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BMS > Signaling Mechanisms Regulating Cell to Cell Communication > Flashcards

Signaling Mechanisms Regulating Cell to Cell Communication Flashcards

1
Q

Cells can both sense their environment and also influence the behavior/function of other cells by producing secreted

A

Signaling Proteins

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2
Q

This form of communication underlies organ/
tissue physiology and homeostasis in adults,
and is fundamental to

A

Embryonic Development

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3
Q

Include all of the proteins and components that transduce the signal to mediate its effect on the cell

A

The Signaling Pathway

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4
Q

What are the reversible ways that cells respond to signals?

A

Become motile or change shape

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5
Q

What are the irreversible was that cells respond to signals?

A

Divide, differentiate or remain undifferentiated, and die

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6
Q

Allow cells to sense their environment by detecting light, stress or pressure, and chemical signals in the environment

A

Receptor proteins

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7
Q

Which receptor proteins detect light?

A

Photoreceptors

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8
Q

Which receptor proteins detect stress or pressure?

A

Death receptors (TNFR) and mechanoreceptors

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9
Q

A molecule or protein that triggers a signal by binding to a receptor-like protein

A

Ligand

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10
Q

Typically in an inactive state until they receive a signal from the environment

A

Receptors

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11
Q

Once stimulated by ligand binding, receptors do not remain active forever. Some receptors are inactivated by specific mechanisms, while others are inactivated by

A

Self-inactivation

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12
Q

Governed by tertiary (3D) structure and non-covalent bonds between amino acid groups

A

Specificity of receptor/ligand interaction

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13
Q

Any molecule, protein or drug that occupies ligand binding sites and stimulates receptor activity (either
partially or fully)

A

Agonists

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14
Q

Any molecule, protein or drug that occupies ligand binding sites and exclude agonists but does not
stimulate receptor activity

A

Antagonists

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15
Q

Induce receptor activation

A

Agonists

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16
Q

Block receptor activation

A

Antagonists

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17
Q

Underlies cancer, neurological disorders, and metabolic disorders

A

Abnormal cell-cell signaling

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18
Q

About 50% of drugs act on

A

Receptors

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19
Q

The remaining 50% of drugs act primarily on

A

Enzymes

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20
Q

What are the four major classes of receptors?

A
  1. ) Ion channels
  2. ) Steroid hormone receptors
  3. ) Protein kinase receptors
  4. ) 7-alpha-helix receptors
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21
Q

Pore-forming proteins that allow the flow of ions across

membranes down an electrochemical gradient

A

Ion channels

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22
Q

Ion channels are present only on

A

Cell surface and intracellular organelles

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23
Q

Classified by the nature of their gating, the species of ions passing through, and the number of gates (pores)

A

Ion channels

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24
Q

What are five types of gating seen in ion channels?

A
  1. ) ligand
  2. ) voltage
  3. ) mechanical or thermal
  4. ) phospholipid
  5. ) lipid
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25
Q

Binding of ligand opens a channel to allow flow of a

specific ion across the membrane, or closes a channel to stop the flow

A

Ligand-gated channel

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26
Q

Ligand gated channels are the basis for

-i.e. where ligands are neurotransmitters

A

Nerve transmission & muscle contraction

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27
Q

GABA, glycine, serotonin, and nicotinic acetylcholine are examples of

A

Ligand neurotransmitters

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28
Q

Mutations in ion channel genes may cause either a loss or a gain of

A

Channel function

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29
Q

Cystic fibrosis is a recessive disease caused by
loss-of-function mutations in the cystic fibrosis
transmembrane conductance regulator (CFTR)
gene which is a

A

Chloride channel

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30
Q

Mutation in the CFTR gene leads to abnormal salt transport across epithelial cell membranes, resulting in thick mucus build-up in

A

Respiratory epithelial cells

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31
Q

The ligand for CFTR is

A

ATP

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32
Q

Typically associated with dominant inheritance of the disease

A

Gain-of-function mutations

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33
Q

Mutations in voltage-dependent sodium channels can result in defective inactivation and late Na+ currents in

A

Paramyotonia, cardiac arrhythmia, and epilepsy

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34
Q

A sodium channel blocker that blocks action potentials in nerves

-Found in pufferfish or Fugu

A

Tetrodoxin

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35
Q

Proteins that function by controlling gene expression

  • hydrophobic and can cross the cell membrane
  • derived from cholesterol
A

Steroid hormones

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36
Q

Steroid hormones bind to receptors located in the

A

Cytosol or nucleus

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37
Q

For estrogen, prior to ligand binding, the steroid hormone receptor is attached to a

A

Chaperone protein

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38
Q

Induces a conformational change in the
receptor that causes dissociation from the chaperone protein and exposes a nuclear import signal, allowing homodimerization and subsequent nuclear entry

