Signal transduction Flashcards

1
Q

endocrine signal

A

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

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2
Q

paracrine signal

A

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

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3
Q

autocrine signal

A

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

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4
Q

cell-cell signalling

A

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

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5
Q

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

A

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

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6
Q

antogonists

A

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

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7
Q

signal amplification

A

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

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8
Q

multi-step transduction pathways allow

A
  1. signal amplification

2. control in multiple places for coordination and regulation

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9
Q

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

A
  1. no receptor for that ligand

2. tissue expresses a different target protein

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10
Q

why must the response process be terminated afterwards?

A

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.

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11
Q

how many human genes code for receptors?

A

around 1,000

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12
Q

which three amino acids are phosphorylated?

A

Tyrosine
Threonine
Serine

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13
Q

3 transmembrane receptors

A
  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
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14
Q

intracellular receptors

A

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

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15
Q

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

A

extracellular signals that trigger GPCR

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16
Q

vision and smell

A

key physiological responses of GPCR

17
Q

GPCR structure

A
7 transmembrane domains
3 extracellular loops
3 intracellular loops
-N outside cell
-C inside cell ("c" for cell)
18
Q

G protein cycle

A
  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
19
Q

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

A

made up of 3 untis:

α-[β-γ]

20
Q

β-γ unit always stays together TRUE FALSE

A

TRUE TRUE TRUE

21
Q

how do G proteins control cAMP levels?

A
Gαi = 'i'nhibits adenylate cyclase and therefore reduces cAMP
Gαs = 'S'timulates adenylate cyclase and therefore increases cAMP
22
Q

Gαq

A

activates Phospholipase C

23
Q

Glucagon is released from…

A

α islets of Langerhans in the pancreas

24
Q

action of glucagon

A
  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
25
Q

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.

A

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.

26
Q

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?

A

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

27
Q

4 ways glycogen breakdown is stopped

A
  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
28
Q

what type of cell receptor does insulin use?

A

receptor tyrosine kinase

29
Q

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

A

ventolin (salbutamol) mimics adrenaline at the beta-adrenoreceptor to treat asthma.

30
Q

what does symlin do in the treatment of diabetes

A

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

31
Q

type I diabetes

A

insulin deficcient

32
Q

structure of RTKs

A

α and β subunits
β spans membrane
kinase domain on β

33
Q

insulin signaling

A

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

34
Q

how do you identify cAMP vs cGMP?

A

cGMP has a double bonded oxygen