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EOM 1 - Test 3 > McCumbee - Cell Signaling > Flashcards

McCumbee - Cell Signaling Flashcards

1
Q

Intracellular Receptors

A

Receptor proteins located inside the cell

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2
Q

Cell Surface Receptors

A

Integral component of the plasma membrane

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3
Q

Signal Transduction Pathways

A

When a signaling molecule binds to its receptor, the receptor undergoes a conformational change that enables it to transmit a signal

These can be activated or inhibited for regulation of functions in target cell

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4
Q

How is the cellular response integrated to different stimulatory/inhibitory signals?

A

Signal transduction pathways for complex network through with certain components in one pathway are able to stimulate or inhibit the activity of components of other pathways

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5
Q

Direct Cell-to-Cell Signaling

A

Involves a signaling molecule expressed on the surface of one cell and a receptor localized on surface of adjacent cell

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6
Q

Endocrine Signaling

A

Signaling molecules = hormones

These released from secretory cells into the blood and carried to distant target tissues

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7
Q

Paracrine Signaling

A

Signaling molecules exert their effects locally on neighboring cells

Reach via interstitial fluid

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8
Q

Neurotransmitters

A

Neural communication is a form of paracrine signaling in which neurotransmitters are released at synaptic junction

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9
Q

Autocrine Signaling

A

Signaling molecules bind to receptors in or on the cells that release them

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10
Q

Gap Junctions

A

Role in cell signaling; small intracellular chemical mediators are able to pass through gap junctions, signaling information can be shared by neighboring cells

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11
Q

Functions of Receptors

A
  1. Recognize and bind specific ligands (hormones, neurotransmitters, drugs, etc)
  2. Elicit a response by the target cell when receptor is occupied by activating one or more intracellular signal transduction pathway
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12
Q

What lessens the probability that a given receptor will be activated by a variety of different compounds?

A

Receptors are highly specific

Receptor binds a specific ligand or a few structurally related molecules

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13
Q

What is the term which means a receptor can bind the ligand at very low concentrations?

A

The receptor has high affinity

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14
Q

What type of interactions usually occur between receptors and ligands?

What does this result in?

A

Non-covalent

Reversible Reactions

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15
Q

What is the result of there being a finite number of receptors in a target tissue?

A

Receptor binding is a saturable process

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16
Q

What allows ligands/receptors to form non-covalent interactions?

A

Complementary shapes, charges, hydrophobicity, or other physical properties of molecules.

  • Ionic Bonds
  • Hydrogen Bonds
  • van der Waals
  • Hydrophobic effects
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17
Q

What term is a quantitative measure of the affinity of a receptor for a specific ligand?

A

Kd

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18
Q

What number is the total number of receptor binding sites?

A

Bmax

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19
Q

What can binding studies help determine?

A

Total number of binding sites (Bmax)

Affinity of the receptor (Kd)

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20
Q

What is the mathematical representation of Ka?

A

Ka = [L*R] / [L][R] = Kf/Kr

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21
Q

Can receptor, [R], be measured direction?

A

No, use binding studies to measure the other values

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22
Q

How is [R] calculated experimentally?

A

Bmax - [L*R]

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23
Q

What is the reciprocal of Ka ?

A

Kd

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24
Q

What is the shape of the plot of many protein and peptide ligands?

A

Curvilinear, due to negative cooperativity

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25
Q

What is the concentration of ligand at with 1/2 of the receptors are occupied?

A

Kd

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26
Q

What is the response of a target tissue to a ligand proportional to?

What does this result in in terms of regulation?

A

Formation of [L*R]

Anything that affects [L], Bmax, and Kd will modulate the response of a target cell to a specific signaling molecule

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27
Q

What are three methods to modulate the response of a target cell to a specific signaling molecule?

A
  1. Changes in the concentration of signaling molecule [L]
  2. Changes in Bmax (up/down regulation)
  3. Changes in Kd (covalent modification, loss of function mutations)
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28
Q

Do all tissues have similar signaling pathways?

Example?

A

No, different tissues have different distributions and different signaling pathways

Example is adrenergic receptors in different tissues in the Fight or Flight reponse

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29
Q

How can specific receptor types for a given ligand be detected?

