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Biochem Winter 2012 > Biochem Hormone Action 2 > Flashcards

Biochem Hormone Action 2 Flashcards

1
Q

How do you define potentcy

A

Graph with hormones with different potencies for a R or receptors with different potetcies for a hormone

within a class of hormones, different lignad molecules may have different POTENCIES, represented by EC50 values

The -log[hormone] at which 50% maximal response is elicited

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1
Q

If ther eis higher potentcy, is midpoint (EC50) increacing potency to left or righ?

A

Left!

Need lower concentration to elicit 50% maximal response

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2
Q

what happens if constant concentrtion of an ANTAGONIST is added?

A

the binding curve for the hormone (agonist) will shift to the RIGHT

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3
Q

How do you define EFFICACY on graph

Agonist vs PARTIAL AGONIST

A

Height of response (maximum is 100%)

Agonist will hve response with 100% efficacty (height of response)

PARTIAL AGONIST which only have 50% maximal response, or 50% efficacy (regardless of hormone concentration)

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4
Q

Efficacy vs Potency

A

Efficacy = height

Potency = midpoint EC50 (concentration of hormone required for half-occupancy of receptor)
depends on both affinity and efficacy

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5
Q

What are the differnt kinds of Regulations of Receptors (3)

A

Down Regulation

Covalent Modification

Up Regulation

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6
Q

Down regulation

A

Desnsitization- Ineternalization of R

loss of receptor number from pPM by sequestration. This change results in DESENSITIZATION of biological response to addition of more agonist.

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7
Q

examples of hormones that down regulate receptors

A 
Insulin
Glucagon
TRH
GH
LH
FSH
catecholamines
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8
Q

Covalent modification of the receptor . Example?

A

Desensitization- frequely Phosphorylation

No change in R number and no translocation occurs.

Hormone binding and effector activaiton systems are uncooupled by covalent modification

I.E. Beta Adrenergic system

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9
Q

Up Regulation

A

Angiotensin II and PROLACTIN

increase their R number as R on the cell surface become occupied

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10
Q

Types of Hormone/Receptor/Diseases

A

Abnormal Receptor Regulation

Inadequate production of hormone

Antibodies directed against a specific hormone

No hormone binding to the R can be detected

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11
Q

What are examples of Antibodies directed against specific hormone

A

Graves Disease
Acanthosis Nigrans (insulin resistant)
Myasthenia Gravis
Asthma

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12
Q

Graves Disease

A

Ab stimulates TSH R

Hyperthyroidism

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13
Q

Acanthosis Nigrans

A

Ab blocks insulin binding

insulin resistant

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14
Q

Myasthenia Gravis

A

Ab enchances turnover of Ach R

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15
Q

Asthma

A

Ab blocks Beta-Adrenergic binding to R

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16
Q

Examples of diseases where there is abnormal Receptor Regulation (2)

A
  1. Obesity - insulin binding is decreased

2. Diabetes mellitus- some form of NIDDM, TYpe II. Insulin binding is decreased; receptor down regulation

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17
Q

Examples of Disease where THERE IS INADEQUATE PRODUCTION OF HORMONE (4)

A
  1. Diabetes Mellitus (insulin-dependent form)
  2. Dwarfism- Deficiency f GH or somatotropin
  3. Gigantism, acromegaly- Excess secretin of GH
  4. Familial Neurohypophyseal diabetes insipidus (FNDI)- mUtations in vasopressin prohormone decrease VP syntehsis
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18
Q

FNDI

A

mutations in vasopressin prohormone decreases VP synthesis

-due to inadequate production of hormone

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19
Q

Diseases where NO HORMONE BINDING TO THE RECEPTOR CAN BE DETECTED (receptor deficiency) (2)

A
  1. congenital neprhogenic diabetes insipidus

Pseudohypoparthyroidism

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20
Q

Congenital Neprhogenic Diabetes Insipidus

A

ADH receptor deficiency

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21
Q

Pseudohypoparathyroidism

A

PTH receptor deficiency

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22
Q

Classification of hormones by mechanism of action (2)

A

Hormones that bind to intracellular receptors

Hormones that bind to cell surface receptors

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23
Q

What kind of hormones bind to intracellular receptors?

