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*Neuroendocrine Exam 3 > Hormone Signaing Pathways > Flashcards

Hormone Signaing Pathways Flashcards

1
Q

Endocrine signaling

A

H released into bloodstream to travel a long distance to reach its target.

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2
Q

Paracrine signaling

A

H released to act on a neighboring cell.

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3
Q

Autocrine signaling

A

H acts on the same cell that secreted it.

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4
Q

Juxtacrine signaling

A

H stays attached to secreting cell and binds to a receptor on an adjacent target cell.

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5
Q

How do hydrophilic Hs signal?

A

Bind to receptor on CM and induce a second messenger system.

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6
Q

What receptors can hydrophilic Hs use?

A

GPCRs

RTKs

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7
Q

Lipophilic Hs signal how?

A

They cross the CM to act as a transcription factor.

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8
Q

What receptors do lipophilic Hs bind?

A

Cytoplasmic receptors

Nuclear receptors

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9
Q

What is the hormone response element (HRE)?

A

The DNA sequence that the hormone-receptor complex (from the cytoplasm) binds to in the nucleus.

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10
Q

What are nuclear receptors bound to?

A

DNA directly

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11
Q

What kind of half-lives do hydrophilic meds have?

A

Very short (sec to min). Given at time of need (ex: Epi).

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12
Q

What kind of half-life do lipophilic meds have?

A

Long half-life (hours to days). Can be taken daily (birth control).

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13
Q

Hoe does an inactive G protein become active? Which enzyme facilitates this?

A

It must exchange its GDP for GTP. GEF causes this transaction.

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14
Q

How does the active GTP become inactivated?

A

There is intrinsic GTPase activity that hydrolysis GTP back into GDP.

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15
Q

What is the function of GTPase-activating protein (GAP)?

A

It accelerates the activity of GTPase, causing an increase in the rate of hydrolysis of GTP to GDP.

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16
Q

What occurs with the alpha, beta and gamma subunits once GTP is active?

A

Beta and gamma subunits remain intact and dissociate, leaving alpha attached to GTP.

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17
Q

How does the Gs pathway function?

What stops the cascade?

A

GTP activates AC —> cAMP —> active PKA —> phosphorylates target.
CAMP is acted on by PDE.

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18
Q

How does the Gi pathway work?

A

GTP inhibits AC and cAMP is not produced.

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19
Q

How does Gt pathway work?

A

Light causes GTP to act on cGMP PDE to convert cGMP to 5’-GMP.

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20
Q

How does Gq pathway work?

A

GTP binds PLC which increases intracellular Ca levels.

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21
Q

When epi binds to a beta adrenergic receptor, what happens? What signaling pathway?

A

Gs.
Relaxation on bronchial SM and intestinal SM.
Contraction of heart.
Increased mobilization of fuels.

22
Q

What pathway does His target? What is the outcome?

A

Gs.

Bronchoconstriction and allergies.

23
Q

What pathway does DA use? What is the outcome?

A

Gi.

Increased HR.

24
Q

What pathway does ACh use? What is the outcome?

A

Gq.

Brochoconstriction and stimulation of salivary glands.

25
Q

What is the anatomy of the RTK receptor?

A

Has an extra cellular domain that binds the ligand, a-helical transmembrane domain and an intracellular domain w/ TK activity

26
Q

How does the RTK system work?

A

Ligand binds —> dimerization.
Dimerized receptor binds tyrosine.
Docking proteins recognize the RTK and trigger either a RAS-dependent or RAS-independent pathway.

27
Q

What is the primary structure of insulin?

A

A chain and a B chain are linked by 2 disulfide bridges.
The A chain has its own disulfide bridge.
21 AAs in the A chain and 30 AAs in the B chain.

28
Q

What is the active form of insulin?

What is the inactive form?

A

Active - hexamer

Inactive - monomer

29
Q

How is insulin synthesized?

A

Preproinsulin mRNA —> preproinsulin protein —> translocated to ER lumen —> cleaved to form proinsulin —> folded in golgi —> released with C peptide.

30
Q

2 phases of insulin release

A
  1. Rapid, but transient release. Comes from a limited pool of granules (<5%) known as the readily releasable pool.
  2. Second phase comes from the reserve pool (>95%). Granules here must undergo mobilization.
31
Q

RAS-dependent insulin signaling (5))

A

Insulin binds to alpha subunit of insulin receptor (an RTK).
Autophosporylation of tyrosine residues in the beta subunit.
Insulin receptor substrate 1 (IRS-1) recognizes the phosphotyrosine residues.
GRB-2 recognizes IRS-1 and triggers the RAS and MAP kinase pathway.
Causes increased transcription of glucokinase.
Glucokinase phosphorylates glucose in the first step of glycolysis.

32
Q

RAS-independent insulin signaling (5)

A

Insulin bind to RTK.
Autophosphorylation.
IRS-1 recognizes the RTK and is phosphorylated.
PI3kinase is recruited by IRS-1.
PIP2 and PIP3 are activated and stimulate recruitment of protein kinase B (PKB).
PKB stimulates glucose uptake/storage.

33
Q

What is the role of PKB in the movement of GLUT 4?

A

It moves GLUT4 from cytoplasm to PM of muscle and adipose to allow Glc to enter.

34
Q

How does PKB promote glycogen synthesis?

A

It inhibits glycogen synthase kinase 3 (GSK-3).

35
Q

How is insulin signaling terminated?

A

The insulin receptor is internalized and degraded or recycled.

36
Q

What is insulin resistance?

A

A down regulation of the insulin receptor.

37
Q

What is the quantifiable parameter of insulin resistance?

A

Measure the amount of glucose cleared from the blood in response to a fixed dose of insulin.

38
Q

Severe insulin resistance can be caused by?

A

Defects in insulin binding domain on extra cellular side or variations of intracellular domains.

39
Q

Phosphorylation of which aa instead of tyrosine in the IR can inhibit activation and signaling?

A

Serine

40
Q

What are orphan receptors?

A

Nuclear receptors discovered by DNA sequencing. Ligands are unknown.

41
Q

3 major domains of nuclear receptors

A

Ligand binding domain (LBD)
Activation function 1 domain (AF1) (aka transcription activating domain)
DNA binding domain

42
Q

What do DBDs bind?

A

HRE

43
Q

Types of estrogen receptors (2)

A

ERa

ERbeta

44
Q

Where is ER alpha expressed most?

A

Female reproductive tract and mammary gland, hypothalamus, endothelium and vascular sm

45
Q

Where is ER-beta mostly expressed?

A

Ovaries and prostate

46
Q

Which ER is believed to be predominant in growth regulation?

A

ER-alpha

47
Q

What is the MOA of ER?

A

Estrogen binds and promotes his tone acetyl transferase (HAT) which activates transcription.

48
Q

MOA of tamoxifen

A

Tamoxifen is metabolized by the liver to 4-hydroxy-tamoxifen —> promotes histone deacetylase activity (HDAC) —> inhibits transcription.

49
Q

What is the general transcription apparatus (GTA) and what is its role in the ER and tamoxifen?

A

It enhances transcription.

ER recruits it, and tamoxifen tries to inhibit it.

50
Q

ER has both:

A

Genomic and non-genomic effects (in cytoplasm and PM).

*Neuroendocrine Exam 3 (27 decks)

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