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ANSC 424 > Powerpoint 4 > Flashcards

Powerpoint 4 Flashcards

1
Q

Activation of the G-proteins leads to the generation of what 3 “second” messengers?

A
  1. cAMP
  2. DAG
  3. IP3
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2
Q

G-Protiin coupled receptors are the most numerous class of receptors with more than ___ members

A

140

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3
Q

What are 4 examples of non-endocrine signals that also act via G-Protiens?

A
  1. Glutamate
  2. Thrombin
  3. Odorants
  4. Photoreceptors
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4
Q

What are some examples of G-Protein coupled RECEPTORS?

A

TRH, GNRH, LH, FSH, TSH, oxytocin

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5
Q

How many times does the G-protein receptor cross the transmembrane domain? What is their shape?

A

7 times, alpha-helices

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6
Q

What do the 7 transmembrane alpha-helices form?

A

a pore

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7
Q

What do G-Proteins use as a switch? Which one activates it and which deactivates it?

A

GTP/GDP

GTP bound = G protein on
GDP bound = G protein off

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8
Q

When the G-Protein is ‘on’, what happens?

A

It moves along and activates adenylate cyclase and/or phospholipase C

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9
Q

What type of structure so G proteins have?

A

Trimeric

  • Alpha subunit
  • Beta subunit
  • Gamma subunit
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10
Q

Which two G-Protein subunits bind together to form heterodimers?

A

Beta and Gamma subunits

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11
Q

What are the two different functional units of G-proteins?

A
  1. G-alpha

2. G-beta/gamma dimer

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12
Q

What happens to the G-protein functional subunits when GTP –> GDP?

A

G-alpha (carries the GDP/GTP) is displaced from G-beta/gamma dimer

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13
Q
  1. G(s)alpha:
  2. G(i)alpha:
  3. G(q)alpha:
  4. G(o)alpha:
A
  1. activates adenylate cyclase
  2. Inhibits adenylate cyclase
  3. activates phospholipase C
  4. activates ion channels
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14
Q

Is it that 1 hormone uses 1 G-protein, or can it use more than 1?

A

may use more than 1

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15
Q

Under what two conditions may G-protein use change?

A
  1. during development

2. depending on the concentration of the hormone or in different tissues

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16
Q

What happens in terms of G-protein function in some with the McCune Albright syndrome? What are 2 side effects?

A

Gain of G(2)alpha function: G-signaling pathway is on despite the absence of a hormone stimulant.

  1. Skin pigmentation (cafe au lait)
  2. breast development
  3. precocial puberty associated with ovarian cysts
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17
Q

What happens endocrinologicaly to someone who has Familial male precocious puberty?

A

High testosterone is produced by Lydia cells despite the absence of LH and FHS –> cells act autonomously

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18
Q

How many isoforms does Adenylate cyclase have? How do they differ?

A

> 10 - differ in their interactions with G-proteins

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19
Q

How many membrane spanning domains are adenylate Cyclades made up of? How many cytoplasmic domains do they have?

A

2 sets of 6 membrane spanning domains

2 cytoplasmic domains

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20
Q

What enzyme converts ATP to cAMP?

A

adenylyl cyclase

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21
Q

What amino acids of CREB does PKA phosphorylate?

A

serines and threonines, activating it

22
Q

What does CREB stand for?

A

cAMP-response element binding protein

23
Q

What is CREB?

A

a transcription factor which switches on genes by binding to the CRE sequence (enhancer sequence) of DNA to induce transcription of cAMP-inducible genes

24
Q

How is the PKA signal terminated?

A

Phospho-diesterases hydrolyse cAMP to 5’AMP – this removes the cAMP from the regulatory subunits allowing them to bind back to PKA and inactivate it

25
Q
  1. What is PIP2?

2. What are DAG and IP3?

A
  1. a minor phospholipid of the cell membrane

2. Second messengers

26
Q

What are the primary actions of DAG and IP3?

A

DAG: activation of PKC
IP3: Release of Ca++ from ER

27
Q

What is a result of increased Ca++?

