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Metabolic Endocrinology > Hormone Action > Flashcards

Hormone Action Flashcards

1
Q

signals are received by cell ____, and passed on to _____, where it is _____, ultimately resulting in ___ or ___

A

receptors
chain of signaling proteins
exponentially amplified
on or off state

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2
Q

the 2 main classes of hormones, based in signalling pathway:

What types of hormones are associated with each?

A
  1. cell-surface receptor pathways (hydrophilic)

2. intracellular receptor pathways (hydrophobic)

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3
Q

basic structure of a cell surface receptor:

A 
outer ectodomain (amino end)
hydrophobic transmembrane domain (crosses plasma membrane)

cytoplasmic domain (carboxyl end)

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4
Q

how many AA are needed at least to cross the cell membrane?

A

25

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5
Q

Characteristics of the ectodomain:

A

NH2 end
rich in cysteine (for S-S bonds)
Often glycosylated

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6
Q

The transmembrane domain usually has a ___ ___ strucutre

A

alpha helix

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7
Q

the ectodomain can also break off and serve as ____ ____ ___. Give an example:

A

hormone binding protein

ex: GH receptor can act as GH binding protein in circulation

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8
Q

What is a possible trigger of Graves disease?

A

TSH receptor ectodomain can induce antibodies -> bind to receptor and mimic TSH -> hyperthyroidism

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9
Q

an activated cytoplasmic domain will induce a ____ ____. How is this done?

A

signal cascade (passing of the signal)

signal passed by phosphorylating proteins, or binding proteins => conformation changes

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10
Q

What AA are common sites for phosphorylation? Why?

A

Serine
Threonine
Tyrosine

Have a polar hydroxyl group that is replaced by phosphate group

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11
Q

What is the phosphate donor in the phosphorylation cascade?

A

ATP

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12
Q

Many signaling proteins are ____, which are activated by _____

A

kinases

phosphorylation

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13
Q

What causes signal amplification?

A

activation of kinase -> can phosphorylate many more kinases -> phosphorylate even more kinases (chain rxn/ripple effect)

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14
Q

True/False: once an activated protein in the signal cascade has phosphorylated the next messenger, it becomes inactive since it loses the phosphate group.

A

False; stays active until inactivated (phosphorylates using ATP, not its own phosphate group)

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15
Q

How do you reverse phosphorylation?

A

phosphatase

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16
Q

Advantages of using protein phosphorylation for signal transduction:

A
  1. rapid (don’t need to synth/degrade proteins)
  2. reversible: easy to reset with phosphatases
  3. easy signal passing: Tyr, Thr, Ser make binding sites for other proteins
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17
Q

____% of all cell proteins are phosphorylated

A

10%

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18
Q

True/False: tyrosines are more abundantly phosphorylated than serine or threonine

A

False: phosphorylated Ser and Thr is 100:1 compared to Tyr

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19
Q

What is special about tyrosine phosphorylation?

A

at beginning of cascade; serve as DOCKING SITE for downstream signal proteins

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20
Q

What are the AA sequence that mediates docking to phosphorylated tyrosines?

A

SH2, SH3 domains (highly conserved; essential)

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21
Q

Types of cell surface receptors? (3)

A
  1. G protein coupled

2. Tyrosine kinase (intrinisc or recruited TK activity)

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22
Q

What are the 2 types of tyrosine kinase receptors?

A

intrinsic TK activity

recruited TK activity

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23
Q

Describe the structure on an intrinsic TK activity receptor

A

inactive intracellular catalytic domain (attached)

binding of dimer signal molecule -> 2 halves of receptor dimerize -> TK activated

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24
Q

Describe the structure on a receptor with recruited TK activity

A

catalytic domain unattached

binding of signal molecule -> 2 halves of receptor dimerize and recruit (summon) intracellular TK -> activated

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25
Q

The general process when a signal binds in a G protein coupled receptor:

A
  1. signal binds
  2. G protein activated
  3. G protein -> membrane enzyme
  4. membrane enzyme activated
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26
Q

How many times does a TK cell surface receptor cross the membrane?

