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Cell Biology > Exam 5 > Flashcards

Exam 5 Flashcards

1
Q

3 cell surface receptors

A
  • G-protein
  • enzyme
  • ion channels
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2
Q

2 categories of intracellular signaling proteins

A
  • cytoplasmic

- nuclear

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3
Q

what type of molecules must use cell surface receptors?

A

large, hydrophilic

peptide

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4
Q

what type of molecules can use intracellular receptors?

A

small, hydrophobic

can diffuse through the hydrophobic phospholipid bilayer) (steroid

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5
Q

mechanism of intracellular receptor

A

molecule (steroid hormone) bind to receptor –> complex binds to control regions of DNA –> transcription

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6
Q

define versatility of signaling molecules

A

molecules can have different signals or effects based on cell type and receptor

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7
Q

example of versatility in signaling molecules

A
  • Ach binds to muscarinic receptors on surface of salivary glands and induces saliva secretion.
  • Ach binds to different subtype of muscarinic receptor in heart muscle and undergoes different intracellular signaling pathway, decrease in the rate and force of contraction.
  • Ach activated surface nicotinic receptor in skeletal muscle which causes depolarization of the membrane and leads to muscle contraction.
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8
Q
  • cell sends a signal to neighboring cell by hormone or cytokine
  • recipient cell must have a specific receptor for the signal in order to be activated or inhibited
A
  • intercellular

- Paracrine

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9
Q
  • same cell that produces the signal molecule has the receptor for the signal as well
  • cell can usually activate itself
A
  • intercellular

- Autocrine

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10
Q

example of autocrine signaling

A
  • T-lymphocyte of the immune system produces the cytokine interleukin t (IL2)
  • these cells have IL2R which is activated by IL2
  • T cells proliferate
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11
Q
  • signal molecule remains attached to membrane of producing cell
  • binds receptor on surface of adjacent target cell
  • target cell will be activated
  • when the cell produces the signaling molecule doesnt want to separate from that molecule and it stays on the surface
A
  • intercellular
  • Juxtacrine
  • “want the signal? here it is, come get it”
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12
Q
  • usually part of a gland
  • release hormone into blood stream
  • only cells with appropriate receptor can respond
  • behavior of target cells change
A
  • intercellular

- Endocrine

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13
Q
  • characteristics of endocrine (long distance signaling over neuronal processes
  • technically paracrine because the signaling cell and target cells are neighbors
  • separated/connected by synapsis
  • NT released, target has receptor that binds NT, change target cell behavior
A
  • intercellular

- synaptic signaling

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14
Q

3 nuclear receptor superfamily and gene regulation types

A
  • Glucocorticoid receptor (GR)
  • Estrogen receptor
  • Thyroid hormone receptor (THR)
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15
Q

GLucocorticoid receptor (GR)

A
  • inactive in cytosol in complex (HSP and immunophilin) (GR-Hsp70-Hsp90-IP)
  • activated complex moves to nucleus and binds to DNA to activate genes (cortisol-GR)
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16
Q

Estrogen receptor

A
  • inactive in nucleus (ER-Hsp90)
  • active in nucleus (ER-estrogen complex)
  • second complex binds forming a DIMER
  • this binds DNA and HAT (HAT is a coactivator)
  • target genes are activated and transcription occurs
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17
Q

Thyroid hormone receptor (THR)

A

In nucleus
in absence of ligand
-complex with HDAC acts as corepressor and gene transcription prevented
in presence of ligand (TH)
-complex with HAT acts as coactivator and transcription is activated

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18
Q

3 methods of growth through growth factors

A
  • mitogen activity
  • trophic factors
  • survival factors
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19
Q

mitogen activity

A

-stimulates mitosis and cell proliferation

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20
Q

trophic factors

A

-cell growth stimulation

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21
Q

survival factors

A

-inhibit programmed cell death (apoptosis)

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22
Q

pleiotropic GFs

A
  • different effects on same target cell type

- same effect on many different cell types

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23
Q

signaling abnormalities may lead to…

A

cancer

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24
Q

regulation of growth hormone (GH) release

A

-GHRH released from hypothalamus
-GH released from pituitary
-GH stimulates muscles, liver, fat (IGF-1 in liver)
Regulation:
-GH and IGF-1 inhibit GHRH release in hypothalamus
-somatostatin and IGF-1 inhibit pituitary release of GH

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25
Q

fibroblast growth factor (FGF) has how many receptors, and what kind are they?

