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Physiology 3 Endocrine > Introduction to Endo - Hormone Receptor Interactions > Flashcards

Introduction to Endo - Hormone Receptor Interactions Flashcards

1
Q

what is the difference between endocrine & paracrine?

A

endocrine - hormones all over body carried by bloodstream

paracrine - local influence

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2
Q

what are pheromones?

what is their other name?

A

chemical messengers released by one species member that affects function of the rest of the group

social hormones

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3
Q

as an example of pheromone kin recognition, rodents have shown to release _____ chemicals that impinge on sensitive _____ receptors and recognize their own kind through odor molecules

A

aromatic chemicals

olfactory receptors

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4
Q

what is the syllabus definition of a hormone?

A

a substance secreted directly into the blood by specialized cells in response to a specific stimulus (neural or blood) that is carried in minute concentrations in blood and influences target cells by interacting with specific receptors

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5
Q

what are the 5 main groups of cells that secrete hormones? and give example(s) of each

A
  1. derivatives of amino acids (epinephrine thyroxine)
  2. small peptides (ADH)
  3. proteins (insulin, gastrin)
  4. glycoproteins (TSH)
  5. steroids (aldosterone sex hormones)
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6
Q

where are steroid hormones synthesized from?

A

cholesterol

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7
Q

how are derivative of amino acid hormones (epinephrine thyroxine) synthesized?

A

derived from tyrosine amino acid

iodination of tyrosine as a part of globulin then released as T3 or T4

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8
Q

how are peptide hormones (ADH) synthesized?

A

prehormone translated from mRNA with short hydrophobic signal sequence at N term

signal sequence leads peptide to rough ER and leaves, leaving begin a prohormone

post-translational cleavage of prohormone = active hormone and non-active peptides

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9
Q

what kind of hormone-recepter interactions does each hormone group have?

  1. insulin
  2. epinephrine, peptides
  3. thyroid hormones
  4. steroids
A
  1. insulin - autophosphorylation of tyrosine residues of receptor –> internalized
  2. epinephrine and peptides - bind to membrane receptors and change ion channel activity or produce secondary messengers (cyclases, phospholipase C)
  3. thyroid - pass through membrane and act within cell nucleus
  4. steroid - lipid soluble, diffuse through membrane and bind to cytoplasmic receptors, mediated by HR complex binding to DNA –> modulate gene trx (expression)
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10
Q

give some examples of hormones that are responsible for each function in the body:

  1. metabolism, energy balance
  2. water and electrolyte balance (renal)
  3. reproduction
  4. satiety
  5. thirst
  6. regulate body rhythms
A
  1. insulin, glucagon, thyroxine, epi, growth hormone, somatostatin, cortisol
  2. ADH, ang2, aldosterone, PTH
  3. sex hormones (hypothalamic-pituitary)
  4. CCK
  5. ang2, ghrelin, leptin
  6. pituitary, adrenal, cortical hormones
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11
Q

what in the hypothalamus specifically controls circadian rhythms?

A

suprachiasmatic nuclei

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12
Q

Explain what a hormone-hormone negative feedback is using TSH and TRH as an example

A

HH negative feedback - when a hormone secreted by endocrine gland is controlled by another hormone from another endocrine gland

ex. hypothalamus secretes TRH which regulates TSH from anterior pituitary –> high levels of TSH inhibits TRH from stimulating TSH release

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13
Q

Explain what a substrate-hormone feedback is using insulin-glucose regulation as an example

A

SH feedback - when a body function/condition is regulated by a hormone

ex. insulin decreases blood glucose in target cells which decreases insulin release (as blood glucose decreases, less of a need for insulin) and vice versa

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14
Q

What are the 5 properties of hormone-receptor interaction?

A
  1. highly specific
  2. simple, bimolecular, reversible
  3. saturable
  4. high affinity
  5. responsive tissue
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15
Q

what is the physiological range for concentrations of circulating hormones?

A

10^-7 M to 10^-12 M

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16
Q

In saturable hormone-receptor interactions, explain what it means to have maximum hormone binding capacity or to be an extra/spare receptor

A

max hormone binding capacity - if amount of hormones exceeds # of receptors, there is saturation of receptors with hormones and hormone binding is limited

extra/spare receptor - hormone may have a response only after partial interaction and those extra un-occupied receptors (when bound to more hormones) increase sensitivity of a cell to the hormone

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17
Q

difference between equilibrium association (Ka) and dissociation (Kd) constant?

