TJ Guide 3

Question 1

What is the dose limiting factor in microtubule inhibiting drugs?

Answer 1

Peripheral neuropathy, can be permanent

Question 2

What is an example of a folate antagonist?

Answer 2

methotrexate

Note: This drug is needed in very high concentrations to inhibit tetrahydrofolate production

Question 3

Antimetabolites terminate DNA production by impersonating real nucleotides. What other enzymes might be inhibited by these antimetabolites and when is this drug most cytotoxic?

Answer 3

RNA reductase
DNA polymerase
DNA ligase
DNA exonuclease

S-phase

Question 4

How does p53 work?

Answer 4

1. Induces p21 (CDK inhibitor) which keeps cell in G-phase

2. Causes cell death

Question 5

What is deleted in cancer that causes degration of p53?

Answer 5

p19/ARF is deleted which in a normal cells keeps MDM2 from degrading p53

Question 6

What is the idea behind alkylating agents?

Answer 6

cause so much crosslinking damage to DNA that that repair systems cant keep up and it can’t conform to the normal structure, preventing RNA synthesis and leading to eventual cell death

Question 7

How do HDAC inhibitors act as anticancer drugs?

Answer 7

They inhibit HDAC which puts acetyl groups on lysine which reduces the +/- attraction of histones to DNA. Loosening of DNA leads to increased transcription. THE MAIN IDEA IS THAT THINGS LIKE P53 WILL GET ACTIVATED AGAIN SO THEY CAN PROGRAM CELL DEATH

Question 8

Why do physicians usually do a CBC before giving chemo drugs?

Answer 8

myelosuppression is usually the dose limiting factor and they want to make sure patients have enough immune cells

Question 9

T or F: Both topoisomerase inhibitors and antimetabolites are cell cycle specific

Answer 9

False, topoisomerases are independent of cell cycle

Question 10

What steps are involved in synaptic signal transmission?

Answer 10

1. Ca2+ channels open in response to AP
2. Ca2+ triggers synapsin kinase to phosphorylate synapsin I
3. Synapsin I triggers the vesicle to bind to the presynaptic terminal
4. Receptors get signal and non-voltage gated Na+/K+ channels open and a graded depolariztion occurs
5. If strong enough an AP is triggered

Question 11

In the event that a neurotransmitter opens a K+ channel will it cause an IPSP or an EPSP?

Answer 11

IPSP - K+ will rush out down its concentration gradient

Question 12

What channel is likely triggered in an EPSP?

Answer 12

a non-specific Na+/K+ channel

Question 13

What two neurotransmitters commonly cause IPSPs?

Answer 13

glycine and GABA

Question 14

What is the result of too many or too few D2 receptors?

Answer 14

Too much D2 = schizophrenia

Too little D2 = parkinsons

Question 15

What type of cholinergic receptor leads to IPSPs in the heart?

Answer 15

muscarinic

Question 16

What are the types of transmitter used at amino acid synapses?

Answer 16

GABA, Glycine –> typically IPSPs

Glutamate, aspartate —> typically EPSPs

Question 17

angiotensin, Substance P, and oxytocin are examples of…

Answer 17

Neuroactive Peptides

Question 18

What is thymosin?

Answer 18

prevents assembly of actin monomers into actin filaments

Question 19

What is profilin?

Answer 19

promotes assembly of actin monomers into filaments?

Question 20

What are formins?

Answer 20

drives the elongation of actin filaments at the plus end of the microfilament

Question 21

Where is bundling protein found?

Answer 21

Filopodia

Question 22

What is the major motor protein for actin?

Answer 22

myosins

Question 23

What is tropmyosin?

Answer 23

side-binding protein that regulates myosin-dependent force generation

Question 24

What is Gelsolin?

Answer 24

actin severing protein that converts actin gel into a more fluid state

Question 25

What are Cadherins?

Answer 25

Found in adherins junctions

Question 26

What is cytochalasin?

Answer 26

binds to the plus end of the microfilament and prevents further polymerization

Question 27

What are phalloidins?

Answer 27

bind tightly along the sides of actin filaments and prevents depolarization

Question 28

What type of cell uses lamellipodia and filipodia to move?

Answer 28

fibroblasts

Question 29

What actin filament design is used to aid in wound healing?

Answer 29

Stress fibers

Question 30

What makes up the focal contacts in movement of a lamellipodium?

Answer 30

stress fibers (anti-parallel) and integrins

Question 31

In what way does gelosin aid in lamellipodia formation?

Answer 31

It breaks down actin so that monomers are available to bind to the ARP complex

Question 32

What is Rho?

Answer 32

Stress fiber formation

- from the rho family of proteins that are active in GTP-bound state and inactive in the GDP bound state.

Question 33

What is Rac?

Answer 33

controls lamellipodia formation

- from the rho family of proteins that are active in GTP-bound state and inactive in the GDP bound state.

Question 34

What is Cdc42?

Answer 34

Controls filipodia formation

- from the rho family of proteins that are active in GTP-bound state and inactive in the GDP bound state.

Question 35

What is membrane anchoring dependent on?

Answer 35

cadherin and actin in cadherins junctions

Question 36

T or F: myosin needs ATP to bind to actin

Answer 36

False, when ATP is not on myosin it binds in the rigor conformation to ATP

Question 37

Step in muscle contraction

Answer 37

1. Ca2+ binds troponin and myosin heads with no ATP bind in the rigor conformation
2. ATP binds myosin and myosin looses affinity for actin filament
3. ATP hydrolyses and myosin moves forward a monomer
4. Pi dissociates and myosin binds tighter
5. ADP dissociates and power stroke occurs