A

4 FGFRs and they are all tyrosine kinase receptors

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26
Q

fibroblast growth factor receptor (FGFR) interacts with ________ and _______ in ECM –> ______ is formed –> induce __________ of cytoplasmic ________ kinase.

A
  • Heparan sulfate (HS)
  • glycosaminoglycans (GAGs)
  • DIMER
  • transphosphorylation
  • tyrosine
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27
Q

3 FGF signal transduction pathway results

A
  • cytoskeletal organization
  • anti-apoptosis
  • MAPKs
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28
Q

basophils are located in

A

circulation

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29
Q

_____ cells are stationary

A

mast cells

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30
Q

2 types of mast cells

A
  • mucosal mast cells (MMC)

- connective tissue mast cells (CTMC)

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31
Q

________ contain mediators

A

granules

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32
Q

4 mediators of granules

A
  • heparin
  • histamine
  • SRS-A (slow reacting substance of anaphylaxis)
  • ECF-A (eosinophil chemotactic factor A)
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33
Q

basophils and mast cells release 5 chemical mediators of immediate hypersensitivity

A
  • Histamine
  • Heparine
  • Prostaglandins
  • Thromboxanes
  • Leukotrienes
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34
Q

causes eosinophils to enter the area of worm infestation or allergen localization

A

eosinophil chemotactic factor (ECF)

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35
Q
  • bilobed nucleus
  • granules stain with acid dyes (eosin)
  • capable of killing microorganisms
A

eosinophils

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36
Q

mast cell degranulation process

A

-mast cells coated with IgE bound to FcR degranulate when allergen cross-links IgEs

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37
Q

histamine signaling process

A

after mast cell degranulation

  • histamine release
  • histamine binds to endothelial and smooth muscles H1 receptors (induces vasodilation)
  • at higher [histamine], acting on eosinophil H4 receptors (induction of migration/extravasation into affected area)
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38
Q

NO-mediated endothelial relaxation intercellular signaling molecules and general pathway

A
  • Ach, histamine, bradykinin, ATP

- cGMP dependent kinases activation –> relaxation

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39
Q

in mast cell activation, the cross linking of IgE by allergen initiates multiple signaling pathways including phosphorylation of ITAMS. These signaling pathways stimulate…

A
  • release of mast cell granule contents (amines, proteases)
  • synthesis of arachidonic acid metabolites (prostaglandins, leukotrienes)
  • synthesis of various cytokines
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40
Q

preformed mediators of type I hypersensitivity

A

from granule release:

  • histamine
  • heparin
  • ECF-A
  • neutrophil chemotactic factor
  • serotonin
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41
Q

newly synthesized mediators of type I hypersensitivity

A

from arachidonic acid:

  • prostaglandins (cyclooxygenase)
  • thromboxanes (cyclooxygenase)
  • leukotrienes (lipooxygenase) (SRS-A)
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42
Q

steps for synaptic transmission at neuromuscular junction

A
  • Ach release in synaptic cleft
  • binds ligand-gated ion channel
  • Na+ influx and depolarizes
  • action potential generated
  • muscle contraction
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43
Q

Role of acetylcholinesterase in the synaptic cleft

A
  • causes Ach to break down into acetate + choline
  • presynaptic cell takes up choline
  • to form Ach, AcCoA + choline which goes to vesicles
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44
Q

ErbB-induced signaling pathway

A
  • ligand binding
  • receptor dimerization
  • tyrosine kinase activation
  • pY tyrosine at COOH terminal tail of ErbB phosphorylation
  • reruitment (SH2 signaling effector or phosphotyrosine binding {PTB})
  • pY-peptide binding
  • to activated receptors
  • ErbB signaling pathways mainly RAS-MAPK
  • gene activation and transcription
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45
Q

structure of ErbB2, 3, &4 receptors

A
  • extracellular has 2 cysteine rich domains
  • transmembrane domain
  • cytoplasmic tyrosine kinase
  • heterodimerization (ErbB2 & ErbB3) or homodimerization (ErbB4 & ErbB4)
  • specificity for heparin binding epidermal growth factor (HB-EGF) and Neuregulin (NRG)
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46
Q

what happens when neuregulin-1 gene knocked out? ErbB2/ErbB4

A

no trabeculation

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47
Q

NRG-1 signals from _______ to ErbB2/ErbB4 heterodimers in the _________

A
  • endocardium

- myocardium

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48
Q

TGF is heavily involved in ________ development and differentiation

A

-embryonic

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49
Q

what kind of receptors do TGF-betas have

A

serine-threonine kinases

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50
Q

loss of the NRG-1 signal to the ErbB2/ErbB4 heterodimers leads to what?

