Bio230 Exam

Front 1

What are the purposes of membrane trafficking?

Back 1

To communicate with other cells and to acquire resources

Front 2

What are the three basic principles of the Biosynthetic-Secretory and Endocytic pathways?

Back 2

1. Polarized trafficking routes

2. Sorting stations

3. Retrieval mechanisms and general balance among routes

Front 3

True or false: both the regulated secretory pathway and the constitutive secretory pathway function in all cells

Back 3

False. The regulated pathway only functions in specialized cells

Front 4

For both of these pathways, how is a mature secretory vessel made?

Back 4

By retrieving Golgi components and concentrating cargo

Front 5

Until when are vesicles stored in the regulated pathway?

Back 5

A signal for docking and fusion is given

Front 6

True or false: regulated secretion provides extra plasma membrane when needed.

Back 6

True.

Front 7

Which of the following does not require extra membrane?

A. Phagocytosis

B. Exocytosis

C. Cleavage furrow

D. Wound

Back 7

B. Exocytosis

Front 8

Which pathway is the counterbalance for the secretory pathway?

Back 8

Endocytic

Front 9

What are the basic steps of endocytosis?

Back 9

Invagination, fission

Front 10

What are the three options for an endocytosed vesicle?

Back 10

Transcytosis, recycling, degradation

Front 11

True or false: recycling is carried out on the apical domain of plasma membrane

Back 11

False. It's carried out on the basal domain; transcytosis takes place on the apical

Front 12

Where does LDL bind?

Back 12

To an LDL receptor in a coated pit

Front 13

What happens after endocytosis?

Back 13

Uncoating of the vesicle and fusion to the early endosome

Front 14

True or false: the whole LDL + receptor unit is recycled

Back 14

False. Only the receptor is

Front 15

How can cells internalize pathogens?

Back 15

Phagocytosis

Front 16

Which organelle is an example of a multivesicular complex?

Back 16

Late endosome

Front 17

After the v-SNAREs and t-SNAREs have bound, what are the steps for fusion?

Back 17

Form stalk, hemifusion, fusion

Front 18

True or false: COPI is the primary driver of vesicle invagination events

Back 18

False. Clathrin is

Front 19

What is the structure of a triskelion?

Back 19

3 heavy and 3 light chains

Front 20

What drives fission events and when?

Back 20

Dynamin after vesicle invagination events

Front 21

Which complex drives budding events?

Back 21

ESCRT

Front 22

True or false: PI(3)P moves with the polyubiquitinated protein from ESCRT-0 all the way to ESCRT-3

Back 22

False. PI(3)P is bound to ESCRT-0 and ESCRT-II, while ESCRT-III is bound by PI(3,5)P; and it's a multiubiquitinated protein

Front 23

What does ESCRT-III do?

Back 23

Builds up borders and prevents proteins from diffusing out

Front 24

Virus particles found in the cytoplasm would need which machinery to leave the cell?

A. COPI

B. Dynamin

C. ESCRT

D. SNAREs

E. Clathrin

Back 24

C. ESCRT

Front 25

What is cargo regulated by?

Back 25

Signal sequences

Front 26

What is transport machinery regulated by?

Back 26

Signaling lipids (PIPs) and small GTPases

Front 27

True or false: a PI(5)P can have a phosphate added to the third carbon to form PI(3,5)P

Back 27

False.

Front 28

True or false: specific PIPs are found at distinct sites in the trafficking network and protein partners will be recruited to these sites

Back 28

True.

Front 29

True or false: GTPase bound to GDP must be phosphorylated to make the complex active

Back 29

False. GEF must help exchange GDP for GTP

Front 30

Where does Rab11 localize to?

Back 30

Recycling endosomes

Front 31

How about Rab5A?

Back 31

Plasma membrane, clathrin-coated vesicles, early endosomes

Front 32

Rab7?

Back 32

Late endosomes

Front 33

How Rab5 recruited to the membrane?

Back 33

1. Rab5-GEF exchanges Rab5-GDP

2. Active Rab5-GTP binds to the membrane with its lipid anchor

3. Rab and PI(3)P work together

Front 34

Microtubules are inherently ___________.