A 
Usually Steroids
estrogen
glucocorticoids
mineralcorticoids
progestins
calcitrol (vit D)
andorgens
thyroid hormones (T3 and T4)
Retinoids
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24
Q

What kind of hormones bind to cell-surface receptors (4)

A
  1. 2nd messenger is cAMP
  2. 2nd messenger is Ca2+ and Phosphatidylinositase
  3. Intracellular effect is a kinase or phosphatase
  4. Messenger is NO
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25
Q

Types of intracellular hormones (general) 3

A

Steroids
Iodothryonines
REtinoids

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26
Q

Types of cell surface hormones (general) 4

A

Polypeptids
porteins
glycoporteins
catecholamines

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27
Q

Solubility of nuclear vs PM hormone

A

Lipophilic vs hydrophilic

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28
Q

PM transport protein needed in nuclear or PM?

A

nuclear- yes

PM- some

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29
Q

Mediator of nuclear vs PM

A

nuclear- receptor-hormone complex

PM
cAMP, P-inositides, kinases, Ca2+ , etc

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30
Q

Mechanism of action of Intracellular (nuclear R) Hormones

A
  1. Hormone delivery to cell passes membrnaes
  2. binds receptor in nucleus
  3. Activates gene Transciption
  4. Protein/enzyme levels increase
31
Q

Do steroid hormones need to be bound to carrier when passing PM?

A

NO! b/c lipohphilic

32
Q

What happens when steroid-type hormone binds to an intracellular R ?

A

intracellular R changes conformation- to homodimer or heterodimer

Complex binds to HRE (hormone response element)

33
Q

What happens when hormone-receptor complex binds to HRE

A

complex binds to specific sequence which results in the Tx of a limited set of genes containing the right upstream regulatory elemnts

34
Q

Three features of Cell Surface Receptor Binding/Cascade

A

Amplification
Reversibility
Rapidity

35
Q

How many subunits is the G protein made up of?

A

three!

Alpah, beta, gamma (different combinations of different types)

36
Q

In the “resting state”, the trimeric Gs protein has what bound to it? GTP or GDP?

A

GDP

37
Q

upon interaction wih occupied R, Gs protein does what

A

exchanges GDP for GTP, it dissociates and alpha,s-GTP subunits is then capable of activiating the cyclase

38
Q

How is this system shut off?

A

By hydrolysis of GTP to GDP by slow, intrinsic GTPase actiity of alpha-s prtein

39
Q

what has GTPase activity>

A

alpha-s, reforms Gs protein with GDP bound to alpha subunit

40
Q

What protein speeds up process of GTP inactivation?

A

GAP
GTPase activating protein, speeds up process by increasing rate of GTP hyrolysis

noe that alpha-i alos has intrinsic GTPase activity

41
Q

What is GNEP?

A

guaninie nucleotide exhchange protein

protein that catalyses reactivation of alpha-i, wich requires an exchange of GTP for GDP

42
Q

Summary of events for second messenger of cAMP

A

Events coupled to G-protein

  1. hormone binds to 7-serpentine R
  2. The R activates a G-protein by GTP exchange
  3. Activated alpha-subunit activates adenylyl cyclase
  4. Adenylyl cyclase produces cAMP form ATP
  5. cAMP activates protein kinase A (and others)
43
Q

What is the effect of Cholera Toxin?

A

it activates G-alpha-s (inhibits GTPase)

irreversably activatves ADENYLATE CYCLASE by preventing GTAse activity of G-alpha-s subunit –> increase cAMP activity –> activates PROTEIN KINASE

44
Q

What are clinical effects of Cholera Toxin

A

Diarrhea!

stimulation of active transprot which leads to massive loss of Na ion and water by gut

45
Q

What is the biochemical cause of cholera toxin

A

ADP-ribosylation on Arg residues of the G prtein whcih the NAD moleucle provides the ADP-ribose

Cholera = CS = cas (alpha s)

46
Q

What happns when ADP is ribosylated Gs

A

GTPase activity is inactivated

Gs constantly activates Adenylate Cyclase

47
Q

What is the cause of Pertussin Toxin

A

inhibits G-alpha-i (blocks GTP on

48
Q

What is clinical effects of Pertussin Toxin

A

DIAHHREA!

irreversibily activates adenylate cyclase by promoting ADP-ribosylation of alpha-i, which prevents alpha-i subunit form being activated

pertussin = pi (for alpha i)

49
Q

What are initiating signal (hormones) for G-alpha-S class?

