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Flashcards in Exam 2 Review Deck (119):
1

two types of functional groups found on the anomeric carbon of straight chain sugars

aldehydes and ketones

2

glycation
-clinical significance

the process of a protein reaction and combining with a sugar without the presence of a cofactor such as an activated sugar
-Hb can be glycated when diabetics dont take their insulin and take too much sugar and can be used in a test to see if people have been compliant

3

polysaccharide, glycolipis, and glycoprotein bond formation requirements

-this process is called glycosylation and it differs from glycation in that cofactors are needed to carry out the reaction
-these are in the form of activated sugar nucleotides

4

glycogen structure

-series of alpha 1,4 linked glucose molecules with alpha 1,6 branches
-the end at which sugars get added is called the nonreducing end

5

glycosaminoglycans GAGs
-what are they
-most common

long, linear sugars with disaccharide repeats that are negatively charged (sulfates)
-can be free or attached to protein
-chondroitin sulfate is the most common

6

chondroitin sulfate

bone, cartilage, cornea formation

7

keratan sulfate

cornea, connective tissue

8

dermatan sulfate

binds LDL to plasma walls

9

heparan sulfate

aortic wall, basement membrane

10

heparin

anticoagulant

11

hyaluronic acid

cell migration, lubricant, (not covalently attached to protein)

12

proteoglycans

-provide part of the ground substance for tissue epithelia, bind growth factors/cytokines and provide cushioning in joints

13

enzymatic glycosylation
-where does it occur

-outside of the cell or oriented outside of the cell except in O-GlcNac
- can be O linked or N linked with a specificity determined by the nucleotide sugar and the substrate
-sugar processing occurs as proteins traffic from the ER through the golgi

14

what enzymes are involved in I cell disease

-there are multiple!!
-results in the accumulation of many biosynthetic materials

15

glycoproteins are critical for...

-biological recognition
-mannose-6-P as a lysosomal targeting signal, influenza or helicobacter, leucocyte adhesion deficiency 2

16

what does lactase insufficiency cause when lactose is consumed

-fluid to rush into the colon causing watery diarrhea and the formation of H2 gas

17

the different mechanisms in which monosaccharides can enter the cell

simple diffusion, facilitated diffusion, active transport

18

Glut 4
-type of transport
-found where
-regulation
-difference between glut 2

-facilitated transporter
-important in fat and muscle
-not found in the liver **
-regulated by insulin
-glut 2 is not regulated by insulin

19

affect of insulin on blood glucose in type 1 diabetics

-blood glucose does not go down nearly as much

20

insulins action on glucose metabolism

-decreases blood glucose by increasing uptake in muscle and adipose tissue (not in the liver)
-increases glycolysis in the liver, increasing acetyl-CoA formation
-decreases gluconeogenic reactions
-decreases glycogen breakdown and increases synthesis

21

purpose of forming G6P from Glu

-locks it into the cell so the exterior glucose concentration doesnt pull it back out of the cell
-this is done by hexokinase everywhere and by glucokinase in hepatocytes
-glucokinase in pancreatic beta cells regulates glycolysis and hence insulin secretion (MODY)

22

glucokinase vs hexokinsae concentrations

-glucokinase is 100 times more concentrated in liver cells than hexokinase is anywhere else in the body
-this makes sure that the liver does not miss any glucose molecules passing through it

23

4 different things you can do with glucose in a general sense

-glycogen synthesis
-glycolysis
-PPS
-glucuronides

24

niacin deficiency

-vitamin B3
-dermatitis
-diarrhea
-dementia (pellagra)

25

thiamine deficiency

-VitB1
-opthalmoplegia
-gait difficulties
-confusion
-beri beri
-wernicke korsakoff

26

riboflavin

-VB12
-cheilosis and glossitis

27

lipopoate

-targeted by arsenic (pyruvate and a ketoglutarate dehydrogenase)

28

ratios of NAD vs NADH and NADPH vs NADP

-NAD+ >> NADH
-NADPH >> NADP
-basically, what the cell wants are NADPH and NAD, these are what are the cell uses as substrates in important reaction
-however, there are reaction within the cell that can convert NADH and NADP back to their original states
-it is an oxidation reduction cycle

29

regulated enzymes of glycolysis

-hexokinase/glucokinase
-phosphofructokinase 1 (PFK1)
-pyruvate kinase

30

ATP producing enzymes of glycolysis

-phosphoglycerate kinase (1,3BPG to 3PG)
-pyruvate kinase (PEP to pyruvate)

31

glycolysis
-where
-yield
-limited by and requires
-deficiencies affect
-regulatory enzymes, reversible?
-what is the most important site of regulation?