A

once

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27
Q

what are 3 examples of ectodomain types that may be coupled with TK domains?

A

cysteine rich domain
immunoglobulin-like domain
fibronectin-type III-like domain

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28
Q

examples of intrinsic TK activity receptors:

A

EGF, insulin, IGF-1, NGF, PDGF, Eph

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29
Q

What holds together the insulin receptor?

A

disulfide bonds

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30
Q

Structure of insulin receptor:

A

hetero-tetrameric

2 alpha, 2 beta chains, S-S bonds

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31
Q

The insulin receptor is formed from _____, through formation of _____ and _____

A

precursor protein

disulfide bonds, cleavage

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32
Q

What cells are highest in insulin receptors?

A

adipocytes, hepatocytes

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33
Q

Cells have between ____ to ___ insulin receptors per cell

A

100 to 200,000

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34
Q

the insulin receptor is similar in structure to the ____ structure

A

IGF-1 receptor

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35
Q

insulin binds to the ____ subunits of the insulin receptor, which causes ______ on the ___ subunits

A

alpha

autophosphorylation, beta

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36
Q

What pathways does insulin binding trigger?

A

PI-3 kinase pathway -> enhances glucose transport

MAPK pathway

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37
Q

3 main steps in sequence of events when insulin binds to receptor:

A
  1. autophosphorylation of intracellular domain
  2. IRS-1 and IRS-2 dock -> get phosphorylated
  3. activate 2 pathways (PI-3 and MAPK)
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38
Q

IRS stands for:

A

insulin receptor substrates

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39
Q

What are the ultimate effects of the PI3-K pathway? (2)

A

maintaining active glycogen synthase -> glycogen synth

more GLUT4 (transporter) moved to surface -> more glucose uptake

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40
Q

IRS -1 is activated by the insulin receptor through _____. Then, active IRS-1 will _____ by binding to _____.

A

phosphorylation

activate PI-3K by binding to its SH2 domain

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41
Q

What is the function of PI-3K?

A

convert PIP2 (membrane phospholipid) into PIP3

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42
Q

___ bound to PIP3 will be activated by ______. Then, it will phosphorylate ______ on a ____ residue, causing it to go (active/inactive).

A

PKB
PDK1
GSK3, Serine
Inactive

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43
Q

What is the role of GSK3?

A

phosphorylate (inactivate) glycogen synthase

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44
Q

When GSK3 is INACTIVE, and PKB is ACTIVE, this indicates a (fed/fasting) state

A

fed

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45
Q

When GS is phosphorylated, and IRS-1 is not phosphorylated, this indicates a (fed/fasting) state

A

fasting

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46
Q

The main enzymes involved in the insulin response/glycogen synthesis pathway:

What is the effect of phosphorylating them?

A 
PI-3K (activated)
PKB (activated)
PDK-1
GSK3 (inactivated)
GS (inactivated)
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47
Q

What is MAPK? What is its role?

A

mitogen activated kinase - target regulatory genes of cell division (c-fos, c-jun)

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48
Q

The MAPK pathway:

_____ is phosphorylated on its ____ residues by the receptor. ____ docks by binding with its ___ domain.

A

IRS-1
Tyrosine
Grb2, SH2

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49
Q

What happens in the MAPK cascakde after Grb2 binds to IRS-1?

A

Sos (sons of seven less) bind to Grb2, then bind/activate to Ras

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50
Q

How is Ras activated in the MAPK pathway?

A

binds to Sos (bound to Grb2), GDP replaced by GTP

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51
Q

Activated Ras (in MAPK pathway) will _______

A

bind/activate Raf-1

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52
Q

What is the role of Raf-1 in the MAPK pathway?

A

phosphorylate/activate MEK (on 2 Serines)

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53
Q

What is the role of MEK in the MAPK pathway?

A

phosphorylate/activate MAPK on Thr and Tyr

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54
Q

What does activated MAPK do?

A

move into nucleus, phosphorylate/activate transcription factors (like Elk1)

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55
Q

How does Elk1 transcription factor function?

