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MCM Test 2 > Cell Signaling > Flashcards

Cell Signaling Flashcards

1
Q

Signaling is important for:

A
  1. normal cell growth
  2. division and differentiation
  3. homeostasis
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2
Q

Steps in cell signaling

A
  1. Signaling cell secretes a signaling molecule (which can be a lipid/water ligand) in response to a stimulus.
  2. Ligand transported to a target cell, where it binds to a receptor
  3. [Ligand-receptor complex] can activate or inhibit cellular pathways.
    a. Effectors alter the activity of components downstream and create 2nd messengers that will elicit a cellular response.
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3
Q

How are signals terminated?

A

Signals are terminated by the removal of the signaling molecule and/or receptor

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4
Q

The effector can be:

A
  1. Metabolic enzyme
  2. Gene regulatory protein
  3. Cytoskeleton protein
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5
Q

Endocrine signaling

A

A signaling molecule (hormones) freely diffuse into the blood to travel long distances to their target.

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6
Q

What is the life of endocrine signals?

A

Short term: the half life is in minutes

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7
Q

Example of endocrine signaling

A

Epinephrine is released by the medulla into the blood to bind to heart muscles.

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8
Q

Paracrine signaling

A

signal diffuses to a receptor of a target cell of a different cell type

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9
Q

Paracrine signaling is _____ and ____-lived

A

Paracrine signaling is LOCAL and SHORT-lived

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10
Q

Example of paracrine signaling

A

Testosterone is made in Leydig cells and act on neighboring Sertoli cells

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11
Q

Autocrine signaling

A

Signal will bind to a receptor on the same cell or the same type of cell

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12
Q

Example of autocrine signaling

A

Interleukin-2 and growth factors use this type of signaling to promote their replication in minutes.

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13
Q

Direct/juxtacrine signaling

A

Direct/juxtacrine signaling involves direct contact. The signal binds signaling cell, which will then bind to a receptor on the target cell

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14
Q

Example of direct/juxtacrine signaling

A

HB-EGF (heparin binding-epidermal growth factor)

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15
Q

What are the 2 types of signaling molecules

A
  1. Water soluble (hydrophillic)

2. Lipid soluble (hydrophibic)

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16
Q

What does the type of signal molecule indicate?

A

it tells us where the receptors are present

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17
Q

How does hydrophilic signaling work?

A
  1. A hydrophilic molecule will bind to a receptor on the cell membrane because it cannot pass through.
  2. Activates a second messenger inside of the cell
  3. Triggers a downstream cellular response
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18
Q

What are receptors that are involved in hydrophilic signaling?

A
  1. GCPRs

2. Tyrosine kinases

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19
Q

Ex. of hydrophilic signals

A
  1. Epinephrine
  2. insulin
  3. glucagon
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20
Q

How does lipophilic signaling work?

A
  1. Lipophilic signal passes the membrane and binds to receptor in the cytoplasm or nucleus.
  2. The [receptor+molecule] will then act as a transcription factor and affect gene expression.
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21
Q

Examples of lipophilic signals

A
  1. steroids
  2. thyroid hormone
  3. retinoids
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22
Q

What happens when a lipophilic molecule binds to a cytoplasmic receptor?

A

The cytoplasmic receptor exists in an inactive complex with HSP 90.

  1. Ligand binds, HSP 90 goes away.
  2. [Hormone+receptor] complex will then move to nucleus where it binds to a DNA sequence called the HRE (hormone response element) and affects gene expression.
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23
Q

What is the DNA sequence called that the hormone+receptor complex of lipophilic molecules bind?

A

HRE

Hormone response element (HRE)

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24
Q

What is the life of lipophilic signals?

A

They have a long half life because they affect transcription

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25
Q

What are the three types of receptors?

A
  1. Ligand gated ion channels
  2. GCPRs
  3. RTKs (receptor tyrosine kinases)
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26
Q

Which type of enzyme is an enzyme-coupled receptor?

