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ENRE > Hormone Signaling Pathways > Flashcards

Hormone Signaling Pathways Flashcards

1
Q

How is cell signalling generally terminated?

A

by removal of signaling molecule or receptor

or attenuation/inactivation of signaling events

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2
Q

What is juxtacrine signaling?

A

signaling molecule stays attached to the secreting cell and binds a receptor on an adjacent targent cell

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3
Q

How is hydrophilic hormone signaling accomplished?

A

hydrophilic signal binds receptor at cell surface –> molecule-receptor complex initiates production of second messenger molecules –> cellular response

main receptors = GPCRs, RTKs

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4
Q

How do lipophilic hormones signal?

A

passively diffuse through plasma membrane of target cell –> bind receptor in PM or on nucleus –> acts as a transcription factor

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5
Q

What are the main hydrophilic hormones?

A

amines: histamine, SE, melatonin, dopamine, NE, epi

From lipid metabolism: Ach

Polypeptides: insulin, glucagon, cytokines, TSH

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6
Q

What are the main lipophilic hormones?

A

steroids: progesterone, estradiol, testosterone, cortisol, aldosterone, Vit D

Thyroid hormone

retinoids

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7
Q

What is the difference in half-lives of hydrophilic and lipophilic hormone medications?

A

hydrophilic = short half lives

lipophilic = long, slow acting

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8
Q

What are the basics of GPCR signaling?

A

inactive trimeric G protein –> GEF exchanges GDP for GTP –> gamma and beta leave = active –> GAP removes Pi –> inactive trimeric w/ GDP

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9
Q

What does a Gs receptor do?

A

stimulates adenylate cyclase –> cAMP –> PKA –> other proteins phosphorylated

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10
Q

What does a Gi receptor do?

A

inhibits Adenylate cyclase –> no cAMP produced

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11
Q

What does a Gt receptor do?

A

light –> GPCR –> cGMP phosphodiesterase

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12
Q

What does a Gq receptor do?

A

Gq –> PLC –> IP3 and DAG –> Ca and PKC

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13
Q

What kind of receptor does histamine bind?

A

Gs

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14
Q

What kind of receptor does Ach bind?

A

Gq

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15
Q

What kind of receptor does dopamine bind?

A

Gi

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16
Q

What is the general structure of an RTK?

A

extracellular domain

alpha-helical transmembrane domain

intracellular TK domain

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17
Q

How does RTK signaling generalling work?

A

ligand binds to extracellular domain –> dimerization –> tyrosines Piate –> recognize adaptor proteins –> RAS-dependent and RAS-independent paths

both Piate spec proteins

18
Q

What is the basic structure of insulin?

A

A chain = 21 aa

B chain = 30 aa

connected by 2 disulfide bridges

1 disulfide bridge within A chain

19
Q

What is the difference btw inactive and active insulin?

A

inactive = stored in body as a hexamer

active = monomer

20
Q

How is insulin synthesized?

A

preproinsulin mRNA –> preproinsulin protein –> goes to ER –> cleaved to proinsulin –> folded and moved to golgi –> packaged and cleaved in golgi –> mature granules = hexameric crystals (3 dimers)

21
Q

What are the 2 pools of insulin corresponding phases of insulin release?

A

readily releasable pool = limited, 5%

reserve pool = 95%, granules must undergo mobilization

22
Q

What does the RAS-dependent signaling of insulin do?

A

insulin binds RTK –> GRB-2 and IRS-1 –> RAS –> Piated proteins –> alterations in gene transcription (increased scrip of glucokinase –> glucose uptake, glucogen synthesis

23
Q

What does the RAS-independent insulin signaling do?

A

insulin binds RTK –> Pi 3-kinase –> PKB –> Piated proteins –> alterations in protein and enzyme activity (more glut4, activation of glycogen synthase) –> glucose uptake, glycogen synthesis

24
Q

How is insulin signaling terminated?

A

insulin-receptor complex is internalized in target cells by endocytosis –> either degraded or recycled

25
Q

How does insulin affect its own receptor?

A

downregulates its receptor

decreases rate of synthesis/increases rate of degradation

26
Q

How is insulin resistance quantified?

A

amount of glucose cleared from the blood in response to a fixed dose of insulin –> failure of expected response = resistance

27
Q

What are the 3 main possibilities for insulin resistance currently being studied?

A

downregulation of insulin receptor

defects in insulin signaling (less GLUT4)

defects in insulin receptor (75 mutations ID’d)

28
Q

What are the main defects in downstream insulin receptor signaling being studied?

A

defects in IRS1 and IRS2

Piation of serine instead of tyr in IR and IRS –> inhibits downstream signaling

Ser/Thr kinase activated by cytokines, FFAs, DAG, ceramide, etc –> impairs downstream signaling

29
Q

Where are nuclear receptors

A

in nucleus

or in cytosol –> translocate to nucleus after ligand binds

30
Q

What are the 3 major domains of nuclear receptors?

A

ligand binding domain (LBD)

activation function 1 domain (AF1) aka transcription activating domain

DNA binding domain (DBD)

31
Q

What does AF1 on a nuclear receptor do?

A

independent of ligand binding

can modify conformation of entire receptor

32
Q

What does DBD on a nuclear receptor do?

A

highly conserved

binds regulatory seq on DNA = hormone response elements (HREs) upstream of target gene

33
Q

What are the primary and secondary responses to steroid hormones?

A

primary = proteins directly induced from steroid-receptor complex

secondary = primary protein shuts off its own genes –> turns on secondary response genes

34
Q

What is ERalpha and where is it found?

A

estrogen receptor = transcription factor

expressed most abundantly in female repro tract

also in mammary gland, hypothalamus, endothelial cells, and vasc smooth muscle

35
Q

What is ERbeta and where is it found?

A

estrogen receptor = transcription factor

expressed most in ovaries, prostate, w/ lower expression in lung, brain, bone, and vasculature

36
Q

What is the mechanism of action of ER?

A

estrogen binds –> ER dimerizes –> promotes HAT activity –> activates transcription

37
Q

How does tamoxifen work?

A

metabolized by liver to 4-hydroxy-tamoxifen –> inhibits ER –> promotes HDAC activity –> inhibits transcription

38
Q

Where is ER located?

A

traditionally thought to be in the nucleus

some evidence that it is in the cytosol

estrogen binding –> dimerization and translocation to nucleus

39
Q

What are the non-genomic ER signaling pathways?

A

some ERs located in the plasma membrane or caveolae in plasma membrane

GPCR and RTK type of receptors

metabolic changes

40
Q

What hormones use a Gs receptor?

A

GCAPALT

glucagon

calcitonin

ACTH

PTH

ADH (V1 receptor)

LH and FSH

TSH

41
Q

What hormones use a Gq receptor?

A

GAGOAT

GHRH

Angiotensin II

GHRH

Oxytocin

ADH (V2 receptor)

TRH

42
Q

What hormones use an RTK to signal?

A

PIGI

prolactin

insulin

GH

IGF-1

ENRE (21 decks)

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