Back 34

Polarized

Front 35

Each protofilament is made ofheterodimers of the monomericproteins ___________ & ____________.

Back 35

a-tubulin and b-tubulin

Front 36

True or false: tubulin monomers bind and hydrolyze ATP

Back 36

False. GTP

Front 37

How many filaments make up one microtubule?

Back 37

13

Front 38

What does gamma tubulin do?

Back 38

Nucleates microtubules at the minus end

Front 39

Plus ends grow (FROM/TO) nucleation sites

Back 39

From

Front 40

What is dynamic instability?

Back 40

How microtubules switch between growing and shrinking to search the full 3D space of the cytoplasm

Front 41

Growing microtubules have a protective cap of __________.

Back 41

GTP-bound tubulin

Front 42

True or false: if the GTP cap is lost, growth can never be started again.

Back 42

False. If it is regained, growth is resumed

Front 43

In general, to which ends of the microtubule do Dynein and Kinesin move?

Back 43

Minus and plus, respectively

Front 44

What motor is likely key for Golgi positioning?

A. Kinesin

B. Dynein

Back 44

B. Dynein

Front 45

When cAMP levels are decreased in male cichlids, what happens to the melanosomes?

Back 45

Kinesin is inhibited and Dynein aggregates the melanosomes to the centre

Front 46

True or false: actin binds and hydrolyzes GTP

Back 46

False. ATP

Front 47

True or false: actin is a monomer like microtubules

Back 47

False. Microtubules are heterodimers

Front 48

What happens when the rate of addition of Actin-ATP is faster than rate of removal ofActin-ADP?

Back 48

A relatively stable "cap" of Actin-ATP subunits can be formed

Front 49

What causes the treadmilling of actin?

Back 49

The ATP-ADP polarity

Front 50

What does the ARP complex do?

Back 50

Nucleates actin filaments and branches them to form 2D networks

Front 51

What protein chops the network to initiate dissociation?

Back 51

Cofilin

Front 52

What do these networks drive?

Back 52

Polarized cell movement

Front 53

What creates protrusive machines?

Back 53

LArge regions of anchored actin networks

Front 54

Integrins

Back 54

Connect the actin cytoskeleton to extracellular matrix molecules

Front 55

What makes up the integrin?

Back 55

a- and b-subunits

Front 56

What acts as an anchor within the cell?

Back 56

Vinculin and talin

Front 57

How is the actin cytoskeleton directed to follow a target?

Back 57

Chemoattractant receptors orient the actin networks

Front 58

When there are chemoattractants present, where will treadmilling be activated?

Back 58

Where the highest concentration activates the most receptors

Front 59

True or false: in epithelial tissue, mechanical stress is supported between cells by cytoskeletal filaments anchored to the matrix and adhesion sites

Back 59

False. The stresses are transmitted from cell to cell

Front 60

The extracellular matrix (DIRECTLY/INDIRECTLY) bears mechanical stress

Back 60

Directly

Front 61

Where is the epithelial tissue located?

Back 61

Lines tissues, surfaces, surrounds organs

Front 62

True or false: connective tissue cells are spread out.

Back 62

True.

Front 63

What are epithelial cells directly connected to beneath?

Back 63

Minimal extracellular matrix

Front 64

What provides the overall structure in connective tissue?

Back 64

Extracellular matrix

Front 65

Connective tissue cells include _________, ___________, and __________.

Back 65

Muscle cells, neurons, immune cells

Front 66

Epithelia are critical for organ ___________ and __________.

Back 66

Structure and function

Front 67

In apical to basal order, name the junctional complexes of the epithelial cell.

Back 67

Tight, adherens, desmosome, gap junction

Front 68

Tight junctions

Back 68

Seals the gap between epithelial cells

Front 69

Adherens junction

Back 69

Connects actin filament bundle in one cell to that of the next cell

Front 70

Desmosome

Back 70

Connects intermediate filaments between cells

Front 71

Gap junction

Back 71

Allows the passage of small water-soluble molecules from cell to cell

Front 72

Hemidesmosome

Back 72

Anchors actin filaments to extracellular matrix

Front 73

What anchors actin filaments to extracellular matrix?

