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Molecular & Cellular Processes of Disease > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

How do phospholipids influence cell membranes

A

impact what molecules can pass through

permeable to uncharged, nonpolar, & small polar molecules

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2
Q

How does cholesterol influence cell membranes

A

membrane packs tightly

allows protein to cluster into functional groups

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3
Q

Diffusion barriers of cholesterol enable what

A

apical-basolateral cell polarization

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4
Q

How do glycolipids influence cell membranes

A

maintained on extracellular leaflet

asymmetry

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5
Q

How does phosphatidyl serine influence cell membranes

A

maintained on intracellular leaflet

asymmetry

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6
Q

What does phosphatidyl serine signal if on he outer leaflet

A

phagocytosis

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7
Q

What are the two types of transporters

A

active or passive

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8
Q

Are transporters fast

A

no, involve a conformation change

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9
Q

What are channels

A

small holes in membrane

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10
Q

Are channels fast

A

yes, do not involve a conformation change

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11
Q

Are channels often selective

A

yes

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12
Q

Do channels require energy or a conformational change

A

no

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13
Q

What are non-gated ion channels (ex?)

A

channels that are always open

K+ leak channels

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14
Q

What are voltage-gated ion channels (ex?)

A

channels that are “gated” electrically

K+ or Na+ voltage-gated channels

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15
Q

Sensors of voltage-gated channels respond to what

A

changing charge on plasma membrane

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16
Q

What are ligand-gated ion channels (ex?)

A

channels that are “gated” and require ligands to bind to open
Na+ ligand-gated channels

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17
Q

Describe the chemical gradient

A

ions concentration difference b/w the inside & outside of the cell

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18
Q

Describe the electrical gradient

A

electrical difference b/w the inside & outside of the cell

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19
Q

What is the electrochemical gradient

A

takes into account both the electrical & chemical gradients of ions

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20
Q

What molecules receive a greater pull to enter into the cell (not considering concentration gradient)

A

positive ions

cell interior is negative

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21
Q

Why is the interior of the cell negative

A

large, negatively charged organic (protein) molecules are on the inside of the cell & cannot leave

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22
Q

Membrane potential depends on what

A

K+ leak channels & Na+/K+ pump

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23
Q

What is membrane potential expressed as

A

voltage

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24
Q

What has to be known in order to calculate membrane potential

A

permeability of membrane to ions & presence of open channels

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25
Q

What factors determine resting membrane potential inside the cell

A

negatively charged, Na+ low, & K+ high

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26
Q

At rest, what channels are open and what channels are closed

A

Na+ closed

K+ leak channels open

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27
Q

Define action potential

A

depolarization of membrane potential

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28
Q

What are the steps of action potential

A

1) stimulus triggers NT ligand to open up the ligand-gated Na channel
2) Na+ starts entering cell, increasing pos charge on the inside
3) increase in pos charge on the inside opens up the voltage-gated Na+ channels to open
4) Na+ rushes in, depolarizing cell
5) secondary gated channels blocks Na+ at a certain concentration
6) depolarization triggers K+ gated channels to open
7) K+ rushes in & balances charges until blocked at a certain concentration
8) Na+/K+ pump returns membrane to its resting potential

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29
Q

Describe hyperkalemia

A

increase in extracellular K+

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30
Q

Does hyperkalemia result in more or less driving force inward

A

more

due to electrochemical gradient

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31
Q

Would hyperkalemia increase or decrease resting membrane potential

A

decrease

become less neg/ closer to 0

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32
Q

How does hyperkalemia impact action potential

A

closer to threshold

more likely to happen

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33
Q

Describe hyponatremia

A

decrease in extracellular Na+

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34
Q

Does hypernatremia result in more or less driving force inward

A

less

due to electrochemical gradient

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35
Q

Would hypernatremia increase or decrease resting membrane potential

A

no effect

Na+ channels are closed at rest

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36
Q

How does hyponatremia impact action potential

A

makes it smaller

shorter peak

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37
Q

What is a common cause of hyponatremia

A

water intoxication

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38
Q

How does hyponatremia as a result of water intoxication occur

A

Na+ ions diluted
water rushes into cell
edema occurs

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39
Q

Where is glycocalyx found

A

attached to extracellular portion of membrane proteins

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40
Q

What is glycocalyx often called

A

membrane decor b/c it is on the extracellular surface of cells

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41
Q

What are the compositions of glycocalyx

A

glycolipds & glycoproteins

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42
Q

Where do glycolipids get their diversity from

A

AA sequence of protein & monosaccharide combos in the polysaccharide

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43
Q

Glyco means what

A

polysaccharide

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44
Q

What are the functions of glycocalyx

A 
immune recognition (self vs non-self)
protective barrier against bacterial invasion
pathogen receptor (viral receptor specificity)
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45
Q

