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Biochem Exam III > Bartling SG > Flashcards

Bartling SG Flashcards

1
Q

Cells detect, amplify, and integrate external signals by way of

A

transduction cassettes

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2
Q

Specific cell surface membrane receptors, Effector signaling elements, Regulatory proteins are components of

A

transduction cassettes

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3
Q

What happens when a ligand binds to a specific receptor protein on the cell surface

A

Change in confirmation

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4
Q

Change in cellular metabolism, function, or development is

A

cellular response

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5
Q

What happens after the cellular response has been activated what happens to the ligand

A

Ligand is removed

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6
Q

After the ligand is removed what happens

A

Ligand is degrated

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7
Q

What is the first step in cell signaling

A

synthesis of ligand

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8
Q

Signaling molecule

A

ligand

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9
Q

What are chemical messengers

A

Hormones

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10
Q

What types of cells makes chemical messengers (hormones)

A

Endocrine cells

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11
Q

Gene expression and protein synthesis are affect by

A

Chemical messengers

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12
Q

Chemical messengers that act on same cell that secreted them

A

Autocrine

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13
Q

Chemical messengers that act on other cells

A

Paracrine

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14
Q

Types of hormones chemical messengers

A

Steroids
Amine
Peptide
Polypeptide

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15
Q

Amino acid-derived chemical messenger

A

Amine

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16
Q

Corticosteroids, Androgens, Estrogens are

A

Cholesterol precursor

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17
Q

Chemical messengers that can cross the cell membrane are

A

lipid soluble

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18
Q

Steroid hormone messengers are

A

lipid soluble

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19
Q

Intracellular (cytoplasmic) receptors for this type of chemical messenger are located inside target

A

Steroid hormones

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20
Q

How do steroid hormones reach there target

A

Through the blood stream

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21
Q

How are steroid hormones are released from the cell that synthesizes them

A

Immediately diffuse out

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22
Q

Steroid hormones are synthesized and released by

A

endocrine cells

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23
Q
  1. Synthesis of the signaling molecule (ligand)
  2. Release of the signaling molecule (ligand)
  3. Transport of signaling molecule to target cell
  4. Binding of the ligand by a specific receptor protein and change in conformation
  5. Change in cellular metabolism, function, or development = cellular response
  6. Removal of ligand, terminating cellular response
  7. Degradation of ligand
A

Know these 6 steps

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24
Q

If a chemical signal is slow acting it has a

A

Longer half-life

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25
Q

Steroid hormones has a longer half-life than

A

peptide hormones

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26
Q

Amine hormones are derived from

A

Tyrosine or tryptophan

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27
Q

How are amine hormones are released from the cell that synthesizes them

A

Stored until needed

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28
Q

What types of cells produce amino hormones

A

Endocrine

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29
Q

Where are the receptors for amine hormones located on target cells

A

Cell surface or intracellular

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30
Q

Hormones that are not imitate;y released into the blood stream

A

Polypeptide

Amine

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31
Q

Type of hormone that is water soluble

A

Polypeptide

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32
Q

Polypeptide are considered to be

A

First messengers

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33
Q

Polypeptide are first messengers because they bind to

A

External receptors

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34
Q

Intracellular effects of a polypeptide hormones are mediated by

A

Second messenger

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35
Q

A second messenger example is

A

cAMP

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36
Q

Second messenger molecules are

A

Low molecular-weight

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37
Q

Another second messenger example is

A

Calcium

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38
Q

Do polypeptide hormone pass immediately into the target cell?