-cytoplasm
-2 ATP per glucose even under anaerobic conditions
-limited by Pi and requires NAD+ (used by G3PDH)
-deficiencies affect mainly RBC's (anemia, pyruvate kinase) and skeletal muscle (exercise intolerance, PFK1)
-glucokinase, phosphofructokinase, pyruvate kinase (liver vs muscle)
-PFK1 is the most important step in glycolysis

32

regulation of PFK1

activators: ATP and F2,6BP
-F2,6BP is particularly important because in its absence, F1,6BP could be used for gluconeogenesis (the opposite of glycolysis)
-inhibitors: ATP and citrate

33

intermediates of glycolysis are used for

-amino acid synthesis
-fats
-nucleic acid

34

posions that affect glycolysis

-2 deoxyglucose inhibits hexokinase
-arsenate inhibits G3PDH
-fluoride inhibits enolase

35

fructose entering the pathway

gets phosphorylated to F1P then aldolase B splits it into DHAP and glyceraldehyde which are both intermediates in glycolysis

36

fructokinase deficiency vs an aldolase B deficiency

fructokinase: less serious, causes essential fructoseria
-aldolase B: more serious as it causes a build up of F1P which blocks glycogen breakdown and glucose synthesis via sequestering Pi, this is called hereditary fructose intolerance

37

matabolic diseases of galactose

-galactokinase deficiency causes minor problems
-Gal-1-P-uridyl transferase causes major problems and is called classic galactosemia

38

what is UDP-Glucoronic acid used for?
-what enzymes does this
-what happens if there is a problem

-conjugated with other molecules such as bilirubin and drugs in order to make them more polar so that they are excreted from the body
-this is done via UGT = UDP-alpha-glucuronyltransferase
-problems cause Gilberts syndrome

39

alcohol is converted into what and then what?
-what cofactors does this process use? What does that lead to

-acetaldehyde by alcohol dehydrogenase and then acetate by aldehyde dehydrogenase
-acetate can then lead to acidosis or be converted to acetyl CoA
-This process uses 2 NAD and produces 2 NADH
-The increased NADH leads to inhibition of gluconeogenesis and increased triglyceride synthesis by blocking the conversion of FA's to Acetyl CoA

40

alternative alcohol pathway, when does this occur

-MEOS (CYTP450) pathway
-uses NADP, creating NADPH
-this is an adaptive pathway and found to be used by alcoholics
-one reason why they can handle more booze

41

production of NADH from ethanol does what

-inhibits gluconeogenesis
-stimulates fat production

42

alcoholics are often deficient in what?

-vitamins, particularly thiamine (VB1)
-this causes W-K and beri-beri

43

PDH is inactivated by

-being phosphorylated by PDH kinase

44

-what activates PDH kinase and what does this cause

-Acetyl CoA, CO2, NADH (products)
-this causes the inhibitions of the TCA cycle, basically this happens when your body is in an energy surplus

45

what inactivates PDH kinase and what does this cause

-via inhibiting the kinase:ADP (low energy), Pyruvate, CoASH, NAD+
-By activating the phosphotase: Insulin, Ca++
-This is when your body has low energy or you have just eaten a high carb meal or you have a build up of the substrate for PDH

46

what macromolecules feed into the TCA cycle

-carbohydrates
-fatty acids
-amino acids

47

where does the great majority of energy derived from glucose come from?

-TCA cycle

48

what products do you get from the TCA cycle?

-3 NADH (isocitrate dehydrogenase, a-KGDH, malate dehydrogenase)
-2 CO2 (isocitrate DH, a-KGDH)
-FADH2 (succinate DH)
-GTP (succinyl CoA synthetase)

49

Regulatory enzymes of the TCA, just their names

-citrate synthase
-isocitrate DH
-a-KGDH
-malate dehydrogenase

50

what regulates citrate synthase

-activator: increased ADP
-inhibitor: NADH, SuccCoA, ATP

51

what regulates isocitrate DH

-activator: ADP, Ca
-inhibitor: NADH, ATP

52

what regulates a-KGDH?