A

defect in the development of the heart ventricles (defective trabeculation of ventricles)

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51
Q

TGF-beta family of signaling molecules (3)

A
  • TGF-beta
  • Bone morphogenetic protein (BMP)
  • Activin mesoderm induction
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52
Q

what is TGF-beta responsible for?

A

proliferation and differentiation of epithelial cells, hematopoietic

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53
Q

what is bone morphogenetic protein (BMP) responsible for?

A
  • organogenesis
  • cell induction
  • osteogenesis
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54
Q

what are the 2 TGF-beta receptor types?

A

TbetaR-I
TbetaR-II
-neither can bind TGF-beta on its own, they have both to build a complex with the ligand (TGF-beta) in order to transduce signals

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55
Q

BMP signal transduction pathway

A

2 pathways
1=signal transmitted via TAK1
-Smad protein pathway=intracellular proteins take signals to the nucleus and promote gene expression
2=MKK phosphorylates protein kinases which activate ATF2 which leads to gene activation

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56
Q

in TGFbeta receptor signaling, Smad pathway activates different gene programs than the _________ pathway

A

TAK1/MEKK1

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57
Q

TAK1/MEKK1 pathways activates 3 transcriptional effectors

A
  • c-Jun N-terminal kinase (JNK)
  • p38
  • mitogen activated protein kinase (MAPK)
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58
Q

which of the following is a proto-oncogene?

JNK, p38, MAPK

A

JNK

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59
Q

left-right symmetry is intitiated by _______

A

sweeping right –> left of potential effector molecules

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60
Q

in left right symmetry, cilia at the _____ play a role

A

node

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61
Q

in left right symmetry, _______ proteins are involved in the movement

A

kinesin

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62
Q

in left sided nodal expression, nodal is a _______ signaling molecule, so is lefty-2

A

TGF-beta like

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63
Q

signal transduction by nodal supports _______

A

leftness

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64
Q

Nodal induces

A

Lefty-1

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65
Q

when nodal induces left-1, it forms a _____ _______ for _______ determinants

A
  • midline barrier

- leftness

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66
Q

are nodal and lefty proteins agonists or antagonists?

A

antagonists

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67
Q

nodal and lefty proteins compete for binding with ______ receptor

A

ActR11

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68
Q

there are EGF-CFC _______ for both nodal and lefty

A

coreceptors

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69
Q

EGF-CFC coreceptors interact with ______ but NOT with ______

A
  • Alk4

- ActR11

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70
Q

nodal and lefty protein action pathway

A
  • nodal signal transduction
  • ActR11R
  • Smad + FAST transcription factors
  • move to nucleus
  • gene activation (Pitx2)
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71
Q

for nodal and lefty proteins, what happens if the lefty receptor binds?

A

no signal transduction

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72
Q

1st step in heart valve development

A

endothelial to mesenchymal transformation

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73
Q

2nd step in heart valve development

A

swelling of cardiac jelly and mesenchymal cells which forms a cushion

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74
Q

final step in heart valve development

A

tapering and thinning to form the valve

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75
Q

what happens when you delaminate endothelial cells?

A

they transform into mesenchymal cells

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76
Q

signaling in heart valve development (A or I)

-Notch –> Snail/slug

A

activation

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77
Q

signaling in heart valve development (A or I)

-TGFbeta –> BMP

A

activation

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78
Q

signaling in heart valve development (A or I)

-VEGF –> Wnt/beta-cat

A

inhibition

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79
Q

signaling in heart valve development (A or I)

-neurofibromin –> NFATc1

A

inhibition

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80
Q

Notch signaling (NOTCH1-NOTCH4) pathway

A
  • signaling pathway increases TGF-beta
  • increases transcription factor (snail or Slug) activity
  • down regulation or VE-cadherin
  • cell-cell adhesion down
  • delamination or endothelial cells
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81
Q