O antigen has what

A

no additional glycocalyx

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46
Q

B antigen has what

A

added galactose

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47
Q

A antigen has what

A

added N-acetylgalactosamine

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48
Q

What does glycocalyx do on the intestinal epithelium

A

increases surface area of microvilli

decreases # of invading pathogens

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49
Q

What cells in the intestinal epithelium have less glycocalyx

A

antigen sampling cells

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50
Q

Why do the antigen sampling cells have less glycocalyx

A

provides access to the luminal contents to sample antigens

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51
Q

Are the antigen sampling cells more or less susceptible to bacterial infection

A

more

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52
Q

Influenza virus hemagglutinin binds to what on epithelial cells

A

glycoproteins w/ sialic acids

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53
Q

Different sialic linkages result in different binding & impacts what

A

where the virus infection is permissible

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54
Q

H1N1 hemagglutinin subtype 1 binds to what

A

alpha 2-6 linked sialic acids

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55
Q

Where is alpha 2-6 linked sialic acids found

A

upper respiratory tract

so this is where H1N1 infects

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56
Q

H5N1 hemagglutinin subtype 5 binds to what

A

alpha 2-3 linked siliac acids

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57
Q

Where is alpha 2-3 siliac acids found

A

avian intestinal mucosa
in humans, lower respiratory tract
so this is where H5N1 infects

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58
Q

What part of SARS-CoV-2 is heavily glycoxylated

A

spike protein

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59
Q

The glycan shield of SARS-CoV-2 limits what

A

potential antibody binding sites

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60
Q

What are the components of ECM

A

fibroblasts, ground substance, & collagen

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61
Q

What do fibroblasts do

A

make collagen & ground substance

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62
Q

What is found in ground substance

A

proteins

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63
Q

What does collagen provide

A

tensile strength

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64
Q

What are glycosaminoglycans

A

GAGs

large, highly neg charged polysaccharides

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65
Q

What are GAGs called when attached to a protein core

A

proteoglycans

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66
Q

What GAG is not attached to a protein core

A

hyaluronic acid

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67
Q

What is the function of hyaluronic acid

A

pulls in H2O
plumps up skin & resists compression
lubricant in joint fluid

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68
Q

GAGs represent < 10% of entire ECM, but they do what

A

occupy most of the space

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69
Q

How do GAGs provide compressive strength

A

form hydrated gels

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70
Q

What causes GAGs to swell

A

neg charge attracts cations

cations pull water in

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71
Q

When do GAGs help with cell migration

A

during development & repair

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72
Q

In certain tissues, GAGs have what function

A

filtration

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73
Q

GAGs serve as what for other molecules

A

binding sites

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74
Q

GAGs act as attachment to what

A

fibrous elements

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75
Q

Do GAGs or glycoproteins branch

A

glycoproteins

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76
Q

Do GAGs or glycoproteins have repeating units

A

glycoproteins

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77
Q

Why do GAGs fill the ECM

A

bend, but cannot fold tightly as a hydrogel

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78
Q

Is collagen the same everywhere

A

no, different types in different tissues

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79
Q

Collagen is synthesized where

A

in the cell

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80
Q

Is collagen constitutively expressed

A

yes

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81
Q

What does collagen require to mature

A

extracellular proteolytic processing

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82
Q

Collagen arrangement defines what

A

tissue strength properties

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83
Q

Strength based on collagen can be what

A

in many directions or one direction

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84
Q

Shar pei skin (slimy-ness) is the result of what

A

overproduction of hyaluronic acid

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85
Q

What direction is skin strong in

A

many directions

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86
Q

What direction are tendons strong in

A

one direction

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87
Q

AA sequence of the glycoprotein can be different how

A

diverse attachment site of protein sequence

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88
Q

Monosacharide combinations in the polysaccharide portion of glycoprotein can be different how