-activator: Ca
-inhibitor: NADH, SuccCoA

53

alcohol is converted into what and then what?
-what cofactors does this process use? What does that lead to

-acetaldehyde by alcohol dehydrogenase and then acetate by aldehyde dehydrogenase
-acetate can then lead to acidosis or be converted to acetyl CoA
-This process uses 2 NAD and produces 2 NADH
-The increased NADH leads to inhibition of gluconeogenesis and increased triglyceride synthesis by blocking the conversion of FA's to Acetyl CoA

54

alternative alcohol pathway, when does this occur

-MEOS (CYTP450) pathway
-uses NADP, creating NADPH
-this is an adaptive pathway and found to be used by alcoholics
-one reason why they can handle more booze

55

production of NADH from ethanol does what

-inhibits gluconeogenesis
-stimulates fat production

56

alcoholics are often deficient in what?

-vitamins, particularly thiamine (VB1)
-this causes W-K and beri-beri

57

PDH is inactivated by

-being phosphorylated by PDH kinase

58

-what activates PDH kinase and what does this cause

-Acetyl CoA, CO2, NADH (products)
-this causes the inhibitions of the TCA cycle, basically this happens when your body is in an energy surplus

59

what inactivates PDH kinase and what does this cause

-via inhibiting the kinase:ADP (low energy), Pyruvate, CoASH, NAD+
-By activating the phosphotase: Insulin, Ca++
-This is when your body has low energy or you have just eaten a high carb meal or you have a build up of the substrate for PDH

60

what macromolecules feed into the TCA cycle

-carbohydrates
-fatty acids
-amino acids

61

where does the great majority of energy derived from glucose come from?

-TCA cycle

62

what products do you get from the TCA cycle?

-3 NADH (isocitrate dehydrogenase, a-KGDH, malate dehydrogenase)
-2 CO2 (isocitrate DH, a-KGDH)
-FADH2 (succinate DH)
-GTP (succinyl CoA synthetase)

63

Regulatory enzymes of the TCA, just their names

-citrate synthase
-isocitrate DH
-a-KGDH
-malate dehydrogenase

64

what regulates citrate synthase

-activator: increased ADP
-inhibitor: NADH, SuccCoA, ATP

65

what regulates isocitrate DH

-activator: ADP, Ca
-inhibitor: NADH, ATP

66

what regulates a-KGDH?

-activator: Ca
-inhibitor: NADH, SuccCoA

67

what regulates malate dehydrogenase?

-inhibitor: NADH

68

what regulates PDH?

-activators: AMP, CoA, NAD+, Ca++, insulin
-inhibitors: ATP, AcCoA, NADH, fatty acids

69

anaplerotic pathways into the TCA cycle (7)

-glutamate into aKG
-I,M,V odd-chain fatty acids into succinyl CoA
-A,P,Y into fumerate
-transamination of amino acids into OAA
-PEP into OAA via PEP carboxykinase
-Pyruvate into OAA via pyruvate carboxylase

70

PPS generates what two important products?

NADPH and ribose-5-P

71

recognition by trypsin, chymotrypsin, and elastase

-trypsin: positive charge
-chymotrypsin: big hydrophobis
-elastase: small hydrophobic
-these are serine proteases

72

what part of the serine protease attacks

-serine 195

73

serine proteases are

-hydrolyases

74

delta G double dagger

-this is the energy of activation
-the larger it is, the slower the reaction

75

catabolism

-breaking down fuel/food to make ATP

76

anabolism

-using ATP to build up complex biosynthetic molecules
-active transport
-mechanical work

77

Km

substrate concentration at 1/2 Vmax

78

enzyme activity respons the most to substrate concentrations where

-near the Km

79

Vmax is used to determine

the amount of enzyme

80

delta G is sensitive to

-substrate concentration

81

delta G not is

constant because the concentrations are worked in already

82

thrombin is made where, what does it reuire, for what, how is it activated, what does the activated form do

-on the membrane surface
-vitamin K and Ca dependent gamma carboxylation
-two proteolytic cleavages result in activated, solube thrombin
-thrombin catalyzes the conversion of fibrinogen to fibrin

83

elastase is inhibitted by what in the lung

-alpha 1 antitrypsin / alpha 1 antiproteinase

84

what secretes elastase in the lung

-neutrophils

85

what does defective alpha 1 antitrypsin lead to

-no inhibition of elastase, degradations of the lung tissue and therefor emphysema

86

competitive inhibs interfere with...