Back 73

Actin-linked cell matrix adhesion

Front 74

What is critical to adhering cells to form epithelia?

Back 74

Strong continuous adhesion belts

Front 75

Tight junctions are made up of ________ proteins while adherins are made up of __________.

Back 75

Claudin, cadherin

Front 76

True or false: cadherins are membrane proteins

Back 76

False. Transmembrane

Front 77

What are the two ways through which cadherin clusters mediate adhesion

Back 77

Homophilic interactions between cadherin receptors and links to the actin cytoskeleton

Front 78

True or false: the C terminus of cadherin is on the inside of the cell

Back 78

True.

Front 79

What happens if there are no adherens junctions?

Back 79

Tissue structure is lost

Front 80

Cadherins are __________ suppressors and the loss epithelial structure is a hallmark of ________.

Back 80

Tumour, cancer

Front 81

True or false: the basal side of an epithelial cell faces the organ lumen while the apical side faces the underlying tissue

Back 81

False. The opposite

Front 82

How does the Na+ driven glucose symport work?

Back 82

Move glucose from low concentration from lumen to high in the cell; need energy so sodium moves from high to low

Front 83

What would happen if tight junctions were removed?

Back 83

Glucose would freely diffuse between cells and there wouldn't be enough in them

Front 84

Tight junctions are formed from interacting strands of _____________ proteins

Back 84

Transmembrane

Front 85

Claudin is a ___-pass transmembrane _________ essential for _______ junction function.

Back 85

4, protein, tight

Front 86

Occludin is a ___-pass transmembrane ___________ needed for ___________ function

Back 86

4, receptor, barrier

Front 87

True or false: claudin and occludin cross both layers of the lipid bilayer

Back 87

True.

Front 88

If occludin were removed, what would happen to the structure of the tight junctions?

Back 88

Not much.

Front 89

In C. elegans, what does the sperm entry point act as?

Back 89

A primary landmark.

Front 90

Primary landmark

Back 90

Used to establish polarity; signals specific structure elaboration

Front 91

Anterior and poster cues form a:

A. Positive feedback loop

B. Negative feedback loop

C. Flip flop device

Back 91

C. Flip-flop device

Front 92

____________ junctions are important landmarks for epithelial polarity.

Back 92

Adherens

Front 93

Which three proteins act as adherens anchors?

Back 93

Arm, a-cat, actin

Front 94

List, in order, the structures made in constructing epithelial polarity.

Back 94

1. Apical cue (anchor and actin)

2. Scribble complex forms

3. Tight junction forms

4. Crumbs complex & Par-etc.

Front 95

Morphogenesis

Back 95

The generation of tissue shapes that form organs and bodies

Front 96

Cell differentiation

Back 96

The generation of different types of cells in tissues

Front 97

In adults, multicellular development will occur continually from _______ cells.

Back 97

Stem

Front 98

How long does epithelial migration from the bottom of the crypt to the top of the villus in the gut take?

Back 98

3-5 days

Front 99

True or false: non-dividing differentiated Paneth cells of the crypt are stem cells.

Back 99

False.

Front 100

What is the purpose of slowly-dividing stem cells?

Back 100

To provide support to the crypt

Front 101

What do embryogenesis, embryogenesis, organogenesis,and stem cell development share?

Back 101

Commonmechanisms of morphogenesis and celldifferentiation.

Front 102

Zona pelucida

Back 102

A jelly-like capsule that houses the pronuclei and the polar body

Front 103

True or false: the polar body is non-viable and will be destroyed

Back 103

True.

Front 104

At 2 1/2 days, the fertilized egg has ___ cells and is called the __________.

Back 104

8, morula

Front 105

Trophectoderms line the blastocyst and will eventually become _______________ tissue.

Back 105

Extra-embryonic

Front 106

What three things does morphogenesis require?

Back 106

Internalization of the cells, elongation of the embryo, fine repositioning of the cells

Front 107

Internalization of the cell during _____________ creates the main three germ layers

Back 107

Gastrulation

Front 108

Name the stages of gastrulation

Back 108

1. Cells start crawling into the inner cavity and become mesoderm cells

2. The endoderm begins to invaginate

3. The ectoderm is on the outside

Front 109

Which tissues, respectively, do the ectoderm, endoderm, and mesoderm form?