A

Using highly specific pharmacological agonists

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30
Q

Nicotinic Receptors location?

A

Skeletal muscles

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31
Q

Parasympathetic nervous system receptors?

A

Muscarinic receptors

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32
Q

Which two Kd values will have a higher affinity?

A

Lower number

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33
Q

Receptor Agonist

A

Structural analog of a naturally occuring signaling molecule that binds the receptor for the signaling molecule and mimics the responses induced by the naturally occuring molecule

34
Q

Receptor Antagonist

A

Structural analogs that bind a receptor for a signaling molecule but to NOT elicit a response. They interfere with the binding of the naturally occuring signaling molecule to the receptor – block the action of that signaling molecule

35
Q

What modulates the activity of signal transduction pathways?

36
Q

What are two broad classes of receptors?

A
  1. Intracellular Receptors
  2. Cell-surface Receptors
37
Q

Intracellular Receptors

A

Signaling molecules for these receptors typically enter the cell by simple diffusion across plasma membrane (e.g. steroid hormones) or by facilitated diffusion (thyroid)

38
Q

Cell-surface Receptors

Type of protein?

A

Bind signaling molecules that are too large or too hydrophilic to pass through the plasma membrane

Transmembrane proteins that can undergo conformational change

39
Q

What three methods does the cell surface receptor transmit the signal to the cell by?

A
  1. Altering flux of ions across the plasma membrane
  2. Turning on enzymatic activity present in the cytoplasmic domain, or by activating a cytoplasmic enzyme that is coupled to the receptor
  3. Regulating the activity of plasma membrane G proteins that are coupled to the receptor
40
Q

Ligand-gated Ion Channels

What causes to open?

A

Binding of the ligand-binding domain of the receptor can induce a conformational change can open or close the channel.

Channel opens when the ACh binding sites are occupied

41
Q

What types of molecules can also bind to receptors on certain ion channels to modulate their activities?

A
  1. ACh binding
  2. Cyclic Nucleotides (cAMP, cGMP)
  3. G proteins binding to receptors
  4. Phosphorylation by kinases
42
Q

Enzyme-linked Receptors

A

Receptors which have a domain that functions as an enzyme–largest family in cytoplasmic domain of the receptor is receptor tyrosine kinase family

43
Q

G Protein Coupled Receptors (GPCRs)

A

Transmit signals by means of intermediary proteins called G Proteins

Largest family of cell surface receptors in the human genome

44
Q

G Proteins (GTP-binding regulatory proteins)

A

Couple cell surface receptors to target proteins.

Heterotrimeric, composed of three subunits: alpha, beta, and gamma

45
Q

What subunits of G proteins are tehthered to the plasma membrane?

A

alpha and gamma by means of covalent bonds with membrane lipids

46
Q

What subunits of the G-protein-coupled receptors (GPCRs) remain coupled during signaling?

A

Beta/Gamma (often refered to as the BettaGamma Subunit

47
Q

What type of binding site is the alpha subunit?

A

Guanine nucleotide binding site

48
Q

Regulator of G Protein Signaling (RGS)

A

Proteins that accelerate the intrinsic GTPase activity of the alpha subunit of hetertrimeric G proteins

Responsible for rapid inactivation of G-protein-coupled signaling

49
Q

What modulates the activity of specific membrane-bound effector proteins?

A

The activated alpha subunit following dissociation

50
Q

Free βγ Subunits

A

In certain cells, these can interact with effector proteins to transduce a signal

51
Q

How is the cAMP intracellular signaling pathway regulated?

A

Specific GPCRs

Adenylyl cyclase

Gproteins that couple the above

52
Q

Adenylyl Cyclase

Regulation?

A

Plasma membrane associated enzyme that catalyzes the conversion of ATP to cAMP

Regulated by two G-proteins:

  1. Gs - stimulatory G protein
  2. Gi - inhibitory G protein
53
Q

How is the cAMP signaling pathway activated?

What can bind with a GPCR to act as a GDP/GTP exchange factor?

A

Gs is inactive when GDP occupies the guaning nucleotide binding site of α-subunit.

Becomes active when GTP occupies the site.

Extracellular signaling molecule can bind GPCR, to act like an exchange factor–following conformational change, binds to Gs protein freely and GDP is released. GTP immediately binds.