Notch signaling is ____ ___ signaling

A

endocardial autocrine

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82
Q

1st event of interatrial and interventricular septum formation

A

septation of the common atrial chamber

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83
Q

2nd event of interatrial and interventricular septum formation

A

septation of the ventricular chamber

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84
Q

3rd event of interatrial and interventricular septum formation

A

proliferation of the endocardial cushions

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85
Q

4th event of interatrial and interventricular septum formation

A

growth of the bulbar ridges that divide the bulbus cordis or outflow tract into the future aorta and pulmonary tract

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86
Q

zinc fingers are located on the _____

A

DNA binding domain

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87
Q

2 methods of heart growth

A
  • adaptive physiological hypertrophy

- maladaptive pathological hypertrophy

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88
Q

growth signals for adaptive physiological hypertrophy of the heart

A
  • exercise

- postnatal growth

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89
Q

growth signals for maladaptive pathological hypertrophy of the heart

A
  • hypertension

- myocardial infarction (heart attack)

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90
Q

the cell cycle is an ordered set of events, culminating in _______ and ______ into 2 daughter cells

A
  • cell growth

- division

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91
Q

phase of no action and no cell division

A

G0

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92
Q

preparative phase, making enzymes, proteins, etc for the actual cell division in mitosis

A

G2

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93
Q

4 phases of the cell cycle

A
  • G1
  • S
  • G2
  • M
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94
Q

what happens in S stage

A

DNA replication

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95
Q

what happens in M stage

A

mitosis

  • nuclear division (chromosomes separate)
  • cytoplasmic division (cytokinesis)
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96
Q

proteins that allow progression through CC (cell cycle)

A

cyclins

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97
Q

cyclins and ____ work closely together

A

CDKs

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98
Q

cyclins work at CC checkpoints by _____ and _______ of proteins which results in activation or deactivation of needed enzymes or other proteins

A
  • phosphorylation

- dephosphorylation

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99
Q

CC inhibitors

A
  • p53
  • p21
  • p27
  • pRB
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100
Q

binds cyclin to CDK blocking entry into S phase

A

p27

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101
Q

breast cancer prognosis is determined by ___ levels

A

p27

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102
Q

_____ levels of p27 predicts a poor outcome for breast cancer patients

A

reduced

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103
Q

G1 cyclin/CDK association

A
  • CyclinD-Cdk4
  • CyclinD-Cdk6
  • CyclinE-Cdk2
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104
Q

S cyclin/CDK association

A

CyclinE-Cdk2

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105
Q

G2 cyclin/CDK association

A

CyclinA-Cdk2

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106
Q

M cyclin/CDK association

A

CyclinB-Cdk1 (called Cdc2)

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107
Q

regulates G1/S and G2/M checkpoints

A

p53

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108
Q

p53 blocks the cell cycle if ________

A

DNA is damaged

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109
Q

severe damage to DNA leads to ____

A

apoptosis

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110
Q

p53 levels are _____ in damaged cells. this allows time for ______ by blocking the cell cycle.

A
  • increased

- DNA repair

111
Q

p53 is the most frequent mutation leading to ____

A

cancer

112
Q

mutated p53 is found in >___% of cancers

A

50%

113
Q

extreme case of p53 mutation

A

Li Fraumeni Syndrome

114
Q

Li Fraumeni Syndrome

A

genetic defect in p53 leads to a high frequency of cancer in affected individuals

115
Q

hypo pRB protein _____ gene transcription needed for transition from ___ phase to ___ phase

A
  • represses
  • G1
  • S
116
Q

pRB phosphorylation pathway

A
  • phosphorylation of Rb
  • breaking Rb-E2F complex
  • transcription of E2F responsive genes needed for DNA synthesis to proceed to S phase
117
Q

3 responses to genetic damage

A
  • DNA repair
  • CC arrest
  • apoptosis
118
Q

_____ phosphorylates CDK and allows progress from G2 to M

A

Cdc25C

119
Q

regulation problems and errors can lead to ___

A

cancer

  • due to faulty regulation of CC
  • loss of normal cell growth and behavior
120
Q

____ triggers progression through the cell cycle (G1 to S to G2 to M)

A

MPF (maturation promoting factor)

121
Q

extracellular growth signals influence ___ and ____ to form a complex. this complex leads to activation of E2F responsive genes via phosphorylation and deactivation of RB

A
  • cyclinD

- CDK4

122
Q

____ acts late in the cycle on CyclinE-CDK2 complex to inhibit movement on to S

A

p27

123
Q

quiescent state means

A

inactive state (G0)