Back 109

Epidermis/nervous system; gut/lung/liver; muscles/connective tissue/blood vessels

Front 110

What is ingression/delamination?

Back 110

A method for cell internalization that involves individual cells separating from the early outer epithelium; epithelial-mesenchymal transition

Front 111

Why are epithelial-to-mesenchymal transitionsdangerous during cancer progression?

Back 111

They can cause benign tumours to metastasize by escaping from the epithelium

Front 112

If a chunk of somites were transplanted from a chicken embryo limb to a quail, what would happen?

Back 112

Epithelial-to-mesenchymal transitions are tightly regulated so the limb would still form but with a mixture of chicken and quail muscle cells

Front 113

What is invagination/involution?

Back 113

When intact epithelial sheets move inside the embryo

Front 114

What changes are required for this process?

Back 114

Microtubules elongate to make columnar cells, apical actin bundles contract to narrow cells' apices

Front 115

Name a developmental example of this process

Back 115

Neural tube development from ectoderm in vertebrates

Front 116

Which TF specifies the cells to undergo mesoderm internalizationin Drosophila?

Back 116

Twist

Front 117

Name the two mechanisms of embryo elongation

Back 117

Cell division and cell shape change; convergent extension

Front 118

How does convergent extension work?

Back 118

Lamellopodia crawl on cells, forcing them to converge and then stretch out

Front 119

True or false: the direction of movement is unregulated

Back 119

False. It's regulated

Front 120

How is the orientation of cell elongation regulated in cell division and shape change?

Back 120

The orientation of cellulose microfibrils and driven by turgor pressure

Front 121

Name the two mechanisms of cell positioning

Back 121

Cell sorting; directed cell migration

Front 122

When cells of the three early germ layers are dissociatedand randomly mixed, the individual cell types re-associateand re-form the germ layers. How?

Back 122

The homophilic adhesion between cadherins may group specific cells together

Front 123

True or false: first-born neurons are deeper in the cortex than last-born

Back 123

True.

Front 124

What kind of cells direct dividing progenitor cells?

Back 124

Radial glial cells

Front 125

How does directed cell migration in the cerebral cortex work?

Back 125

DP cells divide, glial cells get longer; DP moves up and implants in the layer of cortical neurons

Front 126

Where else is directed cell migration required in the nervous system?

Back 126

Axon pathfinding

Front 127

What will the commisural neuron eventually become?

Back 127

The spinal cord

Front 128

True or false: axon pathfinding in the neural tube goes from the floor plate to the roof plate

Back 128

False. Vice versa

Front 129

What is the commisural neuron attracted to, and what are the receptors?

Back 129

Netrin; DCC netrin receptor

Front 130

What is the Slit receptor?

Back 130

Roundabout

Front 131

What is the other repellant?

Back 131

Semaphorin

Front 132

What happens if Slit is removed from the system?

Back 132

It won't bind to the Roundabout receptor so the neuron will not grow toward the brain without the repellant

Front 133

What are the two main mechanisms of cell differentiation?

Back 133

Asymmetric and symmetric division

Front 134

True or false: asymmetric division is when the cells become differentiated by external forces after birth

Back 134

False. Specific proteins/combos go to one side of the cell before the split

Front 135

Direct lateral inhibition

Back 135

Cells begin as all the same but some randomly gain an advantage and become differentiated while inhibiting their neighbours from doing the same

Front 136

The Delta-Notch system is an example of what and how does it work?

Back 136

Lateral inhibition; warring cells until one manages to inactivate Notch to activate Delta and become specialized

Front 137

True or false: if Notch is turned off, the cell will specialize

Back 137

True.

Front 138

Name the three mechanisms for extrinsic cell differentiation

Back 138

Direct lateral inhibition, induction by diffusible signals, regulatory hierarchies

Front 139

Why don't humans sprout wings?

Back 139

Hox genes encode transcription factors with different targets in different species

Front 140

True or false: cells of the auditory hairs regenerate

Back 140

False.