A

activated -> join SRF in nucleus -> stimulate transcript/translation of genes needed for cell division

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56
Q

How does insulin affect synthesis in the body? What enzymes increase for this purpose?

A

muscle: more glycogen synth
liver: more FA and glycogen synth
adipose: more TG synth

increase in: glycogen synthase, acetyl-coA carboxylase, lipoprotein lipase

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57
Q

what cell process/enzyme decrease in presence of insulin?

A

glycogen breakdown; glycogen phosphorylase

58
Q

What enzyme is required for glucose uptake in the liver?

A

glucokinase

59
Q

defects in insulin receptor or pathway leads to ______. What symptoms does this present?

A

insulin resistance syndromes

impaired glucose metabolism, raised insulin concentrations

60
Q

the different severities of insulin resistance syndromes:

A

mild: Type A insulin resistance
Medium: Rabson-Mendenhall syndrome
Severe: Leprachaunism/Donahues syndrome (IUGR, dead <1 yr)

61
Q

recruited TK activity receptors are characterized by _____ and ______

A

4 alpha helices

similar structure of ectodomain

62
Q

the ___ domain in recruited TK receptors can vary, but _____ region is conserved and is involved in ______

A

cytoplasmic
Box 1
triggering cell division

63
Q

Examples of recruited TK kinase activity receptors:

A

GH
PRL
Leptin

64
Q

GH has ____ binding sites, and binds sequentially to ___ molecules.

A

2

2

65
Q

____ of the cytoplasmic regions of GH will initiate signal transduction

A

dimerization

66
Q

The majority of recruited TK activity receptors have ____ dimer formation, except: ______

A

heterodimer or oligomers

GH, PRL, EPO

67
Q

Describe the process of GH binding to the receptor

A
  1. binds to receptor 1
  2. binds to receptor 2 -> form dimeric complex with them both
  3. dimer complex recruit/activate JAK2
68
Q

how many different JAKs are there?

A

4

69
Q

What pathways are activated by the GH binding?

A

MAPK -> gene regulation
JAK2-STAT - gene regulation
JAK2-PI-3 -> insulin-like metabolic effects

70
Q

How does MAPK Pathway differ in GH vs. insulin pathway?

A

in GH: not dependent on IRS-1 (via Shc)

71
Q

How many different STAT regulatory proteins are there?

A

4

72
Q

How are STATs activated?

A
  1. recruited JAKs will cross-phosphorylate (activated)
  2. they phosphorylate the tyrosines on receptor
  3. STATs can dock (via SH2 domain)
  4. JAKs phosphorylate the STATs
  5. STATs dissociate, dimerize (via SH2)
  6. go to nucleus, form transcription complex (bind/affect gene regulation proteins)
73
Q

What does STAT stand for

A

signal transduction and activation of transcription

74
Q

____ syndrome is a type of dwarfism, due to a defective ___ receptor. What are the symptoms?

A

Laron
GH (deletions in exons 3, 5, 6)
severely impaired growth, normal/high levels of GH

75
Q

3 types of ‘second messengers’ generated by G-protein activation:

A

cAMP
DAG (diacylglycerol)
IP3

76
Q

What is the significance of second messengers in GPCRs?

A

amplify and convey signals

77
Q

What is the most numerous type of receptor?

A

GPCRs (>140 members)

78
Q

True/False: GPCRs are not exclusive to the endocrine system

A

True: can be found in non-endocrine signalling as well

79
Q

What are some non-endocrine signal pathways that also use GPCRs? (4)

A

glutamate (NT)
thrombin
odorants
photoreceptors

80
Q

Examples of GPCR endocrine receptors: (8)

A

TRH, GnRH, TSH, LH, FSH, ACTH, GHRH, oxytocin

81
Q

Can GPCRs bind steroid molecules?

A

No; GPCR is cell-surface receptor (steroids act as intracellular signals)

82
Q

What is an easily identifiable feature of GPCRs?

A

serpentine shape, crosses membrane 7 times (forms pore)

83
Q

The GPCR structure consists of 7 ______ that form a ____

A

alpha-helices

pore

84
Q

How do G-proteins function?