A

Estrogen binding

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39
Q

Dimerized receptors bind to an estrogen response element (ERE, a DNA promoter) that activates

A

Activates gene transcription

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40
Q

Overexpressed in cancer cells in 70% of breast cancer cases

A

Estrogen receptors

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41
Q

Estrogen sensitive (ER+) breast cancer cells require signaling for uncontrolled cell division and

A

DNA replication

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42
Q

Involves the use of selective estrogen receptor (i.e., competitive) antagonists, such as tamoxifen

A

Endocrine therapy

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43
Q

In breast tissue, tamoxifen is metabolized into a
protein, hydroxytamoxifen (H-tam) that binds to the
ER and prevents binding of

A

Estrogen

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44
Q

Functions to repress rather than activate estrogen target genes via recruitment of transcriptional co-repressors

A

ER/H-tam complexes

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45
Q

A protein or protein domain with enzymatic
activity that transfers phosphate groups from
high energy donor molecules such as ATP to
specific target molecules.

A

Kinase

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46
Q

Are composed of three domains:

  1. An extracellular domain that binds the ligand
  2. A trans-membrane domain
  3. A cytoplasmic domain that has kinase activity or binds a protein-kinase protein
A

Protein kinase receptors

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47
Q

Active kinase receptors are typically

A

Dimers (or other forms of oligomer)

48
Q

What are the two major subfamilies of protein kinase receptors?

-defined by the amino acid phosphorylated

A
  1. ) Tyrosine kinases

2. ) Serine/threonine kinases

49
Q

One of the most well known receptor tyrosine kinases is the

A

Insulin receptor

50
Q

Describe how the receptor kinase works?

A
  1. ) Ligand binds to extracellular domain of each receptor subunit causing dimerzation
  2. ) The cytosolic protein kinase domains phosphorylate and activate each other (often at multiple positions)
  3. ) Aditional cytosolic proteins are recruited to and bind the phosphorylated receptors
51
Q

A reversible process that can regulate whether a receptor is “on” or “off”

A

Phorphorylation

52
Q

The addition of a phosphate molecule to a polar R
group of an amino acid (like tyrosine) can turn a
hydrophobic portion of a protein into a

A

Hydrophilic one

53
Q

This can give rise to a conformational change which can facilitate interaction with other parts of the protein or with other

A

Molecules

54
Q

Contains an SH2-domain that recognizes tyr-P and binds to phosphorylated receptors

A

Grb

55
Q

Binds to Grb and activates small G-proteins such as Ras

A

SoS (a GEF)

56
Q

SoS binds to Grb and activates small G-proteins such as the prototypic monomeric small G-protein

A

Ras

57
Q

Activate G-proteins by catalyzing the exchange of GDP (inactive) for GTP (active)

A

Guanine Nucleotide Exchange Factors (GEFs)

58
Q

Promote inactivation of G-proteins by stimulating conversion of GTP (active) to GDP (inactive) via hydrolysis

A

GTPase activating proteins (GAPs)

59
Q

Bind guanine nucleotides and act as a molecular switch during signaling

A

G-proteins

60
Q

Have intrinsic GTPase activity

A

G-proteins

61
Q

The GTPase activity of G-proteins is stimulated by

A

GAPs

62
Q

The replacement of GDP by GTP is stimulated by

A

GEFs

63
Q

Receptor bound SoS is

A

ras-GEF (ras-guanine exchange factor)

64
Q

Regulate many aspects of cell function

A

Small G-proteins

65
Q

The Ras protein family is actually a small family of proteins made up of

A

H-, K-, and N-Ras

66
Q

Functions in receptor signaling and cell division

A

Ras family

67
Q

Functions in traffic of membrane vesicles

A

Rab family

68
Q

Functions in nucleus/cytoplasmic traffic

A

Ran family

69
Q

Functions in the actin cytoskeleton

A

Rac family

70
Q

Proteins like the Mitogen Activated Protein Kinae (MAPK) with ras-GTP cause a phosphorylation cascade that activates

-stimulates production of proteins involved in cell division

A

Transcription factors

71
Q

Serves as a convergence point for many signals

A

Ras

72
Q

Ras is one of the most frequently altered proteins in

A

Human Tumors

73
Q

Oncogenic mutations in Ras turn all of its down stream pathways

A

On

74
Q

Most oncogenic mutations of Ras are amino acid substitutions at just two positions. What are the two positions?

A

gly-12/gly-13 or gln-61

75
Q

These mutations affect the structure of Ras and abolish its ability to hydrolyze GTP, so it is always in the

A

Active state

76
Q

What are two ofther Ras-related disease?

A

Neurofibromatosis Type-1 and Noonan Syndrome

77
Q

Caused by a mutation in the NF1 gene, which results in overactive Ras. This gene encodes neurofibromin-1, a Ras-GAP.