Front 141

What initiates a nerve impulse on these hair cells?

Back 141

When the hair bundle tilts to open the ion channel

Front 142

What is another type of permanent cells with specific architecture?

Back 142

Human photoreceptors

Front 143

True or false: bone is degraded by osteoclasts and deposited by osteoblasts

Back 143

True

Front 144

How are the fates o stem cell daughters controlled?

Back 144

Either through divisional asymmetry or environmental asymmetry

Front 145

What is the difference between these?

Back 145

Divisional gets factors that promote stemness and original numbers cannot be restored

Front 146

Stem cells divide (SLOWLY/QUICKLY)

Back 146

Slowly

Front 147

Why do they divide slowly?

Back 147

Protects from mutation and telomere depletion

Front 148

Transit amplifying cells

Back 148

Expand cell numbers before final differentiation

Front 149

The basal lamina provides a _______ for stem cells; from there, the cells ____________ through a linear sequence of cell types.

Back 149

Niche, differentiate

Front 150

Multipotent hemopoietic stem cells differentiate into ______________ and then common ____________ _____________ and ____________ ____________.

Back 150

Multipotent hemopoietic progenitors, lymphoid progenitors, myeloid progenitors

Front 151

In fluorescence-activated cell sorting (FACS), the cells suitable for bone marrow transplant will carry a __________ charge.

Back 151

Negative

Front 152

When a stem cell is to remain a stem cell, what does it bind to?

Back 152

The Kit ligand on the stem cell binds to the Kit receptor on the stromal cell; if it doesn't, it becomes a transit amplifying cell and either differentiates or dies

Front 153

What are the two ways of avoiding immune rejection of embryonic stem cells?

Back 153

Somatic cell nuclear transfer and treating some of the patient’s own cells with a factor known to specify ES cell character(e.g. a combination of Oct3/4, Sox2, Myc and Klf4 can convert differentiated cellsinto cells with ES cell characteristics)

Front 154

Receptor tyrosine kinases

Back 154

Enzyme-coupled receptors used in signalling

Front 155

What do RTKs bind?

Back 155

Secreted or cell surface proteins

Front 156

The RTK domain is in the ___________ of the cell

Back 156

Cytosol

Front 157

Signalling molecules induce the ___________________ of RTKs

Back 157

Transautophosphorylation

Front 158

How does transautophosphorylation work?

Back 158

Ligand binding dimerizes the receptor and the kinase domains are brought together and phosphorylate each other

Front 159

If a receptor tyrosine kinases with a defective kinase domain was expressed together with the normal receptor what would happen?

Back 159

The cell would have no response to the signal (dominant negative mutation)

Front 160

The proteins recruited by RTK have either _____ or ______ domains that bind to ____________ and neighbouring sequences

Back 160

SH2, PTB, phosphotyrosine

Front 161

R7

Back 161

The photoreceptor in Drosophila needed to detect UV light

Front 162

What are the steps in the Sevenless pathway?

Back 162

Boss in the R8 cell is the ligand for Sev RTK; the binding of this ligand activates Sev, then Drk links Sevenless to Sos (Ras-GEF), which activates the Ras protein and downstream signals.

Front 163

True or false: a mutation at any of these steps would cause the fly to become Sevenless

Back 163

True.

Front 164

Ras

Back 164

A monomeric GTPase that is a molecular switch downstream of RTK that leads to cell proliferation or differentiation; in its hyperactive mutant form, it is responsible for 1/3 of human tumours

Front 165

Active Ras activates MAP kinase kinase kinase, and then what?

Back 165

The cascade is phosphorylated (MAP kinase x2 and MAP kinase) until the effector proteins are phosphorylated

Front 166

How is non-specific cross-talk controlled in yeast?

Back 166

Scaffolds bind to specific MAP kinase modules to insulate them

Front 167

Tyrosine kinase-associated receptors are similar to RTKs, but how do they differ?