-substrate binding

87

Ki

-the lower this value is, the more effective the inhibitor
-lower number = tighter binding
-this is exactly how Km relates to substrate affinity

88

how would you define a Km for an allosteric enzyme

-it would be an "apperant" Km

89

what do allosteric enzymes typically have?

-binding sites for affector molecules that change the enzyme confirmation
-either increasing or decreasing activity

90

allosteric enzymes often regulate...

the first step of a reaction pathway that is dedicated to making a specific compound for the pathway

91

what cyclins/CDK are involved in pRB phosphorylation

-Cyclind D/E with 2/4/6
-this allows E2F to begin transcription

92

what can activate p53 and then what can it do?

-oncogenes and DNA damage can activate it
-then it can initiate apoptosis or inhibit Cylcin/CDK complexes via p21

93

what chromosomal changes are associated with burkitts lymphoma

-translocations

94

burkitts lymphoma translocation

-between chromosome 8 and one of three chromosomes containing genes that encode Ab molecules

95

burkitts lymphoma is associated with q

epstein bar virus

96

what is the gene on chromosome 8 that gets moved in burkits lymphoma

-Myc
-encodes a transcription factor
-once transloacted, it is constitutively expressed

97

What can transformation by a DNA tumor cause?

sequestering of pRb and p53 so that the cell is constitutively in proliferation mode

98

HPV
-E7
-E6

binds up tumor supressor proteins
-E7=pRb
=E6=p53

99

mutant epidermal growth factors may...

constantly stimulate growth

100

Ras

-oncogene
-when bound to GTP, it is active and causing the cell to proliferate
-mutant for can be stuck in the GTP bound form
-this is regulated by GAPs (GTPase activating proteins)

101

Neurofibromatosis

-this is caused by a mutation in the NF1 gene which encodes neurofibromin which is a GAP
-a mutation in NF1 is believed to result in a constantly active Ras
-associated with cafe-au-lait spots

102

the six changes in the cell that lead to cancer

-self sufficiency in growth signals (Ras)
-insensitivity to anti growth signals (lose Rb)
-evading apoptosis (produce IGF)
-limitless replicative potential (telomerase)
-sustained angiogenesis
-tissue invasion and metastasis

103

compartments of the mitochondria

-outer membrane,
-intermembrane space
-inner membrane
-matrix

104

mtDNA

-small, circular
-13 oxphos proteins
-some RNA's

105

majority of mitochondrial proteins are

-transcribed from genomic DNA and imported from the cytoplasm using TIM and TOM proteins

106

1st step of ox phos

-electron transfer from NADH and succinate to O2
-this generates NAD+ and H2O
-complexes 1-4

107

2nd step of oxphos

-generation of the electrochemical proton transmembrane potential (negative and alkaline on the matrix side, pociditive and acidic on the intermembrane space side)
-only complexes 1,3, and 4 have proton pumps, NOT 2!)

108

3rd step of oxphos

-use proton motive force to synthesize ATP from ADP using ATP synthase
-complex 5

109

what carries electrons from complex 1 and 2 to 3

-coQ

110

what carries electrons from 3 to 4

-cytC

111

what does the word coupling refer to

-the codependence of the rates of respiration and ATP synthesis
-ie we can not change the rate of respiration without changing the rate of ATP synthesis and vice versa because the gradient is self-limiting

112

rate limiting steps of oxphos

-primary: how much ADP we have
-respiratory chain substrates

113

permeability to NADH

-the inner membrane is impermeable to it
-uses the glycerol phosphate and malate-aspartate shuttles to overcome this

114

glycerol phosphate shuttle

-DHAP is made into glycerol 2 P using a NADH from glycolysis
-therefore, glycerol 3 P is reduced
-glycerol 3 P then makes contact with a protein on the inner membrane which reduced NAD+ in the matrix using glycerol 3 P which makes matrix NADH and reproduces DHAP

115

malate-aspartate shuttle

-OAA is reduced to malate in the cytoplasm using NADH from glycolysis
-malate is then allowed to go through the inner membrane into the matrix where is reduces a NAD+ to NADH and is converted back to OAA
-this OAA is then converted to Asparte which can be shuttled back across the inner membrane to be converted back to OAA in the cytoplasm in order to carry more electrons

116

flavin in oxphos

-prosthetic group on C1

117

heme in oxphos

-this is found in cytC and carries e-

118

Fe-S clusters

-found in C1,2, and 3

119

inhibition of C1

does not completely shut down oxphos
-wherease inhibition of 3 and 4 do