A

permutations in monosaccharide order

branch points add additional complexity

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89
Q

Besides GAGs and fibers, what is the other component of ECM in CT

A

non-collagen glycoproteins

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90
Q

Ehlers-Danlos syndrome is a result of what mutation

A

ADAMTS2 protease

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91
Q

ADAMTS2 protease does what

A

converts pro-collagen to collagen

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92
Q

Ehler-Danlos syndrome causes a defect in collage synthesis called

A

Cutis Hyperelastica

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93
Q

How does Cutis Hyperelastica come about

A

C-terminus of pro-collagen is cut off, but the N-terminus is not removed

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94
Q

What is the functional result of the N-terminus being removed

A

skin has reduced tensile strength

increased stretch

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95
Q

Elastic fibers are a network of

A

elastin molecules

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96
Q

Elastic fibers are abundant where

A

aorta, ligaments, & zonular fibers of the eye

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97
Q

What scaffold helps elastic fibers form myofibrils

A

fibrillin

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98
Q

What species does Marfan Syndrome occur in

A

cattle & humans

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99
Q

What caused Marfan Syndrome

A

mutation in fibrillin

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100
Q

What type of mutation is Marfan Syndrome

A

autosomal dominant

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101
Q

Marfan Syndrome results in what

A

dysfunction in elastic fibers

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102
Q

Those w/ Marfan Syndrome are at risk of what

A

aortic aneurism

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103
Q

What does the first messenger in cellular signaling do

A

receive extracellular signal

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104
Q

What does the receptor/transducer in cellular signaling do

A

transmits signals across plasma membrane (protein)

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105
Q

What does the primary effector in cellular signaling do

A

binds to proteins & regulate their activity

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106
Q

What does the secondary messenger & secondary effector do in cellular signalin

A

pass along the signal

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107
Q

What are primary & secondary effectors

A

proteins or enzymes

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108
Q

What are secondary messengers

A

small molecules

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109
Q

What are the two types of molecular switches

A

phosphorylation & GTP binding

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110
Q

What does protein kinase do

A

use ATP to phosphorylate a protein

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111
Q

Do protein kinases (typically) activate or inhibit proteins

A

activate

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112
Q

What does protein phosphatase do

A

removes phosphates from proteins

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113
Q

Do protein phosphatases (typically) activate or inhibit proteins

A

inhibit

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114
Q

How are molecules activated that use GTP binding

A

GTP replaces the GDP bound to the protein

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115
Q

How are molecules inactivated that use GTP binding

A

phosphate is removed through GTP hydrolysis

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116
Q

What molecules remove GDP so free GTP can bind (activate)

A

GEFs

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117
Q

What molecules convert GTP -> GDP (inactivate)

A

GAPs

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118
Q

Signal ____ on activation and signal _____ before being inactivated

A

in, out

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119
Q

Transmitter gated membrane receptors is a type of what

A

cell surface receptor

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120
Q

How are transmitter gated membrane receptors activated

A

ligand (signal molecule) binds to a receptor

channel opens for ions to flow through

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121
Q

What is an example of a Transmitter gated membrane receptor

A

acetylcholine receptor at neuromuscular junctions

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122
Q

Different G-protein coupled receptors (GPCRs) can be activated by the same signal but do what

A

produce different responses depending on the cells

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123
Q

GPCRs are important as what

A

drug targets

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124
Q

GPCRs activate what

A

alpha subunit of trimeric G-proteins

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125
Q

How do GPCRs activate the alpha subunit of trimeric G-proteins

A

GDP/GTP acivity switch

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126
Q

What are the parts of a trimeric G-protein

A

alpha, beta, & gamma

127
Q

What do trimeric G-proteins allow GPCRs to do

A

become coupled to downstream activities

128
Q

H1 histamine receptor is a type of what

A

GPCR

129
Q

What does the alpha unit of the trimeric G -protein activate, following histamine binding to the H1 histamine receptor