Back 167

They interact non-covalently with cytoplasmic tyrosine kinase

Front 168

Receptor __________________ kinases are the largest class of cell surface receptors in plants

Back 168

Serine/threonine

Front 169

___________ signaling stimulatesthe development ofstems, leaves and flowers

Back 169

Clv1/Clv2

Front 170

True or false: Clv1 and Clv2 get phosphorylated by Clv3

Back 170

False. Clv1 phosphorylates itself and Clv2

Front 171

True or false: histidine-kinase-associated receptors are used by all living things

Back 171

False. They are not used by animals

Front 172

CheA

Back 172

The histidine kinase that phosphorylates itself on a histidine and transfers the phosphate to an aspartic acid on CheY

Front 173

If a repellent binds to the chemotaxis receptor in a bacteria but the bacteria is not supposed to tumble, what happens?

Back 173

CheZ will remove the phosphate on CheY to stop the tumbling

Front 174

Choose the correct statement:

A. Notch is processed in the extracellular space and cut into two fragments

B. The Notch fragment Delta binds to is discarded

C. The Notch tail migrates to the nucleus and activates gene transcription

Back 174

C. It does and inhibits cell specialization

Front 175

If hedgehog signaling were inhibited, what would happen?

Back 175

The transcriptional activator, Ci, would be sequestered in the cytoplasm, phosphorylated, cleaved and put in a complex with a repressor, and transferred to the nucleus were it would inhibit Hh gene transcription. At the same time, Patched would sequester Smoothened in vesicles since nothing would be bound to iHog (Hh receptor)

Front 176

What happens when Hedgehog is on?

Back 176

Patched transfers Smoothened to the plasma membrane where it releases Ci from the inhibitory complex

Front 177

Name the four parts of the cell cycle

Back 177

G1 (cell growth and partial doubling of organelles), S phase (DNA replication), G2, M phase (mitosis and cytokinesis)

Front 178

Cdks

Back 178

Cyclin-dependent kinases; the traffic lights of the cell cycle

Front 179

What two things are required for a Cdk to become active (i.e. to give the "green light" for a checkpoint?)

Back 179

Cyclin and an activating phosphate

Front 180

True or false: the same type of cyclin-Cdk checkpoint can be used at multiple points of the cell cycle

Back 180

False. There are many different cyclins that bind at different points

Front 181

Explain how Cdk becomes fully activated.

Back 181

Cyclin binds to the T-loop on Cdk to make it partially active, and then a phosphate attaches to the active site of the T-loop to make it fully active

Front 182

S-Cdk

Back 182

Activity inhibits an inhibitor of the origin recognition complex to promote DNA replication

Front 183

M-Cdk

Back 183

Phosphorylates (with ATP) multiple targets required to start mitosis

Front 184

What turns Cdks off?

Back 184

Targeted degradation of cyclin

Front 185

APC

Back 185

Anaphase promoting complex; targets M-cyclin to the proteasome for the completion of mitosis

Front 186

p27

Back 186

A Cdk inhibitor protein (CKI); clamps onto cyclin A or cyclin E of Cdk2 to render it inactive

Front 187

Wee1 kinase

Back 187

Adds inhibitory phosphate to Cdk

Front 188

Cdc25 phosphotase

Back 188

Removes the inhibitory phosphate

Front 189

Rb

Back 189

Blocks G1 progression and S phase by inhibiting cyclin synthesis

Front 190

How does Rb do this?

Back 190

By clamping around E2F

Front 191

What is the inactive state of Rb?

Back 191

When it has two phosphate groups

Front 192

Loss of both copies of the Rb gene leads to _____ ___________ since it is a ________ ____________ gene.

Back 192

Eye cancer, tumor suppressor

Front 193

Mitogen

Back 193

Substance that encourages mitosis

Front 194

What induces Myc transcription?

Back 194

Mitogen signaling via a Ras-MAP kinase signaling cascade

Front 195

Myc

Back 195

Increases cyclin synthesis and CKI degradation by regulating transcription

Front 196

What happens when there is too much Myc present?

Back 196

Too much replication

Front 197

Myc is:

A. Oncogene

B. Tumor suppressor

Back 197

A. Oncogene

Front 198

What adds the activating phosphate to Cdk?

Back 198

CAK

Front 199

What initially activates Cdc25?

