Glycogen Metabolism

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Glycogen Metabolism
Chapter 18
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Figure 18-1a Structure of glycogen. (a) Molecular
formula. (b) Schematic diagram illustrating its
branched structure.
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Figure 18-2a X-Ray structure of rabbit muscle
glycogen phosphorylase. (a) Ribbon diagram of a
phosphorylase b subunit.
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Figure 18-2b X-Ray structure of rabbit muscle
glycogen phosphorylase. (b) A ribbon diagram of
the glycogen phosphorylase a dimer.
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Figure 18-2c X-Ray structure of rabbit muscle
glycogen phosphorylase. (c) An interpretive
low-resolution drawing of Part b showing the
enzymes various ligand-binding sites.
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Figure 18-3The reaction mechanism of glycogen
phosphorylase.
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Figure 18-4 The mechanism of action of
phosphoglucomutase.
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Figure 18-5 Reactions catalyzed by debranching
enzyme.
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Figure 18-6 Reaction catalyzed by UDPglucose
pyrophos-phorylase.
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Figure 18-7 Reaction catalyzed by glycogen
synthase.
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Figure 18-8 The branching of glycogen.
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Figure 18-9 The control of glycogen phosphorylase
activity.
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Figure 18-10a Conformational changes in glycogen
phosphorylase. (a) Ribbon diagram of one subunit
(T-state) in absence of allosteric effectors.
a.
(b) Ribbon diagram of one subunit (R-state) with
bound AMP.
b.
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Figure 18-10b Conformational changes in glycogen
phosphorylase. (b) The portion of the glycogen
phosphorylase a dimer in the vicinity of the
dimer interface.
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Figure 18-11a A monocyclic enzyme cascade. (a)
General scheme, where F and R are, respectively,
the modifying and demodifying enzymes.
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Figure 18-11b A monocyclic enzyme cascade.(b)
Chemical equations for the interconversion of the
target enzymes unmodified and modified forms Eb
and Ea.
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Figure 18-12 A bicyclic enzyme cascade.
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Figure 18-13 Schematic diagram of the major
enzymatic modification/demodification systems
involved in the control of glycogen metabolism in
muscle.
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Figure 18-14 X-ray structure of the catalytic
(C) subunit of mouse protein kinase A (PKA).
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Figure 18-15 X-ray structure of the regulatory
(R) subunit of bovine protein kinase A (PKA).
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Figure 18-16 X-Ray structure of rat testis
calmodulin.
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Figure 18-17 EF hand.
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Figure 18-18a. NMR structure of (Ca2)4CaM from
Drosophila melanogaster in complex with its
26-residue target polypeptide from rabbit
skeletal muscle myosin light chain kinase (MLCK).
(a) A view of the complex in which the N-terminus
of the target polypeptide is on the right.
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Figure 18-18b. NMR structure of (Ca2)4CaM from
Drosophila melanogaster in complex with its
26-residue target polypeptide from rabbit
skeletal muscle myosin light chain kinase (MLCK).
(b) The perpendicular view as seen from the right
side of Part a.
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Figure 18-19 Schematic diagram of the
Ca2CaM-dependent activation of protein kinases.
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Figure 18-21 The antagonistic effects of insulin
and epinephrine on glycogen metabolism in muscle.
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Figure 18-22 The enzymatic activities of
phosphorylase a and glycogen synthase in mouse
liver in response to an infusion of glucose.
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Figure 18-23 Comparison of the relative enzymatic
activities of hexokinase and glucokinase over the
physiological blood glucose range.
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Figure 18-24 Formation and degradation of
?-D-fructose-2,6-bisphosphate as catalyzed by
PFK-2 and FBPase-2.
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Figure 18-25 X-ray structure of the H256A mutant
of rat testis PFK-2/FBPase-2.
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Figure 18-26a The livers response to stress.
(a) Stimulation of a-adrenoreceptors by
epinephrine activates phospholipase C to
hydrolyze PIP2 to IP3 and DAG.
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Figure 18-26b The livers response to stress. (b)
The participation of two second messenger systems.
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Figure 18-27 The ADP concentration in human
forearm muscles during rest and following
exertion in normal individuals and those with
McArdles disease.
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Table 18-1 Hereditary Glycogen Storage Diseases.
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