A

Ka - high Ka = high affinity of receptor for hormone
Ka = [HR]/[H][R]

Kd - inverse of Ka = [H][R]/[HR]

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18
Q

when [H] = Kd, what is the ratio of [HR]:[R] and what percentage of the receptors are bound and unbound?

A

the ratio would be 1 meaning [HR] = [R]

that means that half 50% of receptors are bound and the other half 50% of receptors are unbound

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19
Q

T/F: hormones can affect tissues that are unspecific to that hormone

A

FALSE - in order for successful hormone-receptor interaction, tissue must be specific and responsive to hormone

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20
Q

T/F: peptide hormones and amines (water soluble) are non-polar and passively diffuse through lipoprotein membranes and small enough to pass through membrane pores. they initiate their responses inside the target cells by binding to glycoprotein receptors at the nucleus

A

FALSE - peptide hormones and amines (water soluble) are TOO POLAR to passively diffuse through lipoprotein membranes and TOO LARGE to pass through membrane pores. they initiate their responses at the OUTER SURFACE of the target cells by binding to glycoprotein receptors anchored WITHIN THE PLASMA MEMBRANE

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21
Q

what are the 2 groups of membrane receptors?

A
  1. 7 membrane-spanning domains = serpentine receptors

3. single membrane-spanning domain

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22
Q

what are the 3 types of g protein linked receptors? (7 membrane)

A
  1. g protein coupling to adenylase cyclase
  2. g protein coupling to phospholipase C
  3. g protein and others
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23
Q

what are the 4 types of enzyme-linked receptors? (single membrane)

A
  1. tyrosine kinase (TK) receptors
  2. serine/threonine kinases
  3. guanylate cyclase receptors
  4. cytokine receptor family
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24
Q

G proteins are ____ comprised of 3 subunits ___, ____ and ____

A

heterotrimer (remember: 3 subunits)

alpha, beta, gamma

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25
Q

the g protein alpha subunit is a ____, cleaving GTP –> GDP + Pi. since the products of GTP hydrolysis (GDP and Pi) dissociate slowly, the alpha subunit is found predominately bound to ____ in the absence of a hormone which is the (inactive/active) state. when a hormone attaches to receptor, cytoplasmic ____ replaces the ____ at the g subunit binding site and causes the g alpha subunit to dissociate from By subunit. The g alpha subunit binds to ____ and turns hormone response on or off. This is the (inactive/active) state. When the GTP on the g alpha subunit dissociates by GTPase, it will return to ____ state.

A 
GTPase
GDP
inactive
GTP
GDP
effector 
active 
inactive
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26
Q

g protein coupling to adenylase cyclase

many HR interactions lead to activation of adenylate cyclase, a membrane protein that catalyzes the formation of ______ from ____ at inner membrane surface. cyclase activation is mediated by regulatory protein _____, a stimulatory g protein. adenlyate cyclase activated by ____subunit of g protein bound to ____. however, it is not activated by g protein binding to ____.

cAMP activates ____. binding of cAMP to the _____ subunits activates the active _____ subunits by causing them to ____ from the complex.

A 
cAMP
ATP
Gs-alpha 
alpha 
GTP
GDP

PKA
regulatory
catalytic
dissociate

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27
Q

what 2 factors determine how much adenylate cyclase is in the active form? (bound to g protein and GTP)

A

rate of exchange of GTP for GDP

rate of GTP hydrolysis

28
Q

How does PKA affect trx of target genes?

A

catalytic subunits of PKA enter nucleus and phosphorylates CREB which binds to response elements in DNA –> influence trx of nearby genes

29
Q

g protein coupling to phospholipase C

turnover of ____ appears to be a key even in signal transduction of hormones and neurotransmitters. HR interaction here activates g protein ____ which activates ____ rather than adenylate cyclase. PIP2 has 2 pathways:

  1. ____ cleaves PIP2 to ____ and ____, both products being intracellular mediators. ___ mobilizes Ca2+ from vesicular storage sites and ____ which is retained in the membrane, associates with cytoplasmic _____ in the presence of Ca2+ and activates it.
  2. PIP2 also is phosphorylated by ____ to form ____. at the cell membrane, protein kinases called ____ phosphorylates and activates enzyme ____, which then phosphorylates other target proteins like TFs. the enzyme that triggers this cascade is ____.
A

PIP2
Gq-alpha
phospholipase C

1. phospholipase C 
diacylglycerol and IP3
IP3
diacylglycerol
protein kinase C (PKC)
2. PI 3 kinase
PIP3
PDKs
Akt
PI 3 kinase
30
Q

g protein coupling to other effectors

what are the other 3 examples of g protein family members?