A

No

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39
Q

Polypeptide hormones activate their target cells by way of

A

second messagers

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40
Q

What converts ATP to cAMP

A

adenylyl cyclase

41
Q

Adenylyl cyclase is activated by what part of the G-protein

A

α-subunit

42
Q

What activates Adenylyl cyclase

43
Q

What inactivates / turns off cAMP

A

Phosphodiesterase

44
Q

What does cAMP activate

A

Protein kinase

45
Q

Where is the cAMP activated protein kinase located

46
Q

What does G-protein do to the cell signal

47
Q

What do the bacterial toxins target

48
Q

ADP-ribosylates Gs α-subunit

A

Cholera toxin

49
Q

What does cholera toxin do to cAMP

50
Q

What cell does the cholera toxin target

A

intestinal G-protein

51
Q

An increase cAMP within intestinal epithelial cells leads to

A

phosphorylation of Cl

52
Q

Cholera toxin leads to

A

efflux of electrolytes and water

53
Q

Whooping cough is caused by

A

Pertussis toxin

54
Q

Pertussis toxin does what to cAMP

55
Q

An enhance of pertussis toxin does what to neutrophils

A

inhibits functions

56
Q

Pertussis toxin effects

A

neutrophils

57
Q

Ligand binding forms dimer that activates

A

tyrosine kinases

58
Q

Tyrosine kinases does what to downstream targets

A

phosphorylates

59
Q

Does tyrosine kinases have intrinsic enzymatic activity

60
Q

when phosphorylation of tyrosine kinase occurs it activates

A

other protein kinases

61
Q

When ligand binding occurs to an ion channel what happen s

A

confirmation change

62
Q

Ligand binding changes confirmation of ion channel receptor

A

Ions flow through

63
Q

What type of ions flow through ion channels

64
Q

Bacterial toxin that indirectly affects ion-channels

65
Q

Prevents release of acetylcholine neurotransmitter and cleaves proteins involved in docking of neurotransmitter vesicles

A

Botulinum toxin

66
Q

What does Botulinum prevent the release of?

A

acetylcholine

67
Q

What is acetylcholine

A

neurotransmitter

68
Q

Calcium binds to what protein inducing conformational change

A

calmodulin

69
Q

When calcium binds to calmodulin what happens

A

Conformational change

70
Q

What conformational change occurs in the Calcium and calmodulin binding

A

Two globular domains joined

71
Q

What join the two globular domains

A

a long α-helix

72
Q

Calcium/calmodulin complex binds to and modifies

A

protein kinase

73
Q

Calcium/calmodulin complex activates

A

signal cascade

74
Q

Second messenger responsible for calcium mobilization

75
Q

Phosphatidylinositol 4,5-bisphosphate

76
Q

What is PIP2 hydrolyzed by

A

(PLC)

PIP2-specific phospholipase C

77
Q

What PLC generate

A

Two second messengers

78
Q

What are the two second messengers of PLC

A 
Inositol trisphosphate (IP3) 
Diacylglycerol (DAG)
79
Q

Second messenger that is water soluble and mobilizes calcium

A

Inositol trisphosphate (IP3)

80
Q

Second messenger that is anchored in plasma membrane due to hydrophobic fatty acid side chains

A

Diacylglycerol (DAG)

81
Q

Second messenger that activates key protein kinase C (PKC) family

A

Diacylglycerol (DAG)

82
Q

Can be hydrolyzed by other phospholipases to produce other lipid second messengers

A

Phosphatidylcholine

83
Q

Different species of DAG (generated by PLC), Phosphatidic acid (generated by PLD) and Arachidonic acid (generated by PLA2) are

A

Lipid second messengers

84
Q

Key inflammatory and pain mediator

A

Arachidonic acid and prostaglandins

85
Q

Prostaglandins, prostacyclins, thromboxanes, and leukotrienes are precursors of

A

eicosanoids

86
Q

Act like hormones and signal via G-protein coupled receptors

A

Prostaglandins

87
Q

Modulate smooth muscle contraction, platelet aggregation, gastric acid secretion, and salt and water balance

A

Arachidonic acid and prostaglandins

88
Q

Arachidonic acid conversion to prostaglandins involves

A

cyclooxygenase isoforms

89
Q

Nonsteroidal anti-inflammatory drugs (NSAIDs)

A

Aspirin and Ibuprofen

90
Q

Response to inflammatory mediators

91
Q

cyclooxygenase isoforms

A

COX-1 and COX-2

92
Q

Modulate smooth muscle contraction, platelet aggregation, gastric acid secretion, and salt and water balance

A

Arachidonic acid and prostaglandins

93
Q

Anti-inflammatory drugs block cyclooxygenase conversion to

A

prostaglandins

94
Q

Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit

A

cyclooxygenase

95
Q

What irreversibly inactivates both forms cyclooxygenase

96
Q

selective inhibitions of what effective treatments for inflammatory conditions (rheumatoid arthritis)

A

COX-2 (celecoxib)

97
Q

Selective inhibitors of COX-2 (celecoxib) are effective treatments for

A

inflammatory conditions (rheumatoid arthritis)

98
Q

Arachidonic acid can also be converted into what by lipoxygenases

A

leukotrienes

Biochem Exam III (3 decks)

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