A

RTKs

Receptor tyrosine kinases

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27
Q

Structure of GCPRs

A

GCPRs have
1. 7 transmembrane proteins (7 alpha helices)

  1. Extracellular domain (ECD) that binds to the signal
  2. Intracellular domain (ICD) that binds to the G-protein
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28
Q

Trimeric g-protein components

A

There are three components to the G-protein: alpha, beta, gamma

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29
Q

What does an inactivated G-protein look like?

A

Inactivated G-protein has a GDP bound to the alpha subunit, which is bound to beta and gamma subunit

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30
Q

How is the G-protein activated?

A

G-protein is activated by exchanging the GDP for GTP via GEF (built into the GCPR).

The activated alpha subunit will then separate from the B and y subunit

31
Q

What is GEF

A

GEF is guanine nucleotide exchange factor.

It helps to activate the G-protein by replacing GDP with GTP on the alpha subunit

32
Q

How does a G-protein return to its inactive state?

A

The G-protein has intrinsic GTPase activity and will hydrolyze GTP–> GDP via GAP

33
Q

What is GAP

A

GTPase Activating Protein

GAP accelerates the inactivation of a G-protein by hydrolyzing bound GTP into [GDP+Pi].

34
Q

When G-protein is bound to GDP it is

35
Q

When G-protein is bound to GTP it is

36
Q

Steps of GCPR

A
  1. Ligand binds to GCPR, causing a conformational change that facilitates its interaction with the G-protein.
  2. GCPR activates GEF (guanine nucleotide exchange factor), causing the GDP on the alpha-subunit to change into GTP.
  3. The activated alpha subunit will then kick off and attach to a effector molecule, activating or inactivating it.
  4. Effector will then activate 2nd msngers and initiate cascade of events
  5. G-protein has intrinsic GTPase activity and will hydrolyze GTP–> GDP via GAP (GTPase activating protein)
37
Q

4 types of GCPR pathways

A
  1. Gs
  2. Gi
  3. Gq
  4. Gt
38
Q

Gs pathway

A
  1. Gs alpha subunit stimulates AC, causing ATP–> cAMP

2. cAMP activates PKA, which phosphoryaltes target

39
Q

Gi pathway

A
  1. Gi alpha subunit will INHIBIT AC

Thus, cAMP is not made and PKA is not activated to cause phosphorylation

40
Q

Gq pathway

A
  1. Gq alpha subunit will activate the effector [PLC: phospholipase C].
  2. [PLC] will then cleave PIP into IP3 and DAG

—-2 pathways now emerge

A. DAG will activate PKC, which will cause phosphorylation.

B. IP3 will go to the ER and cause Ca2+ to be released from the channels.
    Ca2+ will then bind to 
    Ca2+-calmodulin complex 
    and activate associated 
    proteins
41
Q

What is the second messenger in Gq pathway?

42
Q

Gt pathway

What is the ligand?
What does it activate?

A

Light is the ligand

Activates cGMP phosphodiesterases, which breaks cGMP –> 5’ GMP

43
Q

_____ is a non-selective agonist of all adrenergic receptors. What does this mean?

A

Epinephrine can bind to all adrenergic receptors. It can undergo multiple GCPR pathways.

44
Q

When EPI binds to [B-adrenergic receptors], it undergoes ____ pathway

45
Q

When EPI/NE binds to [a-adrenergic], it undergoes ____ pathway

46
Q

Histamine undergoes ____ pathway

47
Q

ACh undergoes ___ pathway

48
Q

DA undergoes ____ pathway

49
Q

GCPR signaling is diverse. Explain.

A

One ligand can produce different physiological responses in the same target of different cells.

For example:
When EPI binds to B-adrenergic receptors

  1. Causes relaxation of bronchials and intestinal smooth muscle
  2. heart to contract

In both cases, it activates the second msnger cAMP.

Thus, EPI can be prescribed to relieve bronchospasms during an asthma attach or restore cardiac rhythms.

50
Q

cyclic nucleotides are hydrolyzed for what?

A

to regulate cellular levels

51
Q

What does cAMP PDE do?

A

cAMP–>AMP

52
Q

What does cGMP PDE do?

A

cGMP–> 5’GMP

53
Q

How do drugs like Viagra, Levitra and Cialis work?