124
Q

cells enter G0 phase from the _____ point in animal cells or ______ point in yeast

A
  • restriction

- start

125
Q

enter G0 in response to lack of ____ or ____

A
  • growth factors

- nutrients

126
Q

these cells enter G0 almost permanently

A

parenchymal cells of the liver and kidney

127
Q

what is a biochemical alternative for a damaged cell other than apoptosis

A

G0 phase

128
Q

____ are genes that code for proteins that regulate the cell cycle and control the growth of cells. only present in cancerous cells

A

oncogenes

129
Q

phase where the cell is preparing to replicate

A

G2

130
Q

phase where cell is dividing

A

M

131
Q

phase where DNA is replicated

A

S

132
Q

growth phase, occurs just after the cell has split

A

G1

133
Q

Nerve cells spend all of their time in ____ phase because they are unable to replicate

A

G0

134
Q

genes which have the potential to become oncogenes (cancerous)
-essentially very fragile and can become cancerous

A

protooncogenes

135
Q

protooncogenes can become cancerous due to several reasons (6)

A
  • over expression
  • under expression
  • mutation
  • inactivation
  • differing substrates
  • different affinity for substrate
136
Q

___ and ____ are protooncogenes

A

c-Jun

c-Myc

137
Q

c-Jun and c-Myc (protooncogenes) are active around the _____ stage and force the cell out of ___ phase.

A
  • G0/G1

- G0

138
Q

c-Jun and c-Myc are implicated in ______ and ______

A
  • T-Cell leukemias

- lymphomas

139
Q

unregulated cell cycle means

A

cancer

140
Q

5 phases of mitosis

A

-prophase
-prometaphase
-metaphase
-anaphase
-telophase
(interphase is technically not part of mitosis, it is G1, S, G2)

141
Q

this phase has a pair of centrioles present, chromosomes are not visible

A

interphase

142
Q

chromatin condensation, chromosomes are visible under microscope, nucleolus disappears, centrioles move to opposite poles of the cell

A

prophase

143
Q

nuclear membrane dissolves, creation of kinetochores, microtubules attach to kinetochores, chromosomes begin movement

A

prometaphase

144
Q

spindle fibers align chromosomes in middle of cell (metaphase plate), ensure correct separation of chromosomes and each nucleus receives one copy of each chromosome

A

metaphase

145
Q

separation of paired chromosomes at kinetochore, movement to opposite poles of cell

A

anaphase

146
Q

chromosomes arrive at opposite ends of cell, chromosomes disperse into chromatin, cytokinesis may begin

A

telophase

147
Q

cytokinesis splits the cell through the action of ___ and ____ filaments in the contractile ring

A
  • actin

- myosin

148
Q

cytokinesis in animal cells

A

fiber ring contracts pinching the cell into 2 daughter cells

149
Q

cytokinesis in plant cells

A

cell plate synthesis is required between 2 daughter cells

150
Q

metacentric chromosomes

A

short arm p and long arm q, short on top and long on bottom

-overall larger

151
Q

submetacentric chromosomes

A

very small short arm, medium long arm

152
Q

acrocentric chromosomes

A

extremes

  • short arm has stalk and a satellite at the end
  • long arm looks regular, but is just short
153
Q

how many pairs of chromosomes condense during mitosis

A

23 pairs

154
Q

____ stains regions of chromosomes that are rich in base pairs ___ and ____, producing a dark band

A
  • Giemsa dye
  • Adenine (A)
  • Thymine (T)
155
Q

normal male chromosome

A

46,XY

156
Q

normal female chromosome

A

46,XX

157
Q

female with trisomy 21 (down syndrome)

A

47,XX,+21

158
Q

male who is a mosaic of trisomy 21 cells and normal cells

A

47,XY,+21/46,XY

159
Q

male with distal deletion of the short arm of chromosome 4 band designated 14

A

46,XY,del(4)(p14)

160
Q

female with duplication of the short arm of chromosome 5

A

46,XX,dup(5p)

161
Q

a chromosome that has lost one of its arms and replaced it with an exact copy of the other arm

A

isochromosome

162
Q
  • translocation of CH 13 and 14
  • end to end fusion of the 2 chromosomes
  • normal phenotype
  • risks include abnormal child and spontaneous abortion
A