54
Q

What occurs following GTP binding of the α subunit?

A

It will dissociate from the receptor and βγ complex.

Gα​s (tethered to plasma mebrane) associates with and activates adenylyl cyclase–which will catalyze conversion of ATP to cAMP

55
Q

Why is Gα​s activity short lived?

Where does it go following inactivation?

A

The α​-subunit possess at GTPase domain, and hydrolysis of GTP leaves GDP in the binding site

Returns to βγ-complex

56
Q

How to RGSs (Regulator of G-protein-Signaling Proteins) work?

A

Increasing the rate of intrinsic GTPase activity

57
Q

What occurs to adenylyl cyclase activity in the absence of the active form of Gαs?

A

Activity switches off

58
Q

What is the structure of Protein Kinase A (PKA)?

A

Enzyme comprosed of:

2 regulatory subunits [R]

2 catalytic subunits [C]

59
Q

What binds to the regulatory subunits of PKA?

What occurs once these bind?

A

cAMP

[R] and [C] subunits dissociate; catalytic subunits become active

60
Q

When do the subunits of PKA reassociate?

A

When cAMP is metabolized to 5’ AMP by phosphodiesterase

61
Q

What metabolizes cAMP to 5’ AMP?

A

Phosphodiesterase

62
Q

How does PKA activate or inactivate cellular proteins?

A

Catalyzing the transfer of the terminal phosphate group from ATP to specific Ser/Thr residues of target proteins

63
Q

What major proteins are activated by PKA?

A

Enzymes

Other Kinases

Ion Channels

Transcription Factors

64
Q

What can be activated by PKA upon entering the nucleus?

What does this do?

A

Transcription factor CREB (cAMP Regulatory Element Binding Protein)

P-CREB can bind to CRE (cAMP Response Element) in regulatory region of cAMP-inducible genes

65
Q

What does P-CREB have an increased affinity for?

What is the result?

A

CBP/300 (CREB Binding Protein)

This is a coactivator protein that links CREB with the basal transcription machinery

66
Q

A-Kinase Anchoring Proteins (AKAP)

A

Two domain protein, scaffolding.

One binds the regulatory subunit of PKA, one tethers it to a specific subcellular compartment.

Can form multi-protein complexes that can integrate PKA phosphorylation with other signaling events.

67
Q

What can rapidly dephosphorylate proteins?

What determines the level of PKA-phosphorylated proteins within a cell?

A

Protein Phosphatase

Balance between PKA and protein phosphatase activities

68
Q

Although cAMP induces most of its actions by activect on?ating PKA, what else can it have a DIRECT effect on?

A

Ion Channels

69
Q

Cholera Toxin

A

Enteres intestinal epithelial cells and induces process that covalently modifies Gα​s in a way that blocks intrinsic GTPase activity.

Gs remains constantly active.

70
Q

Forskolin

A

Direct stimulatory effect on adenylyl cyclase

71
Q

Caffeine

A

Inhibits phosphodiesterase activity

72
Q

Isoproterenol

A

β-adrenergic receptor agonist

73
Q

Propranolol

A

β-adrenergic receptor antagonist

74
Q

What effect does the α subunit of Gi have on adenylyl cyclase?

A

Direct inhibitory effect

75
Q

What occurs when acetylcholine binds to M2 muscarinic receptors in heart muscle?

A

The βγ subunits bind to an open K+ channels, which hyperpolarizes the plasma membrane

76
Q

Pertussis Toxin

A

Covalently modifies Gαi so it stays in the G form

77
Q

Desensitization

How can Gs protein coupled recepetor desensitization be induced?

A

State of reduced responsiveness of a tissue to an agonist that develops in response to repeated stimulation

  1. Receptor phosphorylation by PKA
  2. β-arrestin binding to the cytoplasmic domain
78
Q

Feedback Repression by PKA

A

Intensity of response of the target to further stimulate will be diminished as long as residues remain phosphorylated.

Affinity is unchanged

80
Q

For a plot of [LR]/[L] as function of [LR] what is Ka and Bmax?

A

Slope = -Ka (1/Kd)

X-int = Bmax (total number of receptor binding sites)

EOM 1 - Test 3 (18 decks)

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