A

GTP bound = ON
GDP bound = OFF

ON => activate adenylate cyclase or PLC

85
Q

True/False: Ras is a type of G-protein

A

False; also activated by GDP replaced with GTP, but serves as ‘relay protein’ in other pathways

86
Q

The types of G-protein (alpha subunits) and their roles: (4)

A

Gs - activate adenylate cyclase
Gi - inhibit adenylate cyclase
Gq - activate PLC
Go - activate ion channels

87
Q

What are the catalytic subunits and second messengers associated with G-proteins?

A

adenylate cyclase -> cAMP

PLC -> Ca, DAG

88
Q

Activated PLC will (increase/decrease) DAG and ___ levels

A

increase

Calcium

89
Q

What is the general structure of G proteins?

A

trimeric structure:
alpha subunit
beta + gamma subunit (heterodimer)

90
Q

How are the alpha, beta, and gamma subunits in a G protein related?

A

beta and gamma form heterodimer

alpha is the activator, can be displaced from beta/gamma and travel through membrane

91
Q

What causes displacement of the G alpha subunit?

A

GDP replaced with GTP

92
Q

What factors affect what G-protein type will be activated by a certain hormone? (3)

A

stage in development
concentration of hormone
tissue type

(alter proximity and # of G proteins in membrane)

93
Q

True/False: a hormone can trigger different types of G receptors

A

True

94
Q

What is McCune Albright syndrome?

A

G-signal pathway (Gs alpha) permanently active; gonads produce sex hormones without hormone stimulation (no LH or FSH)

symptoms: skin pigmentation, precocial puberty

95
Q

Adenylate cyclases have ___ isoforms. What is the general structure?

A

> 10

membrane bound, 2 sets of 6 membrane-spanning domains + cytoplasmic domains

96
Q

What second messenger is generated by adenylate cyclase?

A

cAMP (generated from ATP)

97
Q

What immediate downstream action does cAMP cause in the GPCR pathway?

A

activate PKA

98
Q

True/False: cAMP is required to be bound on the kinase portion of the inactive tetramer in order to free/activate it

A

False; binds onto regulating subunit -> causes to detach

99
Q

How many cAMP are needed to activate a pair of PKA?

A

4

100
Q

How does cAMP activate PKA?

A

cAMP bind to inactive kinase tetramer -> causes removal of the regulating subunit complex -> kinase is freed, become active

101
Q

what is the action of PKA in the GPCR pathway?

A

phosphorylate transcription factor CREB (on Ser and Thr)

102
Q

What is CREB, and what is its role?

A

cAMP response element binding protein

binds to DNA to affect gene expression (bind to CRE enhancer sequence to switch on genes)

103
Q

True/False: activation of CREB alone is not enough to trigger a response

A

True; need other regulatory proteins for transcription

104
Q

How is the GPCR cAMP pathway response terminated?

A

phosphodiesterases hydrolyse cAMP -> 5’AMP (PKA bound up again, inactive)

105
Q

PLC has ___ major isoforms

A

3

106
Q

What is the action of PLC?

A

convert PIP2 (membrane phospholipid) -> DAG, IP3 (second messengers)

107
Q

What are the actions of DAG and IP3?

A

DAG - activate PKC

IP3: release Ca from ER

108
Q

What is the effect of triggering Ca release from the ER?

A

increases Ca -> activates enzymes (kinases) -> phosphorylation cascades

109
Q

How does a cell change its responsiveness to a hormone?

A

of receptors (synth more, bring more to surface, endocytose, etc)

110
Q

___ % occupancy of a cell’s receptor will stimulate a maximal response.

A

3%

111
Q

Why is it important to maintain a large number of ‘empty’ receptors on the cell?

A

act as ‘buffer’ for additional signalling/stimulation -> up/down regulation
(if all receptors filled -> cell no longer responsive until it can make new ones)

112
Q

Why might excessive amounts of pharmacological hormones be detrimental?

A

saturation of cell receptors (cell cannot respond to further signals)

113
Q

What happens to the receptor/signal complex after cell signalling?

