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Home > Documents > Average = 70.0 = B- Approximate Grades: A = 86+B= 73-78C = 60-64 A- = 83-85B- = 67-72C- = 55-59 B+ =...

Average = 70.0 = B- Approximate Grades: A = 86+B= 73-78C = 60-64 A- = 83-85B- = 67-72C- = 55-59 B+ =...

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Chem /B iol472 W 10 E1 0 0.5 1 1.5 2 2.5 3 3.5 0 10 20 30 40 50 61 71 81 91 10 score Frequency Frequency Average = 70.0 = B- Approximate Grades: A = 86+ B= 73-78 C = 60- 64 A- = 83-85 B- = 67-72 C- = 55-59 B+ = 79-82 C+ = 64-67
Transcript

Chem/Biol 472 W10 E1

00.5

11.5

22.5

33.5

0

10

20

30

40

50

61

71

81

91

10

score

Fre

qu

en

cy

Frequency

Average = 70.0 = B-

Approximate Grades:A = 86+ B= 73-78 C = 60-64A- = 83-85 B- = 67-72 C- = 55-59B+ = 79-82 C+ = 64-67

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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Signal amplification!!

Allosteric effectors

Figure 18-11b A monocyclic enzyme cascade.(b) Chemical equations for the interconversion of the

target enzyme’s unmodified and modified forms Eb and Ea.

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Figure 18-12 A bicyclic enzyme cascade.

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Regulation of Glycogen Phosphorylase

• Allosteric control: AMP activates,Glc, G6P, ATP inhibits(T vs. R)

Signal cascade:Phosphorylase KinaseProtein Kinase APhosphoprotein phosphatase (dephosphorylates Glyc phosphorylase and

Phosphorylase Kinase)

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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o= originalm=modified

Figure 18-14 X-ray structure of the catalytic (C) subunit of mouse protein kinase A (PKA).

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PKs have KEY roles in signalling1.7% of human genome = kinases1000 putative kinase genes!

inhibitor

ATP

Figure 18-15 X-ray structure of the regulatory (R) subunit of

bovine protein kinase A (PKA).

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Autoinhibitory domainFits in active site of CKeeps complex inactive

Phosphorylase Kinase

• Senses Ca+2

– Activated by [Ca+2] as low as 10-7M!!

– 4 subunits (αβγδ)4 active structure a tetramer of tetramers!

– Subunit γ has catalytic activity– Others are inhibitory– Subunit δ = Calmodulin (CaM)

Figure 18-16 X-Ray structure of rat testis calmodulin.

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Figure 18-17 EF hand. P

age

642

Figure 18-18a. NMR structure of (Ca2+)4–CaM 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+)4–CaM 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 18-19Schematic diagram of the Ca2+–CaM-

dependent activation of protein kinases.

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 18-21 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 18-26aThe liver’s response to stress. (a) Stimulation of α-adrenoreceptors by epinephrine activates phospholipase C to hydrolyze PIP2 to IP3 and DAG.

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Figure 18-26bThe liver’s response to stress. (b) The participation of two second messenger systems.

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Fig. 19-16 Receptor-mediated activation/inhibition of Adenylate Cyclase

Figure 19-13Activation/deactivation cycle for

hormonally stimulated AC.

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Figure 19-14 General structure of a G protein-coupled receptor

(GPCR).

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Figure 19-51 Role of PIP2 in intracellular signaling.

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Figure 19-21 Schematic diagram of a typical mammalian AC.

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Figure 19-50 Molecular formula of

the phosphatidylinositides.

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Figure 19-52 A phospholipase is named according to the bond that it cleaves on a

glycerophospholipid.

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Figure 19-57 Activation of PKC.

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Figure 19-64 Insulin signal transduction.P

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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 McArdle’s disease.

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(Muscle Phosphorylase Deficiency)

Table 18-1Hereditary Glycogen Storage Diseases.

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Figure 20.2

For diffusion Keq = 1, thus G°’ = 0

Start of “reaction”

equilibrium

For diffusion Keq = 1, thus G°’ = 0

Figure 20.3

“non-mediated”transport

Table 20-1

Figure 20.4

Figure 20-9Valinomycin(K+ complex)

Figure 20-9Monensin(Na+ complex)

Gramicidin ASee Figure 20.11

-hemolysin(Staph. aureus)

“IONOPHORES”

Figure 20.14

Figure 20.15

Figure 20.18

Table 20-3

Figure 20.21

Figure 20.27

“Alfonse, Biochemistry makes my head hurt!!”\


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