A

phospholipase C

130
Q

Phospholipase C cleaves what

A

PIP2 into IP3 & DAG

131
Q

IP3 activates what

A

Ca2+ release from ER

132
Q

DAG & Ca2+ activate what

A

protein kinase C

133
Q

protein kinase C activates what

A

NF-kbeta

134
Q

NF-kbeta causes what

A

inflammation & hives

135
Q

Receptor Tyrosine Kinase (RTK) is a type of what

A

enzyme-linked receptor

136
Q

What binds a signal molecule for RTKs

A

extracellular domain

137
Q

What leads to activation of RTKs

A

dimerization

allows for phosphate binding

138
Q

What are recruited to activated RTKs to pass the signal along

A

relays

139
Q

What generatd many binding sites on the RTK for signaling proteins

A

trans-autophosphorylation after dimerization

140
Q

Ras has what type of activity switch

A

GDP/GTP

141
Q

A mitogen signal for cell division activates what

A

RTK

142
Q

What activates Ras GEF

A

adaptor protein bound to RTK

143
Q

What does Ras GEF do

A

removes GDP from Ras protein

144
Q

Activated Ras initiates what sequence of events

A

Mitogen-activated protein kinase (MAPK) cascade

145
Q

Each step of MAPKKK -> MAPKK -> MAPK involves what

A

ATP hydrolysis

146
Q

After the MAP’s, what happens & what does it lead to

A

change in protein activity & gene expression

leads to cell division

147
Q

Where do pattern recognition receptors (PRRs) operate

A

on cell surface & extracellularly

148
Q

What do PRRs function as

A

act as pathogen sensors

149
Q

PRRs recognize what

A

Pathogen-associated molecular patterns (PAMPs)

150
Q

PAMPs consist of what

A

double-stranded RNA (viruses) or lipolysaccharides (bacteria)

151
Q

PRRs create a signal to activate what

A

an innate immune response

152
Q

What are examples of PRRs

A

Toll-like receptors (TLRs)
NOD-like receptors (NLRs)
C-type lectin receptors (CLRs)
RIG-I-like recpetors (RLRs)

153
Q

PAMP binds to a TLR receptor & the adaptor proteins activate

A

IKK complex

154
Q

IKK complex does what

A

phosphorylates IKB

155
Q

When IKB is phosphorylated, what happens

A

gets degraded in proteosomes

156
Q

Active IKB functions to do what

A

inhibit NF-kbeta

157
Q

Active NF-kbeta does what & causes what (different answer than hives one)

A

alters gene expression; innate immune response

158
Q

Cytokine binding to cytokine receptors causes what

A

dimerization

159
Q

Dimerization of cytokine receptors results in

A

activation of JAK kinase

160
Q

Phosphorylation of JAK kinase does what

A

recruits STAT proteins

161
Q

Phosphorylated STATs do what

A

dimerize & translocate to nucleus to alter gene expression

162
Q

What is the source of somatotropin (GH) & how is it transported through the body

A

anterior pituitary

thus, GH sent through cardiovascular system

163
Q

What are the target tissues for GH

A

skeletal muscle, adipose tissue, bone, & liver

164
Q

MAP kinase cascade causes what type of growth effects

A

direct & systemic

165
Q

MAP kinase cascade involves Ras signalling that leads to the transcription & translation of factors that cause what

A

cell cycle entry -> proliferation

166
Q

GH signaling w/ MAP kinase cascade involves

A

Ras signaling & enzyme-linked receptor (RTK)

167
Q

GH via MAP kinase cascade stimulates what

A

muscle, chondrocyte (cartilage), & bone growth during childhood

168
Q

JAK-STAT pathway for GH stimulates what

A

induction of IGF-1 in liver

169
Q

Production of IGF-1 in liver promotes what

A

growth of liver, bone growth, protein synthesis, increased muscle mass, & activation of stored fat

170
Q

JAK-STAT pathway involves what molecules

A

growth hormone
GH receptor (dimerizes)
JAK kinases
STAT proteins

171
Q

Do Great Danes or Chiuahuas have more IGF-1

A

Great danes

172
Q

Elevated GH in mice results in

A

gigantism

173
Q

GH deficiency in mice results in

A

dwarfism

174
Q

GH insensitivity in mice leads to

A

dwarfism

175
Q

Over the long run, decreased GH signaling leads to

A

a longer lifespand

176
Q

What does bovine somatotropin do

A

stimulate IGF-1 production -> survival of mammary alveolar cells

177
Q

Recombinant bovine somatotropin results in what changes in the cow

A

increased milk production

increased growth

178
Q

Glycogen breakdown is stimulated in muscle by

A

adrenaline (epinephrine)

