific activity of [gamma-32P]ATP in adipose and other tissue preparations incubated with medium containing [32P]phosphate.

T J Hopkirk, R M Denton.   

Abstract

The specific activity of the gamma-32P position of ATP was measured in various tissue preparations by two methods. One employed HPLC and the enzymatic conversion of ATP to glucose 6-phosphate and ADP. The other was based on the phosphorylation of histone by catalytic subunit of cAMP-dependent protein kinase (Hawkins, P.T., Michell, R.H. and Kirk, C.J. (1983) Biochem. J. 210, 717-720). The HPLC method also allowed the incorporation of 32P into the (alpha + beta)-positions of ATP to be determined. In rat epididymal fat-pad pieces and fat-cell preparations the specific activity of [gamma-32P]ATP attained a steady-state value after 1-2 h incubation in medium containing 0.2 mM [32P]phosphate. Addition of insulin or the beta-agonist isoprenaline increased this value by 5-10% within 15 min. Under these conditions the steady-state specific activity of [gamma-32P]ATP was 30-40% of the initial specific activity of the medium [32P]phosphate. However, if allowance was made for the change in medium phosphate specific activity during incubations the equilibration of the gamma-phosphate position of ATP with medium phosphate was greater than 80% in both preparations. The change in medium phosphate specific activity was a combination of the expected equilibration of [32P]phosphate with exchangeable intracellular phosphate pools plus the net release of substantial amounts of tissue phosphate. At external phosphate concentrations of less than 0.6 mM the loss of tissue phosphate to the medium was the major factor in the change in medium phosphate specific activity. It is concluded that little advantage is gained in employing external phosphate concentrations of less than 0.6 mM in experiments concerned with the incorporation of phosphate into proteins and other intracellular constituents. Indeed, a low external phosphate concentration may cause depletion of important intracellular phosphorus-containing components.

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Year:  1986        PMID: 3511972     DOI: 10.1016/0167-4889(86)90089-3

Source DB:  PubMed          Journal:  Biochim Biophys Acta        ISSN: 0006-3002


  6 in total

1.  Comparison of the effects of insulin and adrenergic agonists on the phosphorylation of an acid-soluble 22 kDa protein in rat epididymal fat-pads and isolated fat-cells.

Authors:  T A Diggle; R M Denton
Journal:  Biochem J       Date:  1992-03-15       Impact factor: 3.857

2.  Activation and phosphorylation of the 'dense-vesicle' high-affinity cyclic AMP phosphodiesterase by cyclic AMP-dependent protein kinase.

Authors:  E Kilgour; N G Anderson; M D Houslay
Journal:  Biochem J       Date:  1989-05-15       Impact factor: 3.857

3.  Insulin stimulates the tyrosyl phosphorylation and activation of the 52 kDa peripheral plasma-membrane cyclic AMP phosphodiesterase in intact hepatocytes.

Authors:  N J Pyne; W Cushley; H G Nimmo; M D Houslay
Journal:  Biochem J       Date:  1989-08-01       Impact factor: 3.857

4.  The binding of Ca2+ ions to pig heart NAD+-isocitrate dehydrogenase and the 2-oxoglutarate dehydrogenase complex.

Authors:  G A Rutter; R M Denton
Journal:  Biochem J       Date:  1989-10-15       Impact factor: 3.857

5.  Analysis of insulin receptor phosphorylation sites in intact rat liver cells by two-dimensional phosphopeptide mapping. Predominance of the tris-phosphorylated form of the kinase domain after stimulation by insulin.

Authors:  T Issad; J M Tavaré; R M Denton
Journal:  Biochem J       Date:  1991-04-01       Impact factor: 3.857

6.  Phosphorylation state of the GLUT4 isoform of the glucose transporter in subfractions of the rat adipose cell: effects of insulin, adenosine, and isoproterenol.

Authors:  H Nishimura; J Saltis; A D Habberfield; N B Garty; A S Greenberg; S W Cushman; C Londos; I A Simpson
Journal:  Proc Natl Acad Sci U S A       Date:  1991-12-15       Impact factor: 11.205

  6 in total

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