A
  1. uncoupled

2. endocytosis -> hormone removed and receptor recycled, or digested and synth new receptor

114
Q

___ and ____ hormones are lipid soluble, so they target ___ receptors due to their ability to _____.

A

thyroid; steroid
intracellular
cross the cell/nuclear membrane

115
Q

Do lipophilic hormones generate second messengers? How does this affect their function?

A

No (act as transcription factors themselves directly)

SLOW response, need to diffuse in, no signal amplification, cannot reuse

116
Q

What features of intracellular receptor hormones make them slower than cell-surface receptor hormones?

A
  1. must synthesize as needed (can’t store)
  2. can’t reuse
  3. no second messengers (no amplification, must diffuse in)
  4. affects protein transcription/translation -> slower effects
117
Q

A steroid hormone entering a cell will only trigger an effect if: _____

A

the receptor is present inside

118
Q

there are ___ members in the steroid/thyroid receptor family

A

> 150

119
Q

What is an orphan receptor?

A

receptor without identified ligand

120
Q

structure and domains of intracellular receptors:

A

single peptide structure

AF2 (hormone-specific binding domain, C terminus)
DNA binding domain
AF1 (transcription activating domain; hypervariable)

121
Q

Which of the intracellular receptor domains display the least, and most variability?

A

least variation (highly conserved): DNA binding domain

highly variable: AF1

122
Q

intracellular receptor classes

A

Class 1: cytsolic - binds hormone, then travel to DNA sequence
Class 2: Nuclear: already bound to DNA, waiting for hormone

123
Q

True/False: domains of intracellular receptors are interchangeable

A

True

124
Q

DNA binding of steroid hormone receptors is mediated by _____, which are normally covered with _____.

A

2 zinc fingers (loops with Zn)

heat shock proteins (inhibitor)

125
Q

What causes activation of a steroid hormone receptor?

A

binding of hormone -> conformation change -> inhibitor removed, DNA binding zinc fingers exposed

126
Q

Class ____ receptors are ___ hormones, and form complexes with ____ when inactive

A

Class I
steroid
heat shock proteins (hsp)

127
Q

Class I receptors are partitioned betweeen the ___ and ____

A

cytoplasm

nucleus

128
Q

What happens after a Class I steroid hormone is activated?

A

2 activated receptors -> go inside nucleus -> form HOMODIMER -> bind/regulate DNA transcription

129
Q

the class I hormone receptor will bind to ____ on DNA

A

HRE (hormone response element)

130
Q

How is the class I hormone receptor homodimer arranged?

A

the two halves face opposite directions

131
Q

What is the arrangement of a Class II hormone receptor when activated?

A

form hetero or homodimers, or monomeric; faces same direction

132
Q

What is the action of an activated Class II hormone receptor?

A

recruit co-activators, TIC (transcriptor initiation complex) => stimulate RNA polymerase to transcript target gene

133
Q

What causes androgen insensitivity syndrome?

A

defect in androgen receptor (lower #, less binding, or problems with dimerizing)

134
Q

Defects in the Calcitriol receptor leads to:

A

calcitriol-resistant rickets

135
Q

Androgen receptor defects lead to increased risk of _____

A

breast or prostate cancer

136
Q

why might target cells need to further modify hormones?

A

convert to active form (T4 -> T3)

deactivate to prevent cross-reactions (deactive cortisol in kidney to prevent from interfering with aldosterone receptor)

137
Q

What converts T4 to T3?

A

removal of 5’ iodine by tissue specific deiodinase

138
Q

How does the kidney ‘protect’ cells from accidental activation of the aldosterone receptor?

A

converts cortisol to cortisone to prevent from binding to aldosterone receptor

139
Q

Testosterone serves as a prohormone in the ____, where it is converted to _____; and also in the _____, where it is converted to _____.

A

hypothalamus; estradiol (feedback)

prostate; DHT

140
Q

What converts testosterone to DHT?

A

5 alpha reductase (prostate)

Metabolic Endocrinology (6 decks)

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