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By A. Chadwick Cox (auth.), Thomas Briggs Ph.D., Albert M. Chandler Ph.D. (eds.)

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Their characteristics are summarized in Table 3-6. long outer branches McArdle's Disease phosphorylase Muscle I,N Hers'Disease phosphorylase Liver I,N VII phosphofructokinase Muscle I,N VIII phosphorylase kinase Liver I,N Type I II V VI Table 3-6. Glycogen Storage Diseases: Nomenclature and Effects on Glycogen *1 = increased; N = normal levels or structure; A = abnormal structure. For example, the dynamics of two types of glycogen storage diseases that are sometimes encountered are as follows: • von Gierke's Disease: Due to the failure of glycogen breakdown, the liver is greatly enlarged and loaded with glycogen.

This is end-product or feedback inhibition. Allosteric Effector Examples: Enzyme threonine (-) homoserine dehydrogenase methionine (-) homoserine succinylase threonine deaminase aspartate transcarbamoylase phosphofructokinase isoleucine (-) cytidine triphosphate (-) adenosine triphosphate (+) fructose-6-phosphate (+) pyruvate carboxylase acetyl-CoA ( + ) Kinetics (Figure 2-6). Allosteric enzymes do not follow Michaelis-Menten kinetics. A sigmoidal rather than hyperbolic curve is obtained when reaction rate is plotted against substrate concentration.

These kinases then catalyze the phosphorylation of one or more target proteins using A TP as the phosphate donor. In the case of glycogen degradation, the target protein is phosphorylase kinase. Phosphorylation of this protein converts it from an inactive form to an active form. Activated phosphorylase kinase in turn phosphorylates inactive phosphorylase b converting it to phosphorylase a. This is the active form of phosphorylase. The cyclic AMP-dependent protein kinase that activates phosphorylase kinase is also known as phosphorylase kinase kinase.

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