A

Neurofibromatosis type 1

78
Q

Caused by a mutation in the PTPN11 gene which encodes SHP2. This results in a gain of function phenotype which leads to hyperactive Ras

A

Noonan Syndrome

79
Q

The most abundant class of receptors

A

7-α-helix receptors

80
Q

Most receptor targeted drugs are directed at

A

7-α-helix receptors

81
Q

What are four physiological roles for 7-α-helix receptors?

A

Vision, smell, mood, and autonomic nervous system

82
Q

Opsins (7-α-helix receptors), such as rhodopsin, convert electromagnetic radiation (light) into

A

Cellular signals

83
Q

7-α-helix receptors for neurotransmitters bind serotonin, dopamine, GABA, and glutamate to affect

A

Mood

84
Q

Both sympathetic and parasympathetic nervous systems are regulated by G-Protein-coupled

A

7-α-helix receptors

85
Q

7-α-helix receptors are coupled to trimeric “large G-proteins” whose α-subunits contain

A

Ras-like domains

86
Q

Ligand binding to 7-α-helix receptors causes exchange of GDP by GTP and activation of the G-protein, initiating

A

Signaling Cascade

87
Q

The 7-α-helix receptor itself thus acts as a

A

GEF

88
Q

Dissociate from ligand-bound receptors and regulate activity of downstream proteins

A

α and βγ subunits

89
Q

What are the three main subclasses of large G-proteins α-subunits?

A

Gs-α, Gi-α, and Gq-α

90
Q

Activates adenylate cyclase which activates protein kinase A (PKA)

A

Gs-α

91
Q

Inhibits adenylate cyclase, which inhibits protein kinase A (PKA)

A

Gi-α

92
Q

Activates phospholipase-Cβ (PLC) which affects Protein kinase C (PKC)

A

Gq-α

93
Q

Desensitization/dialing back the response, is when the receptor signaling diminishes or terminates, even in the presence of

A

Ligand

94
Q

7-α-helix receptor that binds the adrenal-gland hormone epinephrine and the neurotransmitter norepinephrine.

A

β-adrenergic receptor

95
Q

The ligand-bound β-adrenergic receptor becomes substrate for

A

β-adrenergic receptor kinase (BARK)

96
Q

The phosphorylated β-adrenergic receptor is bound by

-blocks interaction with Gs

A

β-arrestin

97
Q

Ligand-bound β-adrenergic receptor is inactivated by a
protein kinase and

-terminates signaling even in the presence of the ligand (desensitization)

A

β-arrestin

98
Q

Cytosolic calcium is maintained at a very low
concentration by calcium pumps in the plasma
membrane and the

A

Smooth ER (SER)

99
Q

Triggers many events in cells such as muscle contraction, regulated secretion, and cell division

A

Receptor-mediated calcium influx

100
Q

Gi-α inhibits adenylyl cyclase, which then prevents PKA from becoming active. This prevents

A

Calcium influx

101
Q

Gs-α activates adenylyl cyclase, which in turn activates PKA, which allows for

A

Calcium influx

102
Q

Gq-α-GTP activates phospholipase-C (PLC) and triggers

A

Ca2+ release from the Smooth ER (SER)

103
Q

Gq-α-GTP activates phospholipase C (PLC), which hydrolyzes membrane phosphatidyl inositol-
4,5-diphosphate (PiP2) into

A

iP3 and diacyl glycerol (DAG)

104
Q

Triggers release of Ca2+ from lumen of SER into cytoplasm

A

iP3

105
Q

DAG and Ca2+ then activate

A

Protein kinase C (PKC)

106
Q

Most kinases are inactive because they are

A

inhibited

107
Q

Frees kinases from inhibition

A

Receptor activation

108
Q

Inactive because its active site is filled with an N-terminal pseudosubstrate peptide, held in place by its
C1 and C2 domains

A

PKC

109
Q

Bind DAG in membranes

A

C1 domains

110
Q

In the presence of Ca2+ the C2 domain binds

-found in the inner leaflet of the plasma membrane

A

Phosphatidyl Serine (PS)

111
Q

This removes the pseudosubstrate from the active site and PKC becomes active. It can then be cleaved proteolytically and PKC is then

A

Constitutively (permanently) active

112
Q

A calcium-binding protein that regulates the activity of many proteins

-binds 4 Ca2+ ions

A

Calmodulin

113
Q

Is closely related to the calcium-binding subunit
of the protein troponin which regulates muscle
contraction

A

Calmodulin

114
Q

Ca2+ bound calmodulin activates many proteins,

including another self-inhibited kinase known as

A

Calmodulin-activated protein kinase (CAMK)

115
Q

An important mediator of learning and
memory and has been implicated in AD

-others are involved in cancer and musculoskeletal diseases

A

CAMKII

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