Robertsonian Translocation Karyotype

163
Q

FISH (chromosomal disorders test) can be used to test chromosomes for

A
  • additions

- deletions

164
Q

in FISH, the labelled probe hybridizes to chromosomes from these 3 phases

A
  • metaphase
  • prophase
  • interphase
165
Q
  • form of duplication using only mitosis
  • produces only genetically identical offspring
  • method of reproduction is rapid and effective allowing the spread of an organism
A

Asexual (vegetative) reproduction

166
Q

sexual reproduction is the formation of new individuals by a combination of 2 ____ sex cells (gametes)

A

haploid

167
Q

combination of genetic information from 2 separate cells that have 1/2 the original genetic information

A

fertilization

168
Q

female produces

A

egg

169
Q

male produces

A

sperm

170
Q

gametes are ___ with a single set of chromosomes

A

haploid

171
Q

individual with 2 sets of chromosomes (diploid)

A

zygote

172
Q

process to convert a diploid cell to a haploid gamete while causing a change in genetic information to increase diversity

A

meiosis

173
Q

DNA replication in a diploid cell (2N) cell preceded the start of ______

A

meiosis I

174
Q
  • dyad pairs alight to create tetrads (bivalents)

- non sister chromatids connect and trade sections at a chiasma

A

prophase I

175
Q

bivalent has ___ chromosomes and ____ chromatids

A
  • 2

- 4

176
Q

trading sections at a chiasma is called

A

crossing over

177
Q
  • nuclear membrane disappears
  • 1 kinetochore forms per chromosome rather than 1 per chromatid
  • spindle fibers attach to each dyad (2 chromosomes) at kinetochore
  • chromosomes attach to spindle fibers begin to move
A

prometaphase I

178
Q
  • bivalents align at metaphase plate
  • orientation is random (either parental homologue on a side)
  • 50-50 chance for daughter cells to get mothers or fathers homologue for each chromosome
A

metaphase I

179
Q
  • chiasmata separate
  • chromosomes each with 2 chromatids mocve to separate poles
  • each daughter cell is now haploid (23 chromosomes) but each has 2 chromatids
A

anaphase I

180
Q
  • cell pinching

- nuclear envelope may reform or cell may quickly start meiosis 2

A

telophase I

181
Q

cell splits

A

cytokinesis 1

182
Q

meiosis 2 is similar to _____

A

mitosis

-just no S phase which means no DNA replication in interphase 2

183
Q

in meiosis 2, chromatids of each chromosome are no longer indentical because of ____

A

recombination

184
Q

process where meiosis 2 separates the chromatids producing 4 haploid daughter cells each with 23 chromosomes, and each chromosome has only 1 chromatid

A

spermatogenesis

185
Q

process where 3 haploid nuclei form polar bodies and only one nucleus remains to make the nucleus of the egg

A

oogenesis

186
Q

one set of chromosomes

A

haploid (n)

187
Q

two sets of chromosomes

A

diploid (2n)

188
Q

are eggs and sperm haploid or diploid?

A

haploid (n)

189
Q

are most plant and animal cells haploid or diploid?

A

diploid (2n)

190
Q

___ is when cells have multiples of 23 chromosomes

  • called polyploid (triploidy 69Chr)
  • spontanous abortion of such conceptions
  • if born alive, dont survive long
A

euploidy

191
Q

result of meiotic disjunction

  • consist of trisomies (sometimes survive)
  • consist of monosomies (always lethal)
A

aneuploidy

192
Q

when 2 chromosome homologs migrate to the same daughter cell instead of disjoining and migrating to different daughter cells
-produces monosomic and trisomic offspring

A

meiotic nondisjunction

193
Q 
trisomy 21-autosomal aneuploidy
-most common surviving trisomy
-extra chromosome (maternal contribution 95%)
problems:
-mental retardation
-respiratory infections
-leukemia
-congenital heart defects
-GI tract obstruction
A

Down Syndrome

194
Q

some cell lines are normal, shows a milder phenotype
-condition in which an individual has 2 or more genetically distinct cell lines derived from a single zygote, but differing because of mutation or nondisjunction

A

mosaicism

195
Q

the prevalence of down syndrome _______ with age of the mother, especially after what age?

