ATP-dependent protein

In the initial experiments, we resolved reticulocyte lysates on DEAE-cellulose into two crude fractions Fraction 1, which contained proteins not adsorbed to the resin, and Fraction 2, which contained all proteins adsorbed to the resin and eluted with high salt. The original aim of this fractionation was to get rid of hemoglobin, which was known to be in Fraction 1, while most non-hemoglobin proteins of reticulocytes were known to be in Fraction 2. We found that neither fraction was active by itself, but ATP-dependent protein degradation could be reconstituted by combination of the two fractions [13]. The active component in Fraction 1 was a small, heat-stable protein we have exploited its stability to heat treatment for its purification to near homogeneity. We termed this protein at that time APF-1, for ATP-dependent Proteolysis Factor 1 [13]. The identity of APF-1 with ubiquitin was established later by Wilkinson et al. [14], subsequent to the discovery in my laboratory of its covalent ligation to protein substrates, as described below. 

Zachowski, A., Henry, J.P. and Devaux, P.F., 1989, Control of transmembrane hpid asymmetry in chromaffin granules by an ATP-dependent protein. Nature, 340 75-76... 

Members of the protein kinase C family promote signal transduction by catalyzing ATP-dependent protein phosphorylation [general EC number 2.7.1.37] in response to various signals that promote lipid hydrolysis. The primary activator is diacylglycerol. See also Cal-cium/Calmodulin-Dependent Protein Kinase... 

In another rare inherited disorder, called Wilson s disease, excessive amounts of copper accumulate in liver and brain tissue. A prominent symptom of the disease is the deposition of copper in greenish-brown layers surrounding the cornea, called Kayser-Fleischer rings. Wilson s disease is now known to be caused by a defective ATP-dependent protein that transports copper across cell membranes. Apparently, the copper transport protein is required to incorporate copper into ceruloplasmin and to excrete excess copper. In addition to a low copper diet, Wilson s disease is treated with zinc sulfate and the chelating agent penicillamine (p. 123). Describe how these treatments work. (Hint Metallothionein has a greater affinity for copper than for zinc.)... 

Armstrong et al. (1995) [4] showed that ABA induced anion efflux is independent of ABIl in tobacco. However, phosphorylation and dephosphorylation events are involved in control of anion efflux. Kinase antagonists or removal of ATP inhibits ABA induced slow anion channels in V faba guard cells suggesting that an ATP-dependent protein kinase is necessary for anion efflux. Down-regulation by removal of ATP can be reversed by the phosphatase inhibitor okadaic acid. Thus, the induction of slow anion channels by ABA is mediated by an ATP-dependent protein kinase and inhibited by a phosphatase. The phosphatase is distinct from ABIl which is not inhibited by okadaic acid [7], Furthermore,... 

LHCII and several PSII thylakoid proteins are phosphorylated by an ATP dependent protein kinase (1,2), which is under control of the redox state of the PQ pool (3). This protein phosphorylation leads to rearrangements in the lateral organization of the thylakoid membrane... 

---