179
Q

Glycogen breakdown is stimulated in the liver by

A

glucagon

180
Q

What makes cAMP

A

adenylate cyclase (AC)

181
Q

What breaks cAMP

A

PDE

182
Q

What is protein kinase A (PKA)

A

dimer of dimers

183
Q

cAMP has what effect on PKA

A

removes regulatory part

allows catalytic part to be active

184
Q

Adrenaline & glucagon are signal molecules that first activate what to lead to glycogen breakdown

A

GPCR

185
Q

Activation of the alpha subunit of the trimeric protein results in activation of what in glycogen breakdown

A

adenylate cyclase (AC)

186
Q

AC causes the conversion of what into cAMP

A

ATP

187
Q

cAMP activates PKA, resulting in

A

glycogen -> glucose 1-phosphate

188
Q

If GH hormone releasing hormone stimulates a similar cascade to glycogen breakdown, what does PKA activate instead

A

CREB

189
Q

Activated/phosphorylated CREB does what

A

results in gene transcription of GH

190
Q

What is the source of adrenaline

A

adrenal medulla

191
Q

What are the physiological effects of adrenaline

A

increased heart rate
increased resp rate
pupil dilation
glycogen breakdwon

192
Q

alpha 1 activates what, leading to what intracellular signaling events

A

phospholipase C
leads to PIP3 -> IP3 + DAG
Ca2+ release

193
Q

Ca2+ release as a result of alpha 1 causes what

A

smooth muscle contraction of GI & peripheral blood vessels

194
Q

alpha 2 does what, leading to what

A

represses AC

decreased levels of cAMP

195
Q

Decreased cAMP as a result of alpha 2 causes what

A

smooth muscle contraction of GI sphincter

196
Q

beta does what, leading to what

A

activates AC

increased levels of cAMP

197
Q

Increased cAMP as a result of beta causes what

A

heart muscle contraction (increases heart rate), smooth muscle relaxation, glycogenolysis, & opening of bronchioles

198
Q

What kind of molecule is caffeine

A

xanthine alkaloid

199
Q

What is the source of caffeine

A

leaves, seeds, & fruits of some plants

200
Q

What are the physiological effect of caffeine

A

neurostimulant

increased heart rate

201
Q

How does caffeine act as a neurostimulant

A

counteracts inhibitory effect of adenosine

202
Q

How does caffeine increase heart rate

A

PDE inhibited
cAMP conc increases
PKA activity increases

203
Q

What is the source of cholera toxin

A

vibrio cholerae

204
Q

What are the physiological effects of cholera toxin

A

efflux of ions & water into small intestine

205
Q

What molecules does cholera toxin affect

A

alpha subunit of GPCR

206
Q

What effect does cholera toxin have on the alpha subunit of GPCR

A

permanently activates it

207
Q

How does cholera toxin permanently activate the alpha subunit of GPCR

A

catalyzes a covalent modifcation

ADP-ribose from NAD+ locks onto an Arginine side chain

208
Q

When the alpha subunit is permanently activated by the cholera toxin, what occurs

A

AC stimulated
levels of cAMP & PKA increase
chloride channels open

209
Q

What is a drug that represses AC

A

enkephalin

210
Q

What are the phases of the cell cycle

A

G1, S, G2, & M

G0

211
Q

G1 phase involves

A

cell growth

copy of organelles

212
Q

S phase involves

A

DNA synthesis

chromosome replication

213
Q

G2 phase involves

A

cell growth

synthesis of proteins/ organelles

214
Q

M phase involves

A

mitosis

chromosomes separated

215
Q

G0 phase involves

A

cell cycle arrested

216
Q

Cyclins do what

A

activate CdK

217
Q

Cyclins allow for control during the cell cycle b/c they undergo

A

synthesis & degradation

218
Q

What are examples of the different types of cyclins

A

G1/S cyclin
M cyclin
S cyclin

219
Q

What does CdK stand for

A

cyclin-dependent kinase

220
Q

When are CdKs active

A

only when their cyclin activator is present

221
Q

What do CdKs do

A

phosphorylate other molecules to activate them

222
Q

Is CdK expression constant

A

yes

223
Q

Activity of CdK rises & falls corresponding to

A

cyclin binding

224
Q

What is CAK

A

CdK activating kinase

225
Q

Cyclins cause CdK to undergo a conformation change, which allows what to happen

A

CAK phosphorylates CdK (on threonine)