Back 199

The phosphorylation of M-Cdk

Front 200

What kind of feedback loop is it when active M-Cdk inhibits Wee1?

Back 200

Positive feedback since it is also promoting phosphorylation by Cdc25

Front 201

p53

Back 201

Stops the cell cycle in response to damage

Front 202

What happens when p53 gets phosphorylated?

Back 202

Mdm2 detaches and active p53 activates transcription of p21

Front 203

p21

Back 203

Cdk inhibitor protein

Front 204

p53 is

A. Oncogene

B. Tumor suppressor

Back 204

B. Tumor suppressor

Front 205

Caspase

Back 205

Cysteine proteases that cleave target proteins at specific aspartic acid residues and trigger apoptosis

Front 206

How are caspases activated?

Back 206

Inactive procaspases are cleaved at two sites; the prodomains are degraded and the small subunits of two bind to create an active caspase

Front 207

True or false: caspase 8 is an executioner caspase

Back 207

False. Caspase 3 is; caspases 8, 9, and 10 are initiator caspases

Front 208

True or false: a Fas receptor is an extrinsic signal for a caspase cascade.

Back 208

True.

Front 209

How does Fas work?

Back 209

The ligand on the killer lymphocyte binds to the Fas death receptor; FADD and the procaspase attach to form the DISC; procaspase 8/10 is cleaved to form caspase and the cascade is activated; apoptosis is triggered

Front 210

How is apoptosis triggered intrinsically?

Back 210

Apoptotic stiumulus leads to the release of cytochrome c from the mitochondria, which attaches to Apaf1; this oligomerizes and recruits procaspase 9, which cleaves and recruits executioner caspases

Front 211

True or false: caspase 8 and 9 are used for extrinsic apoptosis signaling

Back 211

False. 8 and 10 are used for extrinsic.

Front 212

How do healthy cells avoid cell death?

Back 212

They create lots of decoy receptors that bind the Fas ligand but don't contain death domains (extrinsic) or they mimic initiator caspases without a proteolytic domain

Front 213

Bcl2

Back 213

Inhibits channel formation in the outer mitochondrial membrane

Front 214

What happens when there is too much Bcl2?

Back 214

Inactivates BH123 and does not allow the release of cytochrome c so may lead to cancer since there would be no cell death

Front 215

IAPs

Back 215

(Inhibitors of apoptosis) block caspase activity in the cytoplasm when procaspases accidentally bump into each other

Front 216

If apoptosis is supposed to happen but IAPs are present, what happens?

Back 216

Anti-IAPs will bind the IAPs and allow the caspases to do their jobs

Front 217

Name three examples of survival factors that would block apoptosis

Back 217

Activated gene regulatory protein transcribes lots of Bcl2; Akt kinase inactivates Bad; MAP-kinase inactivates Hid which normally inhibits IAPs

Front 218

True or false: tumor cells will have a mixture of which X chromosome is inactivated

Back 218

False. All cells will have the same one inactivated

Front 219

Carcinoma

Back 219

Epithelial cell cancers

Front 220

What is the difference between a benign and a malignant tumor?

Back 220

Benign tumors are contained whereas malignant tumors invade the surrounding tissue.

Front 221

How do cancer cells usually invade other parts of the body?

Back 221

Blood vessels or lymphatic vessels

Front 222

What is the Ames Test and how does it work?

Back 222

Tests whether a chemical is a mutagen; mix the test compound and a culture of histidine-dependent Salmonella on an agar plate without histidine and if the culture grows, the compound is a mutagen

Front 223

True or false: oncogenes are gain of function mutations

Back 223

True

Front 224

True or false: p53 and Rb are oncogenes

Back 224

False. They are tumor suppressors and their loss of function can lead to cancer

Front 225

True or false: tumor suppressor genes are dominant

Back 225

False. Recessive

Front 226

How are oncogenes produced?

Back 226

Proto-oncogenes undergo a mutation or gene amplification or chromosome rearrangement

Front 227

When polarity is lost, metastases ___________.

Back 227

Increase

Front 228

What does Gleevec target and how does it work?

Back 228

The Bcr-Abl protein; binds where ATP normally would and stops phosphate signal for cell proliferation and leukemia

Front 229

What are the two ways from which cells receive signals?

