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BECOM Exam 2 > Cell Signaling > Flashcards

Cell Signaling Flashcards

1
Q

Signals are produced by the target cell that stays within the target

A

Intracrine

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2
Q

Secondary messengers are _____ signals

A

Intracrine

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3
Q

Signals produced by the target cell that are secreted and affect target itself or nearby cell of same type via a receptor

A

Autocrine

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4
Q

Immune cells are ______ signals

A

Autocrine

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5
Q

Signals that target cells in the vicinity of the emitting cell

A

Paracrine

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6
Q

Neurotransmitters are _____ signals

A

Paracrine

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7
Q

Signals that target distance cells.

A

Endocrine

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8
Q

Cells that produce hormones that travel through bloodstream to reach all parts of body.

A

Endocrine

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9
Q

Hormones are _____ signals

A

Endocrine

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10
Q

Signals that target adjacent cells.

A

Juxtacrine

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11
Q

Signals that are transmitted along cell membranes via protein or lipid components integral to the membrane

A

Juxtacrine

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12
Q

Signals that are capable of affecting either the emitting cell or cells immediately adjacent

A

Juxtacrine

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13
Q

Gap (tight junctions, notch signaling) are _____ signals

A

Juxtacrine

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14
Q

3 types of cell surface receptors

A
  • Ion channels/ionotrophic receptors
  • Enzyme-linked receptors
  • G-protein coupled receptors
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15
Q

Intracellular receptors

A

Nuclear hormone receptors

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16
Q

Ca++ is a _______ messenger

A

2nd

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17
Q

What is a molecule that is released in response to a first stimulus that triggers downstream cell responses often to a profound effect?

A

2nd messenger

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18
Q

How are cytosolic Ca++ levels kept low?

A

Ca++ ATPase pumps

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19
Q

What kind of channels are plasma membrane Ca++ channels?

A

Ligand gated or voltage gated channels

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20
Q

What kind of channels are ER Ca++ channels?

A

IP3 gated channels

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21
Q

2 ways increased Ca++ concentration activates effectors

A
  • Directly

- Via Ca++ binding calmodulin

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22
Q

What causes genetic channelopathies?

A

Mutated genes that cause abnormal or absent channel proteins

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23
Q

What causes autoimmune and toxic channelopathies?

A

Antibodies or toxins that bind to channels

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24
Q

What causes transcriptional channelopathies?

A

Abnormal transcription of normal genes that causes aberrant expression of normal proteins

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25
Q

Which signal transducer protein goes with Tyrosine Kinase Receptor?

A

SH2 domain

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26
Q

What does Tyrosine Kinase Receptor bind with?

A

growth factor

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27
Q

What signal transducer protein goes with JAK-STAT Receptor?

A

STAT

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28
Q

What does JAK-STAT Receptor bind with?

A

cytokine

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29
Q

What signal transducer protein goes with Serine-Threonine Kinase Receptor?

A

Smad

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30
Q

What does Serine-Threonine Kinase Receptor bind with?

A

cytokine dimer

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31
Q

What facilitates enzymatic reactions that would not be favorable in the monomeric state to make it much more likely that they will phosphorylate each other due to their proximity?

A

dimerization or oligomerization

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32
Q

What causes transphosphorylation?

A

ligand-binding, dimerization

33
Q

What do RTKs do?

A

Regulate:

Cell proliferation
Cell growth
Cell differentiation
Cell migration

34
Q

Which receptors have a cysteine-rich domain?

A
  • EGF receptor
  • Insulin receptor (IGF-1 receptor)
  • Eph receptor
35
Q

Which receptors have an immunoglobulin-like domain?

A
  • NGF receptor
  • PDGF receptor
  • M-CSF receptor
  • FGF receptor
  • VEGF receptor
  • Eph receptor
36
Q

Which receptor has a fibronectin type II-like domain?

A

Eph receptor

37
Q

Which receptor has disulfide bonds?

A

Insulin receptor, IGF-1 receptor

38
Q

Phosphatidylinositol is phosphorylated by kinases to make __________

A

PI 4,5-bisphosphate

39
Q

What cleaves PI 4,5-bisphosphate to make DAG and IP3 second messengers?

A

phospholipase C

40
Q

PI 3-kinases is phosphorylated by what?

A

PI 4,5-bisphosphate

41
Q

What does phosphorylation of PI 3-kinase produce?

A

PI 3,4,5-triphosphate

42
Q

What creates the docking site for proteins that contain pleckstrin homology (PH) domains?

A

PI 3,4,5-triphosphate

43
Q

What is a good example of divergence in the pathway of signal transduction?