A
  1. inhibit adenylate cyclase
  2. activate k+ channels (Gi-alpha)
  3. stimulate cGMP phosphodiesterase (Gt-alpha or transducin)
31
Q

tyrosine kinase receptors

many receptors have ____ kinase activity (insulin, EGF, PDGF) in cytoplasmic domains. signal transduction requires ____ of agonist-receptor complexes and ___ of Tyrosine residues of the receptor itself. this is called ______. it increases both receptor kinase activity and affinity for substrates.

A

intrinsic
dimerization
phosphorylation
auto-phosphorylation

32
Q

serine/threonine kinases

similar to TK kinases in that after binding to a ligand (hormone), they ____ and ____ cytoplasmic substrates called _____. These substrates then move into the ___ where they influence gene trx. serine/threonine kinases interact with ____ inhibitory substance and ___ (both hormones).

A 
dimerize
phosphorylate
Smads
nucleus
Mullerian
inhibin
33
Q

guanylate cyclase receptors

the receptor for ____ has guanylate cyclase activity in cytoplasmic domain. binding of ANP to receptor increases cytoplasmic levels of ____ that mediate actions of hormone. Some of these actions result from ___ activation of ____.

A

ANP
cGMP
cGMP
protein kinase G

34
Q

cytokine receptor family

this family includes hormones like ___ and ____ and include receptors like ____ and _____. this family lacks ______ activity. however, they associate with ____ after they bind to ligand and ____. JAKS interact with dimerized receptors and phosphorylate factors called ____ that move into nucleus and regulate trx of specific genes.

A 
growth hormone and prolactin
erythropoeitin and other hematopoietic growth factors
intrinsic enzymatic activity
JAKS 
dimerize
STATs
35
Q

receptor mediated endocytosis

define: coated pits
coated vesicles
clathrin
adaptins

although internalized hormones are degraded in lysosome, receptors/degradation products may act within a cell to further ______. receptors that aren’t degraded can be ______ to cell surface.

A

coated pits - cluster of HR complexes in regions of the membrane

coated vesicles - coated pits that invaginate and pinch off from membrane

clathrin - protein in inner surface of membrane that forms membrane coat

adaptins - protein complexes also found in coat, recognize receptors cytoplasmic domains and trap them within the coated pit

mediate a biological response
recycled

36
Q

intracellular receptors - steroid hormones

steroid hormones act by regulating ____ in responsive cells. ligands are lipid (soluble, insoluble) so they passively diffuse across membrane and bind to receptors in cytoplasm or nucleus and bind to ____.

hormone binding to steroid receptors causes _____ of associated proteins like HSP90 (heat shock) that prevents __________ when the ligand is absent. HR complex then _____ and translocates to nucleus.

at the nucleus, they interact with sites on DNA called ____ that have ____ sequences. the _____ of HR complexes favors interaction of each receptor subunits with one of the two identical half sites of _____.

A

gene expression
soluble
DNA

dissociation
receptors from interacting with DNA
dimerizes

HREs
palindromic sequences
dimerization
HRE

37
Q

What are HREs?

A

hormone response elements on DNA (binding sites for HR complex on DNA)

38
Q

intracellular receptors - thyroid hormones

these receptors associate with HREs even in the (presence/absence) of the hormone. these receptors are NOT associated with ____ but with _______ that modulate gene trx downstream.

A

absence
HSP90
nuclear proteins

39
Q

what are the 3 structural domains that intracellular receptors share?

A
  1. C term hormone binding region
  2. highly conserved DNA binding domain
  3. variable N term
40
Q

what is the role of intracellular receptor N term domain?

A

participates in TF recruitment

41
Q

in intracellular receptors, the DNA binding domain is rich in ____ residues and recognizes specific ___. they are unmasked upon interaction of hormone binding region with _____.

A

cysteine
HREs
ligands (hormones)

42
Q

Showcase how steroid hormones may have non-genomic actions within the cell (hormone actions too rapid for nuclear events to take place)

ex. aldosterone

A

aldosterone affects RBCs and fibroblasts in knockout mice without aldosterone receptor

non-genomic because RBCs have no nucleus

43
Q

what are the 2 factors of cellular response to a hormone?

