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BPM DLA1 > Lecture 20 > Flashcards

Lecture 20 Flashcards

1
Q

3 ways of cellular communication

A
  1. synaptic signaling (neurotrasnmitter)
  2. endocrine signaling (hormone)
  3. direct contact (paracrine or autocrine) e.g. thromboxane
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2
Q

2 types of receptor

A
  1. Intercellular receptor
    - on cell surface, which produce secondary messengers and thus signal transduction cascade
  2. Intracellular receptor
    - bind to cytosolic protein receptor or DNA sequence
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3
Q

2 ways that hormone can be released

A
  1. Endocrine - directly into bloodstream

2. Exocrine - first secreted into duct and then into bloodstream

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4
Q

How is hormone controlled? (2)

A
  1. Coordinated counter-regulatory of opposing pathways (Gs and Gi)
  2. Antagonistic action of other hormone
    eg. insulin and glucagon
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5
Q

What is Bmax?

A

max hormone binding (analogue to Vmax)

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6
Q

What is Kd?

A

dissociation constant of receptor-hormone complex (same as half the receptors which have formed receptor-hormone complex) = 1/2Bmax (analogue to Km)

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7
Q

How is cascade reaction switched off? (2)

A
  1. hormone will dissociate from membrane receptor and removed from circulation by liver.
  2. Then cAMP is degraded by phosphodiesterases producing AMP.
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8
Q

How can cAMP degradation be inhibited?

A

Phosphodiesterase inhibitors such as methylxanthine can be used which potentiates the effect of cAMP

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9
Q

4 Principle groups of receptors

A
  1. Type 1 : Ligand-gated ion channels
  2. Type 2: G-protein-coupled receptors (GPCR)
  3. Type 3: Enzyme-linked receptor (tyrosine kinase)
  4. Type 4 : Steroid hormone receptors
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10
Q

Example of Type 1 receptor

A

nicotinic cholinergic neuroreceptors

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11
Q

Mechanism of type 1 receptor

A

Binding of neurotransmitter opens the receptor, allowing a rapid influx of ions into cytoplasm. When terminating signal, the neurotransmitter at synaptic cleft is cleaved or degraded by enzyme (eg acetylcholinesterase)

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12
Q

Structure of Type2 receptor (3)

A

GPCR contain 7 transmembrane alpha helices (heptahelical receptor)
Extracellular domain interact with ligand (hormone or neurotransmitter)
Intracellular domain interact with G proteins.

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13
Q

Mechanism of type2receptor

A
  1. Ligand binds to receptor which cause GTP to bind to G protein alpha subunit, causing conformational change.
  2. As a result, alpha subunit of G protein dissociates from beta and gamma subunits, then activates adenylyl cyclase, which convert ATP to cAMP.
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14
Q

Glucagon interaction with GPCR

A
  1. glucagon binds to GPCR which cause GTP to bind to G protein alpha subunit, causing conformational change.
  2. Alpha subunit of G protein dissociates and activates adenylyl cyclase which turns ATP to cAMP.
  3. cAMP then activates protein kinase A which stimulates glycogenolysis and inhibits hepatic glycolysis (inhibit pyruvate kinase by phosphorylating it)
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15
Q

2 ways of termination of glucagon

A
  1. Hydrolysis of GTP

2. Hydrolysis of cAMP to AMP by phosphodiesterase

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16
Q

2 ways G-protein can activate other protein

A
  1. Gs activates adenylyl cyclase which convert ATP to cAMP
  2. Gq activates phospholipase C which react with PIP2 (localized inner membrane leaflet of membrane), producing IP3 (produced to cytoplasm) and DAG (produced in membrane)
17
Q

Which type of G protein is linked with beta 1 receptor

A

Gs linked with B1 Receptor

18
Q

Which type of G protein is linked with alpha 1 receptor?

A

Gq linked with alpha 1 receptor

19
Q

Which type of G protein is linked with alpha 2 receptor?

A

Gi (inhibitory) linked with alpha 2 receptor

20
Q

What does Gq protein activate?

A

Phospholiapse C > PIP2 >IP3+DAG

21
Q

What does Gs protein activate?

A

activate adenyly cyclase

22
Q

What does Gi protein activate?

A

inhibit adenylyl cyclase by replacing GTP with GDP

23
Q

Epinephrine has higher affinity for Beta or alpha receptor?

A

Beta1 receptor

24
Q

Norepinephrine primarily acts through which receptor?

A

alpha receptor

25
Q

Effect of IP3

A

Increase calcium influx causing smooth muscle contraction

26
Q

Effect of DAG

A

activate PKC

27
Q

Effect of activation of Gi (3)

A
  1. inhibit adenylyl cyclase leading decrease cAMP
  2. Increased opening of K+ channel, leading to membrane hyperpolarization
  3. increased closing of neuronal calcium channel, leading to decreased NE release from nerve terminal
28
Q

What is difference between beta 1 and beta 2 receptor?

A

beta 2 is more specific to epinephrine while beta 1 has equal binding to epinephrine and norepinephrine

29
Q

Effect of binding of epinephrine to beta-adrenergic receptors on skeletal myocytes (2)

A
  • stimulate glycogenolysis

- inhibit glycogenesis

30
Q

Factors that affect arterial BP

A

Cardiac output (heart rate, stroke volume) peripheral resistance

31
Q

What is Type 3 receptor made up of?

A

single transmembrane protein Kinase

32
Q

How does Type 3 receptor work?

A
  1. hormone binds to receptor which activates protein kinase that phosphorylates intracellular proteins.
33
Q

Mechanism of insulin receptor

A
  1. insulin binds to receptor which activates tyrosine kinase activity in intracellular domain of Beta subunit.
  2. Then, tyrosine residue of beta subunit are autophosphorylated.
  3. Then, tyrosine kinase phosphorylates tyrosines in other proteins such as insulin receptor substrates (IRS).
  4. Phosphorylated IRS promote activation of protein kinases and phosphatases, leading to the metabolic effects of insulin.
34
Q

What is insulin receptor made up of?

A

two alpha and two beta subunits
alpha subunits held by disulfide bond induce conformational change that stimulates tyrosine kinase acitvity of beta subunit.

35
Q

Effects of insulin (3)

A
  • rapid increase in glucose transport into cytoplasm of adipose and muscle tissue
  • stimulate transcription of specific genes for glycolytic enzyme such as hepatic glucokinase & phosphofructokinase
  • activate lipogenesis in adipocytes and inactivate lipolysis
36
Q

What is difference between lipid-soluble hormones (type 4 receptor) to other types of signals?

A
  • target intracellular receptors which bind to regulatory regions of DNA that induce or repress specific genes.
  • have longer half life
37
Q

Mechanism of cortisol receptors

A
  1. Cortisol binds to cortisol receptors in cytosol which leads to dissociation of Hsp from receptor (Usually bound to receptor to make it inactive)
  2. Activated receptor then homodimerize and translocate to nucleus where they bind to DNA at hormone response element (HRE) in the promoter region, controlling gene expression.
  3. Thus it increase transcription of gluconeogenic enzyme.
38
Q

Why does steroid hormones have similar structures with minor changes bring about different cellular function?

A

Because they bind to different receptors which causes different cellular function
e.g. testosterone and progesterone (male/female)

BPM DLA1 (47 decks)

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