A

insulin receptor

44
Q

What kind of processes does calmodulin mediate?

A
  • Inflammation
  • Metabolism
  • Apoptosis
  • Muscle contraction
  • Intracellular movement
  • Short-term memory
  • Long-term memory
  • Nerve growth
  • Immune response
45
Q

G-proteins store and transmit information based upon what?

A

their conformational state

46
Q

Is the GDP-bound conformation of the G-protein active or inactive?

47
Q

Is the GTP-bound conformation of the G-protein active or inactive?

48
Q

Which G-protein conformation can bind downstream effectors?

A

GTP-bound conformation (active)

49
Q

What speeds up activation (exchange of GDP for GTP) of G-proteins?

A

Guanine Nucleotide Exchange Factor enzymes (GEF)

50
Q

What promotes inactivation of G-proteins?

A

GTPase-activator protein enzymes (GAP)

51
Q

How does GAP enzymes inactive G-proteins?

A

speed up GTP hydrolysis

52
Q

What are G-protein direct effectors?

A
  • Ion channels
  • PLC
  • Adenylyl cyclase
  • Phosphodiesterases
  • GEFs (for Rho family GTPases)
53
Q

There are more _______ than G-proteins or effectors.

54
Q

Often a cell will only contain a few different _______.

55
Q

Why is there only a few different GPCRs for olfactory?

A

If many odorant receptors were expressed, there would be no way to discriminate which one was active because they all couple to the same effectors

56
Q

What is the basal state of heterotrimeric G-proteins?

A

Ga subunit:

  • bound to GDP
  • in complex with Gby subunits
57
Q

Ligand binding to the GPCR causes what?

A

1- Activation of the GPCR
2- Conformational changes
3- Induces GEF activity

58
Q

Which subunit does the GDP for GTP exchange occur?

A

Ga subunit

59
Q

Where does the conformational change take place?

A

Ga subunit

60
Q

What does the conformational change of the Ga subunit lead to?

A

Dissociation of the Ga subunit from:

  • Receptor
  • Gby subunit
61
Q

What activates adenylyl cyclase?

A

heterotrimeric G-proteins

62
Q

What enzyme degrades cAMP?

A

phosphodiesterase

63
Q

What are most of the effects of cAMP mediated through?

A
  • Protein kinase A (PKA)

- EPAC

64
Q

What is EPAC?

A

GEF for Rap1 and Rap2

65
Q

What happens when cAMP binds to the regulatory subunit of PKA?

A

dissociation of the catalytic subunit

66
Q

What happens when cAMP binds to EPAC?

A

relieves auto inhibition of the GEF activity of the protein

67
Q

In the GTP-bound form of Ras, which phosphate group on the bound nucleotide is involved in H-bonding?

A

gamma phosphate group

68
Q

What does the gamma phosphate group H-bond to?

A

the main chain of atoms of conserved Threonine and Glycine residues

69
Q

What happens when the gamma phosphate group H-bonds to T and G?

A

conformational rearrangements of the switch I and II regions of the protein

70
Q

What are the steps of the Ras MAP Kinase pathway?

A

1- Growth factor binding and dimerization
2- Autophosphorylation
3- Binding of adaptor proteins such as Grb2
4- Complex assembly
5- Guanine nucleotide exchange and activation of Ras
6- Ras binds and initiates MAP kinase pathway
7- AP-1 (jun and fos) and transcription factor activated
8- Induction of myc and fos
9- Cell proliferation

71
Q

Are ligands lipophobic or lipophilic molecules?

A

Lipophilic

72
Q

What are some nuclear hormones?

A
  • Steroid hormones
  • Thyroid hormones
  • Retinoids
73
Q

Where do steroid hormones come from?

A

Cholesterol (sex hormones, vitamin D, cortisol)

74
Q

Where do thyroid hormones come from?

75
Q

Where do retinoids come from?

76
Q

What are the steps of the lipophilic hormone pathway from the blood to the cell?

A

1- Hormone passes from the blood plasma through the plasma membrane

2- Hormone binds to a receptor protein in the cytoplasm or nucleus

3- Hormone-receptor complex binds to hormone response element on DNA regulating gene transcription

4- Protein synthesis

5- Change in protein synthesis is cellular response

77
Q

What does glucagon release cause?

A
  • Increased glycogenolysis
  • Increased gluconeogenesis
  • Increased lipolysis
  • Decreased liver glycolysis
78
Q

What does insulin release cause?

A
  • Increased glycogen synthesis
  • Increased FA synthesis
  • Increased TAG synthesis
  • Increased liver glycolysis

BECOM Exam 2 (9 decks)

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