A
  1. free hormone availability

2. cell sensitivity to hormone

44
Q

T/F: secretion, uptake, degradation rates of hormone influence cellular response

A

TRUE

45
Q

T/F: concentrations of plasma proteins are NOT involved in regulating cellular responses to hormone

A

FALSE - plasma proteins carry hormones to target cells so they DO affect cellular responses to hormones

46
Q

T/F: free hormone, the biologically inactive form, is in equilibrium with carrier bound hormone

A

FALSE - biologically active

47
Q

T/F: free hormone, the biologically active form, is in excess compared with carrier bound hormone

A

FALSE - equilibrium

48
Q

Free hormone, the biologically active form, is in equilibrium with carrier bound hormone:

explain the example given in the syllabus
ex. alpha-feroprotein levels in baby vs puberty mice

A

alpha-feroprotein in mice binds to testosterone and estradiol with high affinity –> gradually declines from high levels in newborn mice to low levels in mice just before puberty

overtime, alpha-feroprotein releases sex hormone so increasing amounts of free sex hormone

49
Q

explain negative cooperativity

A

binding of a hormone molecule to a receptor influences affinity of neighboring binding sites

increasing receptor occupancy decreases affinity of remaining receptors for that hormone

50
Q

T/F: there is high cell sensitivity (receptor affinity) at low hormone concentrations and vice versa

A

TRUE

51
Q

T/F: there is low cell sensitivity (receptor affinity) at low hormone concentrations and vice versa

A

FALSE - high cell sensitivity = low hormone levels

52
Q

explain down regulation of a hormone

A

decrease in # of receptors or loss of binding sites to a hormone to protect cells from over-stimulation

decrease overall effect of hormone

53
Q

explain how g protein uncoupling contributes to decreased cell sensitivity to a hormone

ex. in beta-adrenergic system

A

beta-ARK and free By mediate phosphorylation of receptor which reduces affinity for g protein

beta-arrestin binds phosphorylated receptor and blocks g protein interaction

54
Q

how are these hormonal groups inactivated?

peptide
internalized
steroid

A

peptide - proteases

internalized - lysosome

steroid - liver

55
Q

T/F: in hormone radioimmunoassay standard curve, increased radioactivity means that there is more cold insulin/hormone that binds to receptors

A

FALSE - cold means unlabeled so if there if increased radioactivity, it means more labeled hormones are bound to receptors

56
Q

what is androgen insensitivity syndrome?

Describe the cause, effects, long term effects, diagnosis of androgen insensitivity syndrome

talk about - dihydrotestosterone, female phenotype, LH role in high testosterone, aromatase

A

no synthesis of functional androgen receptor

cause = during development, testis of XY (male) makes testosterone normally BUT target tissues of testosterone fail to develope –> no differentiation of these tissues

effects = ineffective dihydrotestosterone (uses same defective receptor), no differentiation of prostate/male external genitalia so you have female phenotype

normally, you have increased LH production by pituitary gland which increases testosterone but since no receptor, testosterone levels skyrocket and stay like that

long term = person has female phenotype because some testosterone becomes estrogen by enzyme aromatase.

diagnosis = disorder diagnosed at puberty (no menstruation)

57
Q

What does arrestin do?

A

blocks receptors from binding to g proteins

58
Q

can steroid hormones enter the nucleus with the presence of heat shock proteins?

A

NO - heat shock proteins are bound to receptors and inhibit them from entering nucleus

59
Q

What are hormone response elements?

A

HRE - palindromic sequences at specific sites on DNA that bind to steroid hormone-receptors complexes

60
Q

what hormones have receptors associated with g protein activation? (utilize cAMP as secondary messenger)

A 
catecholamines 
glucagon
ACTH
glycoprotein hormones (LH, TSH, FSH, hCG)
ADH
PTH
MSH
prostaglandins
histamine
secretin
VIP
61
Q

T/F: in all responsive cells, a max biological response occurs only when all receptors are occupied

A

FALSE - can also occur in receptors that are partially occupied

62
Q

T/F: every cell synthesizes receptors for all circulating hormones

A

FALSE - only specific hormones, not all

63
Q

T/F: downregulation refers to the decrease in rate of hormone secretion by endocrine cells

A

FALSE - loss of binding sites (decrease in # of receptors)

64
Q

T/F: the pituitary gland increases LH production at puberty

A

TRUE - which is why people with androgen insensitivity syndrome have such levels of testosterone at puberty

65
Q

increasing hormone concentration also increases free ______ on the membrane and therefore increases potential for receptor ______ to the hormone

A 
free By (beta-gamma)
desensitization

(G protein uncoupling)

66
Q

T/F: G protein alpha (Ga) is bound to By when the receptor is inactive

A

TRUE - not bound to hormone

67
Q

T/F: Ga is bound to By when the receptor is active

A

FALSE - Ga is bound to effector protein when hormone/ligand is bound –> leaving free By component of the membrane

Physiology 3 Endocrine (9 decks)

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