A

activation of many enzymes including kinases (phosphorylation cascade)

28
Q

How is the # of receptors regulated in cell membranes?

A

it constantly changes with the cell cycle, development, and cell differentiation - cells become more/less responsive to a hormone

29
Q

A cell will have maximal response to its receptor if it that receptor occupies how much of the cell membrane?

A

3 %

30
Q

A receptor may be up or down regulated in response to _______ stimulation.

A

hormonal

31
Q

When are receptor complexes inactivated? In what 2 ways can it become inactivated?

A

After cell signalling has been initiated

  1. uncoupling
  2. endocytosis
32
Q

What two types of hormones bind to a family of INTRACELLULAR receptors which are structurally related?

A
  1. steroid hormones

2. thyroid hormones

33
Q

Where are intracellular hormone receptors located?

A

in the cytoplasm or the nucleus

34
Q

What do intracellular hormone receptors function as?

A

Transcription factors

35
Q

What is the response rate of intracellular hormone receptors? Why?

A

slow because transcription and translation of proteins is necessary

36
Q

The family of steroid and thyroid receptors is made up of how many members?

A

> 150 (about 100 are orphan receptors as their ligand has not been identified)

37
Q

Steroid and thyroid receptors are made up of how many peptides?

A

single peptide

38
Q

What are the 3 domains of steroid and thyroid receptors?

A
  1. AF2: DNA hormone-specific binding domain with a region responsible for hormone dependent transcription activation at the C-terminus
  2. Highly conserved DNA-binding domain
  3. AF1: Transcription activating domain. Hypervariable, not dependent on the type of hormone. Can activate transcription continuously

Domains are interchangeable

39
Q

What are the 2 main hormone receptor classes?

A
  1. cytosolic

2. nuclear

40
Q

What is characteristic of DNA-binding domains?

A

2 loops that forms a “zinc finger”

41
Q

What is the difference between Class 1 and Class 2 DNA-binding receptors?

A

Class 1:

  • ligands = steroids
  • form complexes with heat shock proteins
  • form homodimers
  • ex: hsp 70, hsp 90

Class 2:

  • ligands = T3
  • already bound to DNA
  • can form heterodimers/homodimers or be monomeric
  • activated by hormone binding
42
Q

What 3 clinical effects are a result of a defect in the androgen (AR) nuclear receptor?

A
  1. partial or complete androgen insensitivity syndromes
  2. brast cancer
  3. prostate cancer
43
Q

What clinical effect is a result of a defect in the glucocorticoid (GR) nuclear receptor?

A

generalized inherited glucocorticoid resistance

44
Q

What clinical effect is a result of a defect in the Oestrogen (ER) nuclear receptor?

A

Usually lethal Oestrogen resistance

45
Q

What clinical effect is a result of a defect in the Calcitriol (VDR) nuclear receptor?

A

calcitriol-resistance rickets

46
Q

Hormones which act via nuclear receptors many be modified by _________.`

A

Target cells

47
Q

What are two examples of modifications to nuclear receptor hormones that happen due target cells?

A
  1. conversion of thyroxin (T4) to the active T3 (removal of 5’-iodine by tissue specific deiodinase)
  2. Deactivation of cortisol to cortisone in aldosterone-responsive kidney cells (cortisol cross reacts with the aldosterone receptor)
48
Q

What enzyme converts cortisol to cortisone?

A

Type 2 11-beta HDS

49
Q

What receptors does cortisol bind to?

A

aldosterone receptor in addition to its own receptor

50
Q

How does the convention to cortisone “protect” the cell?

A

by preventing inappropriate activation of the aldosterone receptor by cortisol

51
Q

What enzyme in the hypothalamus converts the inactive testosterone (pro hormone) into an active form? What is this new active molecule called?

A
  1. aromatase

2. new molecule = estradiol

52
Q

What enzyme in the prostate converts the inactive testosterone (prohormone) into an active form? What is this new active molecule called?

A

5-alpha-reductase

DHT

ANSC 424 (7 decks)

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