Back 229

Cell-surface and intracellular receptors

Front 230

What is the main difference between these?

Back 230

Cell-surface signals must be hydrophilic whereas intracellulars ones must be hydrophobic

Front 231

Contact-dependent signaling

Back 231

Signals are retained on the cell surface and occurs over short distances

Front 232

Paracrine signaling

Back 232

Signals are released from cells but act locally; movement is restricted

Front 233

Synaptic signalling

Back 233

Neurons extend axons to contact distant targets

Front 234

Endocrine signaling

Back 234

Endocrine cells secrete hormones into the bloodstream for long-range distribution

Front 235

Signal transduction

Back 235

The conversion of extracellular signals into intracellular signals; signal creates a signaling cascade that goes down to the effector proteins

Front 236

Second messengers

Back 236

Small intracellular signalling molecules that bind and alter effector proteins

Front 237

What are the potential steps of the signal transduction pathway?

Back 237

Extracellular signal, scaffold, relay, transduce and amplify, integrate (coincidence detector), spread, anchor, modulate, effector protein activation

Front 238

SH2 and PTB bind ________________-containing sequences

Back 238

Phosphotyrosine

Front 239

PH domains bind _______________

Back 239

Phosphoinositides

Front 240

SH3 domains bind _____________-rich sequences

Back 240

Proline

Front 241

What is the difference between synaptic and endocrine signaling specificity?

Back 241

The same synaptic signaling molecules can be used in all connections (target-specific) whereas the receptors on the target cells are different for the endocrine pathway.

Front 242

What prevents an upstream signal from activating all of the pathways?

Back 242

A scaffold; either a designated scaffold, a phosphorylated receptor scaffold, or a PI docking site scaffold

Front 243

Coincidence detector

Back 243

Only activate downstream signals when two upstream signals are both detected

Front 244

Biphasic switches promote _______________.

Back 244

Differentiation

Front 245

The circadian rhythm is an example of a __________ feedback loop with a ________ delay.

Back 245

Negative, long

Front 246

True or false: nuclear receptors are always in the nucleus

Back 246

False. They can be in the cytosol, but once they bind to a signalling molecule, they go to the nucleus

Front 247

Orphan nuclear receptors

Back 247

Part of the nuclear receptor superfamily but their ligands are unknown

Front 248

True or false: the ligand-binding domain of a receptor is closer to the C terminus

Back 248

True.

Front 249

True or false: ion channel transport is active

Back 249

False. Passive

Front 250

Na levels are _______ within the cell, while K levels are ______.

Back 250

Low, high.

Front 251

The cell must contain _________ amounts of positive to negative charges

Back 251

Equal

Front 252

What are the three states of a voltage-gated channel?

Back 252

Open, closed, and inactivated

Front 253

How do chemical synapses transmit signals?

Back 253

Synaptic vesicles release neurotransmitters that open ligand-gated ion channels that then depolarize and allow electrical signals to pass through

Front 254

GPCR

Back 254

G-protein coupled receptors are 7 pass transmembrane proteins that respond to proteins, small molecules, and light

Front 255

What are the components of a G-protein and what binds to it?

Back 255

Alpha, beta, gamma; GTP/GDP binds the alpha subunit

Front 256

GPCRs signal into the ______________.

Back 256

Cytoplasm

Front 257

How does this path get turned on and off?

Back 257

GPCR is activated by a small extracellular signal and acts as a GEF on the G-protein and the altered subunits bind downstream proteins. The system is turned off by RGS which acts as a GAP

Front 258

Why do dogs have a better sense of smell than humans?

Back 258

They have more types of GPCRs and so can recognize many different odourants

Front 259

IP3 is a hydro_______ molecule that diffuses through the __________while DAG is a hydro________ molecule that diffuses _______ the ________ ____________.

Back 259

Hydrophilic, cytoplasm, hydrophobic, plasma membrane

Front 260

How does GPCR signal via calcium?

Back 260

GPCR activates production of IP3 and DAG; IP3 goes to the ER and acts as a channel ligand to release Ca and activate protein kinase C