A
  • increases

- age 35

196
Q

45,X

A

turner syndrome

197
Q
  • characteristically broad “webbed” neck
  • reduced stature
  • poorly developed secondary sex characteristics
  • usually infertile because of gonadal dysgenesis
  • rarely undergo menarche
  • estrogen treatment
  • 30-40% mosaic, mostly 45,X/46,XX
A

turner syndrome

198
Q

cell death by acute injury, mechanical damage, lytic viral infection, toxic chemicals

A

necrosis

199
Q

programmed cell death, signals can be external or internal

A

apoptosis

200
Q

apoptosis plays a major role from ______ development to ________

A
  • embryonic

- senescence

201
Q

______ is evolutionarily conserved

A

apoptosis

202
Q

4 general steps of apoptosis

A
  • collapse of cell
  • protein degradation
  • DNA fragmentation
  • rapid engulfment by neighboring cells and phagocytes
203
Q

growth of organs is controlled by rate of:

  • ______
  • ______
  • ______
A
  • cell division (proliferation)
  • growth
  • death
204
Q

______ hormone induces morphogenetic events

A

thyroid

205
Q

in a mature organism, apoptosis is needed for normal _____ ______

A

tissue turnover

206
Q

______ undergoes apoptosis and by puberty, it is virtually gone

A

thymus

207
Q

place where t-cells are developed

A

thymus

208
Q

apoptosis is needed to destroy cells that pose a potential threat such as

  • cells infected with ____
  • self reactive immature __ or __ cells (prevents autoimmune reactions
  • cells with ____ damage
  • _____ cells
A
  • viruses
  • B or T cells
  • DNA
  • cancerous
209
Q

functional unresponsiveness

A

anergy

210
Q

_____ is the basic requirement for the immune system to work in order to not attack own cells

A

tolerance

211
Q

what makes a cell decide to commit suicide?

A
  • withdrawal of positive signals

- receiving negative signals

212
Q

3 examples of withdrawal of positive signals

A
  • growth factor for neurons
  • IL2 (T-cells)
  • loss of matrix adhesion
213
Q

3 examples of negative signals

A
  • increased levels of oxidants within the cell
  • DNA damage
  • death activators
214
Q

3 examples of death activators

A
  • tumor necrosis factor alpha (TNF-alpha)
  • lymphotoxin (TNF-beta)
  • Fas ligand (FasL)
215
Q

what type of signaling is th IL2 pathway?

A

autocrine

216
Q

IL2 synthesis is controlled by _____ signals

A

costimulatory

217
Q

CTLA-4 is a ______ homologue that is synthesized after activation of T-cells

A

CD28

218
Q

what happens when CTLA-4 ligates B7?

A

blocks activation signals so no more IL-2 is synthesized, leading to cell death

219
Q

CD28 + B7 = _____

A

T-cells active

220
Q

CTLA-4 + B7 = ______

A

apoptosis (IL2 synthesis blocked

221
Q

Necrosis or Apoptosis?

-cellular swelling

A

Necrosis

222
Q

Necrosis or Apoptosis?

-membranes remain intact

A

apoptosis

223
Q

Necrosis or Apoptosis?

-requires ATP

A

apoptosis

224
Q

Necrosis or Apoptosis?

-cell lyses, eliciting an inflammatory response

A

necrosis

225
Q

Necrosis or Apoptosis?

-ladder-like DNA fragmentation

A

apoptosis

226
Q

Necrosis or Apoptosis?

-ATP is depleted

A

necrosis

227
Q

Necrosis or Apoptosis?

-membranes are broken

A

necrosis

228
Q

Necrosis or Apoptosis?

-cellular condensation

A

apoptosis

229
Q

Necrosis or Apoptosis?

-in vivo, individual cells appear affected

A

apoptosis

230
Q

Necrosis or Apoptosis?

-in vivo, whole areas of the tissue are affected

A

necrosis

231
Q

Necrosis or Apoptosis?

-cell is phagocytosed, no tissue reaction

A

apoptosis

232
Q

Necrosis or Apoptosis?