Downstream signal

A

Beta adrenergic amines
glucagon
parathyroid hormone (PTH)
others

Dwnstrm signal: Stiulate Adenylate cyclase

50
Q

What hormones serve as initiating signal for G-alpha-i?

Whas is the downstream signal

A

Acetycholine
alpha-adrenergic amines
NTs

Downstream sgl: Inhibits adenylatec cyclase

51
Q

What are initiating signals of G-alpha-q? Downstream signal?

A

Acetylcholine
alpha-adrenergic amines
many NTs

Downstream: Increases IP3 and intracellular Ca

52
Q

What are initiating factor of G-alpha-t

A

Photons

Stimulates cGMP phosphodiesterase

53
Q

G alpha 13

A

Thrombin

Stimulates Na/ H exchange

54
Q

Describe activatino of protein kinase A (PKA or camp-dependent protein kinase)

A

PKA is activated by any mechanism that activates cAMP

CaMP binds to regulatory subunit and causes dissociation of catalytic subunit of PKA

55
Q

Function of PKA

A

phosphorylates a wide variety of proteins: (enzymes, membrane proteins, nuclear proteins)

Residues that are phosphorylatd are Ser or Thr residues (NOT tyrosine)

56
Q

How can PKA system be turnef OFF?

A

cyclica AMP PHOSPHODIESTERASE

57
Q

what kind of agents inhibit phosphodiesterase?

A

METHYLXANTHINES like coffee or theophylline)

amplifies response by preventing or slowing the destruction of cAMP
treats asthamticsby raising intracellular cAMP which leads to relaxation of SM

58
Q

How can the adrenergic receptor be “desensitized”

A

by phosphoyraltion by a specific kinase, BARK

for beta adrenergic receptor kinase

B-arrestin then binds to this phosphoyralted domain

59
Q

Process if Epinephrine is stimulus

A

B-adrenergic R

Gs

Ad Cyclase

Glycogen breakdown

60
Q

Serotonin

A

Serotonin R

Gs

Ad cyclase

Behavrioal sensitization and learnign in APLYSIA

61
Q

Light

A

rhodopsin

Transducin

cGMP PDE

Visual excitation

62
Q

Odornats

A

olfactory R

G olf

Ad cyclase

olfaction

63
Q

fMET

A

chemoatactic R

Gq

PLC

Chemotaxis

64
Q

Ach

A

Muscarinic R

Gi

K+ channels

Slowing of pacemaker activity

65
Q

What does Ras do?

A

Regulates CELL GROWTH through serine-threonine protein kinases

66
Q

What does Rho do?

A

REORGANIZES CYTOSKELETON through serin-theronine protein kinases

67
Q

What does Arf do?

A

Activates ADP-ribosyltransferase of the cholera toxin A subunis;

regulates VESICULAR TRAFFICKING pathways; activates phospholipase D

68
Q

What does Rab do?

A

Plays a key role in SECRETORY and ENDOCYTOTIC pathways

69
Q

What does Ran do

A

Functions in the TRANSPORT of RNA and protein into and out of nucleus

70
Q

What is neurofibromatosis

A

variety of benign and malignant tumors of CNS and PNS

dominantly inherited genetic disorder

71
Q

cuause of Neurofibromatosis

A

deletion or loss of function mutation in the nfl gene

72
Q

What are clinical signs

A

cafe au lait macules (spots)

73
Q

What is Neurofibromin

A

GTPase activating protein (GAP) for Ras (and other smll G-proteins)

74
Q

What happens with loss of neurogbromin?

A

loss of GTPase activity which inactivates Ras and tehrefore Ras stays on in its GTP-bound form

75
Q

What is Nf2?

A

tumor suppressor gene associated with neurofibromatosis

76
Q

Describe mechanism of hormones that use Ca or phosphatidylinostides (or both)

A
  1. hormone binds to 7 TM serpentine
  2. Receptor activates a G-protein by GTP exchange
  3. activated alpha-subunit activates PLC
  4. Two second messengers are produced
    5/ Protein Kinase C is activated

Biochem Winter 2012 (10 decks)

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