A

These drugs are [cGMP PDE inhibitors].

when cGMP PDE is inhibited, levels of cGMP increases leading to

smooth muscle relaxation and vasodilation

54
Q

How does caffeine work?

A

Caffeine is a cAMP PDE inhibitor, which leads to increased heart rate.

55
Q

Viagra is a ___________ inhibitor.

56
Q

Caffeine is a _________ inhibitor.

57
Q

Nitrous oxide (nitrates) causes ______ and ______. It _____ blood pressure

A

Nitrates cause

  1. relaxation of smooth muscle
  2. vasodilation

Decreases blood pressure

58
Q

Nitrous oxide (nitrates) cause the relaxation of smooth muscle and vasodilation. How?

A

Nitrous oxides cause the relaxation of smooth muscle by diffusing into cells [guanylate cyclase–> cGMP].

Increasing cGMP causes smooth muscle relaxation and vasodilation. BP decreases

59
Q

What drugs should those on nitrates avoid?

A

cGMP PDE inhibitors (which increase cGMP).

Can cause hyper-vasodilation and a fatal drop in BP.

60
Q

Cholera toxin prevents the _________ of ___.

A

Cholera toxins prevent the INactivation of Gs.

61
Q

Pertussis prevents the _____ of ___.

A

Pertussis prevents the ACTIVATION of Gi.

62
Q

Cholera toxin and mechanism of action

A

Cholera occurs when one drinks contaminated water.

Cholera prevents Gs proteins from being inactivated due to ADP ribosylation of Arg , which decreases GTPase activity.

Thus, Gs proteins is constantly stimulating AC, leading to an increase in cAMP.

Too much cAMP opens Cl- chanells, causnig loss of electrolytes and water resulting in diarreah.

63
Q

Pertussis and mechanism of action

A

Pertussis prevents Gi proteins from being activated due to ADP ribsosylation of Cys.

The alpha subunit cannot dissociate from the G complex to inactivate AC.

Thus, AC is less inhibited, increase cAMP.

Causes loss of fluids and excess mucous in airway.

64
Q

In Cholera and Pertussis, how is there excess H2O secretion?

A

Toxins activate AC, producing cAMP.

cAMP activates the CFTR, opening up Cl- channels. A negative charge is built across the membrane and Na+ follows to offset, creating NaCl.

NaCl creates a gradient, which leads to water secretion.

65
Q

Desensitization

A

our ability to turn off or “ignore” a signal

66
Q

What 4 ways can signal densensitization occur?

A
  1. Hormone levels drop, leading to decrease AC activity, decrease cAMP, decrease PKA
  2. Use a PDE to remove the signaling molecule
  3. Receptor sequestration via a endosome
  4. Receptor destruction via a endosome + lysosome
67
Q

What does GRK stand for?

A

G-protein receptor kinases

68
Q

What do GRK’s do?

A

G-protein receptor kinases (GRKs) impair downstream activity of GCPRs.

  1. Activated GPCR stimulates GRK to phosphorylate the GCPR on multiple sites.
  2. Arrestin will then bind to the 3rd intracellular loop, preventing the Galpha subunit from binding.
  3. GDP does not get converted to GTP and the GCPR is densensitized
69
Q

Structure of tyrosine kinases

A
  1. EDC has the binding site (ligands tend to be growth factors)
  2. Single helix that spans the membrane
  3. ICD that has tyrosine kinase activity

IT IS MONOMERIC!!!

70
Q

What binds to RTKs?

A

growth factors and insulin

71
Q

RTK pathway

A

When the ligand binds it causes:

  1. Ligand binds to receptors and causes dimerization.
  2. Dimerized receptor will phosphorylate tyrosine residues in the ICD.
  3. Phosphorylated tyrosines are recognized by adaptors and docking proteins (SH2 of GRB2), which can activate 2 pathways: RAS dependent and RAS independent
72
Q

RAS dependent pathway is facilitated by _____

73
Q

RAS dependent pathway is facilitated ____

A

other kinases

74
Q

Both the RAS dependent and RAS independent trigger what?

A

Both trigger the phosphorylation of proteins in the nucleus, plasma membrane and cytoplasm

leading to alterations in gene transcription

MCM Test 2 (12 decks)

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