Signal transduction

Question 1

endocrine signal

Answer 1

released from a gland and travel in the blood to a distant target organ e.g. insulin

Question 2

paracrine signal

Answer 2

released from cells to act upon adjacent cells e.g. ACh at neuromuscular junction

Question 3

autocrine signal

Answer 3

act upon same cell type they’re released from e.g. growth factors

Question 4

cell-cell signalling

Answer 4

signal attached to cell and binds to receptor e.g. t-cell activation

Question 5

interaction of _______ and receptor leads to a ________ change in the receptor protein

Answer 5

interaction of ligand and receptor leads to a conformational change in the receptor protein

Question 6

antogonists

Answer 6

drug which binds to receptor similarly to native ligand, and blocks the binding site

Question 7

signal amplification

Answer 7

at each step in the pathway, number of activated products is much greater than preceeding step. Thus, small ammount of hormone required

Question 8

multi-step transduction pathways allow

Answer 8

1. signal amplification

2. control in multiple places for coordination and regulation

Question 9

how can millions of cells, which all use cAMP as a second messenger, create different responses to a ligand?

Answer 9

1. no receptor for that ligand

2. tissue expresses a different target protein

Question 10

why must the response process be terminated afterwards?

Answer 10

so that the cell can respond to new signals. Failure to terminate will lead to consequences and disease e.g. cholera toxin locks g protein.

Question 11

how many human genes code for receptors?

Answer 11

around 1,000

Question 12

which three amino acids are phosphorylated?

Answer 12

Tyrosine
Threonine
Serine

Question 13

3 transmembrane receptors

Answer 13

1. G protein-coupled receptor - g proteins & second messengers
2. receptor tyrosine kinases (RTKs) - phosphorylation cascades
3. Ligand-gated ion channel receptors - ions bind and channel opens

Question 14

intracellular receptors

Answer 14

small or hydrophobic chemical crosses the membrane readily and bind to receptors on the nucleus or free in the cytoplasm

Question 15

Ca2+, light, proteins, peptides, small molecules…

Answer 15

extracellular signals that trigger GPCR

Question 16

vision and smell

Answer 16

key physiological responses of GPCR

Question 17

GPCR structure

Answer 17

7 transmembrane domains
3 extracellular loops
3 intracellular loops
-N outside cell
-C inside cell ("c" for cell)

Question 18

G protein cycle

Answer 18

1. GPCR activated
2. conformational change, activates (heterotrimeric) G protein
3. GTP replaces GDP
4. α unit separates from β-γ unit
5. αGTP binds to Adenylate cyclase
6. Adenylate cyclase is activated and makes cAMP from ATP
7. GTPase activity of αGTP hydrolyses GTP to GDP
8. α unit returns to β-γ unit
   RESTARTS

Question 19

what is meant by the phrase “G proteins are heterotrimeric”

Answer 19

made up of 3 untis:

α-[β-γ]

Question 20

β-γ unit always stays together TRUE FALSE

Answer 20

TRUE TRUE TRUE

Question 21

how do G proteins control cAMP levels?

Answer 21

Gαi = 'i'nhibits adenylate cyclase and therefore reduces cAMP
Gαs = 'S'timulates adenylate cyclase and therefore increases cAMP

Question 22

Gαq

Answer 22

activates Phospholipase C

Question 23

Glucagon is released from…

Answer 23

α islets of Langerhans in the pancreas

Question 24

action of glucagon

Answer 24

1. binds to glucagon receptor on liver cell
2. activates Gs - adenylate cyclase active
3. cAMP increases
4. PKA activated
5. PKA phosphorylates and activates phosphorylase kinase (phosphorylase b becomes a)
6. glycogen broken down to glucose

Question 25

adrenaline (aka __________) is released from the ________ glands in the _________ and circulates in the blood to the _________ tissue, where it bonds to the receptor __________ _________. It then activates the ____ protein and induces a conformational change. The process which follows is the same as with _________. Results in increased blood _______ levels.

Answer 25

adrenaline (aka _epinephrine_) is released from the _adrenal_ glands in the _kidneys_ and circulates in the blood to the _muscle_ tissue, where it bonds to the receptor _epinephrine_ _receptor_. It then activates the _Gs_ protein and induces a conformational change. The process which follows is the same as with _glucagon_. Results in increased blood _glucose_ levels.

Question 26

fuel can't be stored at the same time as being degenerated, so how is glycogen synthesis stopped when glucagon is released into the blood stream?

Answer 26

the PKA produced through the action of glucagon also phosphorylates glycogen synthase a to the inactive glycogen synthase b

Question 27

4 ways glycogen breakdown is stopped

Answer 27

1. hormones that stimulated it are no longer present 2. GTPase activity of Gα subunit inactivates the g protein 3. phosphodiesterase converts cAMP to AMP 4. Phosphatase removes phosphate from from phosphorylases thereby inactivating them

Question 28

what type of cell receptor does insulin use?

Answer 28

receptor tyrosine kinase

Question 29

ventolin (salbutamol) mimics _________ at the __-___________ to treat _______.

Answer 29

ventolin (salbutamol) mimics _adrenaline_ at the _beta_-_adrenoreceptor_ to treat _asthma_.

Question 30

what does symlin do in the treatment of diabetes

Answer 30

mimics amylin - reduces eating and causes weight loss but is rapidly metabolised

Question 31

type I diabetes

Answer 31

insulin deficcient

Question 32

structure of RTKs

Answer 32

α and β subunits β spans membrane kinase domain on β

Question 33

insulin signaling

Answer 33

insulin binds to α, triggers conformational change, leading to autophosphorylation of the tyrosine residues

Question 34

how do you identify cAMP vs cGMP?

Answer 34

cGMP has a double bonded oxygen