226
Q

Do cells in G0 have a lot or a little of CAK

A

little

227
Q

Wee1 kinase does what

A

phosphorylates active (phosphorylated) CdK to temporarily inactivate it

228
Q

What does Wee1 kinase allow to happen

A

cell to grow during G2

229
Q

Wee1 mutants are what

A

small

230
Q

Cdc25 phosphatase does what

A

removes the inactivating phosphate to activate CdK

231
Q

CKI stands for

A

cyclin dependent kinase inhibitor

232
Q

Two types of CKI

A

p21 & p27

233
Q

CKI (p21 & p27) do what

A

bind to the cyclin-CdK complex to inactivate it

234
Q

When are CKIs expressed

A

during G0 to prevent cell cycle entry

235
Q

What does E3 ligase SCF do

A

degrades inhibitor p27

makes cyclin-CdK complex active again

236
Q

What events does E2F activation lead to

A

S-phase gene transcription -> G1/S cyclin -> activated S-CdK -> S phase

237
Q

What does Rb do when active

A

inactivates E2F

prevents transcription of S-cyclin

238
Q

Rb arrests cells at what checkpoint

A

G1/S

239
Q

What does Ras do after it receives a mitogen signal

A

indirectly inactivates Rb

240
Q

What events happen when Rb is inactivated

A

EF is liberated
cells pass through the G1/S checkpoint
cell division occurs

241
Q

What events lead to the indirect activation of Rb by Ras

A

MAP kinase cascade
activation of G1 cyclin transcription
G1 & cyclin-dependent kinase activation
G1-CdK dependent phosphorylation of Rb

242
Q

What does mdm2 (E3 ligase) do

A

binds & inactivates p53

243
Q

What does mdm2 promote

A

protease degradation of p53

244
Q

p53 leads to what cellular events

A

cell cycle arrest, DNA repair, & cell cycle restart

apoptosis

245
Q

p53 promotes what

A

cellular & genetic stability

246
Q

p53 is active at what checkpoint

A

G2/M

247
Q

DNA damage leads to the activation of p53 by

A

phosphorylation

248
Q

Activated p53 binds to the regulatory region of what

A

p21 gene

249
Q

After p53 binding, translated p21 does what

A

inactivates G1/S-CdK & S-CdK complexes

250
Q

The inactivation of the G1/S-CdK & S-CdK complexes leads to

A

cell cycle arrest & DNA repair

251
Q

What is the G1/S checkpoint

A

start transition

restriction point

252
Q

In the G1/S checkpoint, the cell checks on what

A

cellsize
nutrients
growth factors
DNA damage

253
Q

After the G1/S checkpoint, what happens

A

enter S phase or G0

254
Q

What is the G2/M checkpoint

A

gap to mitosis transition

255
Q

In the G2/M checkpoint, the cell checks on what

A

DNA damage

DNA replication

256
Q

After the G2/M checkpoint, what can happen

A

enter M phase
pause to repair damage
undergo apoptosis

257
Q

What is the M/G1 checkpoint

A

metaphase-to-anaphase transition

258
Q

In the M/G1 checkpoint, the cell checks on what

A

chromosome attachment

259
Q

Non-functional Rb leads to what

A

no break before S phase

aggressive cancer

260
Q

Hyperactive Ras (meaning Ras activates too early) promotes what

A

activation of MAP-kinase cascade
cells divide inappropriately b/c Rb is inactivated
aggressive cancer

261
Q

p53 mutations in the DNA binding domain make it unable to promote transcription of p21, so what happens

A

inability to inactivate G1/S-CdK & S-CdK complexes
cell progresses right into S phase
aggressive cancer

262
Q

Apoptosis is described as what type of process

A

controlled developmental process

263
Q

Apoptosis is considered what type of pathway for cells if they are not provided with what type of factors