-DNA fragmentation is random or smeared

A

necrosis

233
Q

_____ is a protrusion or bulge caused by cytoskeleton

A

blebbing

234
Q

results of apoptosis

A
  • prevent tumor formation

- homeostasis between cell death rate and mitosis rate

235
Q

results of necrosis

A

-inflammation

236
Q

6 morphological events of apoptosis

A
  • cell shrinkage
  • organelle reduction
  • mitochondrial leakage
  • chromatin condensation
  • nuclear fragmentation
  • membrane blebbing and changes
237
Q

during blebbing, cells break down into apoptotic bodies and are _____ by neighboring cells or _____

A
  • phagocytosed

- macrophages

238
Q

_____ are the central executioners of apoptosis

A

caspases

239
Q

caspases are a family of proteases that have a _____ at the active site and cleave their target proteins at specific _______

A
  • cysteine

- aspartic acid

240
Q

caspases are synthesized as ______ precursors called ______

A
  • inactive

- procaspases

241
Q

procaspases are usually activated by cleavage at aspartic acids by _______

A

other caspases

-results in amplifying proteolytic cascade

242
Q

initiator caspases

A
  • 8
  • 9
  • 10
  • 12
243
Q

effector caspases

A
  • 3
  • 6
  • 7
244
Q

pro-apoptotic stimulus

A

p53

245
Q

3 mechanisms of caspase activation

A
  • proteolytic cleavage (pro-caspase 3)
  • induced proximity (pro-caspase 8)
  • oligomerization (Cyt c, Apaf-1, caspase 9)
246
Q

caspase targets ICAD inhibitor of DNase –>

A

DNA fragmentation

247
Q

caspase targets nuclear lamins –>

A

fragmentation of nucleus

248
Q

caspase targets cytoskeletal proteins actin, myosin, alpha-actinin, tubulin, and vimentin –>

A

cell fragmentation and membrane blebbing

249
Q

caspase targets golgi matric proteins –>

A

fragmentation of the golgi

250
Q

ICAD

A

inhibitor of caspase activated DNase

251
Q

extrinsic apoptosis pathway

A
  • death ligands
  • death receptors
  • initiator caspase 8
  • effector caspase 3
  • apoptosis
252
Q

intrinsic apoptosis pathway

A
  • DNA damage and p53
  • (ROS-reactive oxygen species)
  • mitochondria/cytochrome C
  • initiator caspase 9
  • effector caspase 3
  • apoptosis
253
Q

the members of the BCL2 family regulate apoptosis at the _______ level

A

mitochondrial

254
Q

the BCL2 family is divided into 2 groups

A
  • anti-apoptotic

- pro-apoptotic

255
Q

BCL2 family proteins influence the _____ of the mitochondrial membrane

A

permeability

256
Q

BCL2 family anti-apoptotic proteins

A
  • Bcl-2

- Bcl-XL

257
Q

BCL2 family pro-apoptotic proteins

A
  • Bax
  • Bak
  • Bid
  • Bim
  • Bad
  • Noxa
  • Puma
258
Q

p53 induces apoptosis through transcriptional activation or ______ _____ such as puma, noxa, bax, and apaf-1

A

pro-apoptotic genes

259
Q

p53 can also directly induce apoptosis by localizing to mitochondria via interactions with BCL2 family protein ____ and facilitating ____ oligomerization

A
  • Bcl-XL

- Bax

260
Q

2 functions of p53

A
  • activate apoptosis

- inhibit factors that inhibit apoptosis

261
Q

is a nucleus required for apoptosis?

A

NO

262
Q

are ALL the proteins involved in apoptosis ALWAYS expressed?

A

YES

263
Q

4 inhibitors of apoptosis

A
  • antiapoptotic members of the BCL2 family
  • IAPs (inhibitors of apoptosis)
  • FLIP (FADD like inhibitory protein)
  • AKT
264
Q

FADD

A

Fas associated protein with death domain

265
Q

DISC

A

death inducing signaling complex

266
Q

homeostasis disorders occur when the _____ rate does not equal the _____ rate

A
  • proliferation

- apoptosis

267
Q

cell loss disorders

A
  • AIDS
  • neurodegradation
  • ischemic injuries
268
Q

cell accumulation disorders

A
  • autoimmunity
  • viral infections
  • cancer
269
Q

Systemic Lupus Erythematosus (SLE)

A
  • autoimmune disorder

- damages several organs from skin, to kidney, to lungs, etc.

270
Q

purpose of mitotic catastrophe

A
  • prevention of aneuploidy formation

- prevent oncogenesis

271
Q

main facotrs responsible for control of mitotic catastrophe

A
  • Cdk1 (M-cyclin)
  • p53
  • caspases
  • BCL2 family
272
Q

procaspases are activated by ___

A

cleavage

273
Q

active caspase consists of 2 _____ and 2 _____

A
  • large subunits

- small subunits

274
Q

once one caspase is activated, will more be activated, or will more be repressed?

A

more will be activated

Cell Biology (2 decks)

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