A

default, survival

264
Q

Apoptosis is initiated by

A

viruses
organ/ tissue development
DNA damage

265
Q

Apoptosis promotes what

A

homeostasis

266
Q

Does apoptosis involve single cells or clusters

A

both

267
Q

Does apoptosis involve cell swelling or shrinkage

A

shrinkage

268
Q

Does apoptosis involve controlled or random DNA fragmentation

A

controlled

269
Q

Does apoptosis involve intact or broken cell membranes

A

intact

270
Q

Does apoptosis release the cytoplasm through pores or bodies

A

apoptotic bodies

271
Q

Does apoptosis involve inflammation

A

no

272
Q

Caspase have what active site & cleave where

A

active site cysteine

cleave at aspartic acid

273
Q

What do adaptor proteins do to caspases

A

dimerize, activate, & cleave the initiator caspase

274
Q

The active initator caspase does what

A

cleaves the executioner caspase to activate it

275
Q

The active executioner caspase does what

A

cleaves multiple subunits

276
Q

The cleavage of multiple subunits leads to what

A

apoptosis

277
Q

Each cleavage results in what

A

conformational change

278
Q

Cells are removed in a controlled fashion as what happens

A

caspases amplify their signals

279
Q

A few activated caspases lead to

A

cleavage of cytosolic protein

280
Q

Many activated caspases lead to

A

clavage of nuclear lamin

281
Q

Intrinsic pathway of caspase activation is via what type of pathway

A

mitochondrial

282
Q

Intrinsic pathway is activated by

A

intracellular factors (oxidative stress, hypoxia, nutrient deprevation, & DNA damage)

283
Q

Intrinsic pathway results in what

A

mitochondrial membrane permeabilization

cytochrome c leakage into the cytoplasm

284
Q

What binds to cytochrome c in the cytoplasm

A

adaptor proteins

285
Q

Adaptor proteins w/ cytochrome c form what

A

apoptosome

286
Q

Apoptosome recruit what that forms what

A

caspases

forms an active initiator caspase

287
Q

Active iniatiator caspase does what

A

activates executioner caspases

288
Q

Executioner caspases lead to

A

cellular breakdown

apoptosis

289
Q

What molecule creates pores for cytocrhome c to leak out

A

Bax

290
Q

Is Bax pro-apoptotic or anti-apoptotic

A

pro-apoptotic

291
Q

What does Bcl2 do

A

inhibits Bax

292
Q

Is Bcl2 pro-apoptotic or anti-apoptotic

A

anti-apoptotic

293
Q

What does Bad do

A

sequesters Bcl2

allows Bax to create pores

294
Q

Is Bad pro-apoptotic or anti-apoptotic

A

pro-apoptotic

295
Q

What molecule promotes the aggregation of Bax so that it can create pores

A

p53

296
Q

What does the extrinsic pathway for caspase activation involve

A

damaged cell displayes a death receptor on its surface

297
Q

What recognizes the death receptor

A

killer lymphocyte

298
Q

Cell-cell binding of the killer lymphocyte to the target cell results in

A

assembly of adaptor proteins into a death-inducing signaling complex

299
Q

The death-inducing signaling complex leads to what & ultimately what

A

activates executioner caspases

apoptosis

300
Q

Cells constantly decide if they will

A

divide, differentiate, or die

301
Q

Sculpting organs requires

A

proliferation, survival, & apoptosis

302
Q

Inadequate apoptosis in b/w digits leads to

A

syndactyly

303
Q

Too little proliferation causes

A

Microphthalmia - small eye phenotype

304
Q

Microphthalmia is a result of

A

genetic, environmental, or infectious

ex: maternal Vit A deficiency

305
Q

Too much proliferation causes

A 
Protein myostatin
Mighty mice
Texel sheep
Belgian blue cattle
Whippets
306
Q

Protein myostatin is what

A

differentiation factor

prevents myogenesis

307
Q

Mighty mice are transgenic mice mutants with

A

increased muscle mass & fiber number

308
Q

Belgian blue cattle are often called what and have a mutation in what leading to what

A

double muscled
mutation in myostatin
more myocytes

309
Q

Whippets have what after a mutation in myostatin

A

increased muscle mass

310
Q

Examples of second messengers

A

Ras, cAMP, IP3, & DAG

311
Q

What does GH stimulate in adipose tissue

A

release of FAs

312
Q

What does GH stimulate in skeletal muscle

A

increase nutrient uptake & utilization

313
Q

What does GH stimulated in bone

A

bone growth

314
Q

What does GH stimulate in liver

A

increased IGF-1

Molecular & Cellular Processes of Disease (2 decks)

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