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MCM Final > Receptors And Cell Signaling > Flashcards

Receptors And Cell Signaling Flashcards

1
Q

Endocrine signaling

  1. Definition
  2. Example
A
  1. Signal (hormone) is transported via the blood to a cell a long distance away.
  2. Epinephrine released by adrenal medulla acts on heart muscle; hormones
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2
Q

Paracrine

  1. Definition
  2. Example
A
  1. Signal (paracrine factor) diffuses to neighboring target cell of a different cell type. LOCAL
  2. Testosterone—Leydig cells synthesize and secrete testosterone that induce spermatogensis by acting on Sertolli and germ cells
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3
Q

autocrine signaling

  1. Definition
  2. Example
A
  1. Secreting cells express surface receptors for the signal they are producing. Self activation
  2. Chemokines, interleukin-1 produced by T-lymphocytes promote their own replication in immune response
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4
Q

Direct/Juxtacrine signaling

  1. Definition
  2. Example
A
  1. Signal binds to cell that produces the signal and then binds to receptor on the target cell. This creates a bridge between the two cells.
  2. Heparin-binding epidermal growth facto-like growth factor binds to EGF receptors
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5
Q

Hydrophilic signaling

  1. Receptors involved
  2. Mechanism
  3. Examples
A
  1. G-protein coupled receptors (GPCRs) and receptor tyrosine kinases.
  2. Signal—receptor complex initiate production of second messenger (small and derived from AA, or through lipid metabolism) which triggers a downstream cellular response.
  3. Epinephrine, insulin, and glucagon.
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6
Q

Lipophilic Signaling

  1. Receptors involved
  2. Mechanism
  3. Examples
A
  1. Cytoplasmic receptor, nuclear receptor
  2. Lipophilic signals are able to move through the cell membrane and activate receptors in the cell
  3. Steroid hormones, thyroid hormones, retinoids
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7
Q

How does a cytoplasmic receptor work?

A

Exist in inactive complex with HSP90.
When ligand binds, HSP dissociates.
Hormone receptor complex is translocated to the nucleus, which then binds to a specific DNA sequence called HORMONE RESPONSE ELEMENT (HRE) in the promoter region of specific genes.

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8
Q

How does a nuclear receptor work?

A

These receptors are already present in the nucleus and bound to DNA. The hormone ligand allows for interactions with additional proteins to activate the complex.

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9
Q

Three types of receptors

A
  1. Ligand gated-ion channels, usually stimulated by neurotransmitters
  2. G-protein coupled receptors
  3. Enzyme-coupled receptor class—receptor tyrosine kinases
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10
Q

Structure of the G-protein coupled receptor (GPCR)

A
  • Extracellular domain binds signal
  • Transmembrane domain is composed of 7 alpha helixes
  • intracellular domain interacts with G-proteins
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11
Q

Overview of the step of GPCR signaling

A
  1. Ligand binds to ECD causes conformational change in GPCR
  2. ICD activates G protein (exchange GDP for GTP)
  3. GTP bound protein interacts with membrane bound effector protein, usually an enzyme that produces secondary messenger
  4. Signal is terminated, various methods
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12
Q

Methods of termination of cell signaling

A
  1. Dissociation of signaling molecule
  2. Inactivation of the G-protein
  3. Reduction of concentration of the secondary messenger
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13
Q

A trimeric G protein has what function that monomeric G proteins lack?

A

Trimeric G proteins have intrinsic GEF (guanine exchange factor) and GAP (GTP-ase activating protein) capabilities.

Monomeric G proteins will need to have an external GEF and GAP force.

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14
Q

Different types of GPCR signaling (4)

A
  1. Gs—stimulates adenylate cyclase
  2. Gt—stimulates cGMP phosphodiester are
  3. Gi—inhibits adenylate cyclase
  4. Gq—activates phospholipase C
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15
Q

Gs signaling

A

Stimulates adenylate cyclase

  1. Ligand binds
  2. G-protein activates
  3. Activate G protein stimulates adenalylcyclase (AC) to create cAMP
  4. cAMP activates PKA (the effector enzyme)
  5. PKA phosphorylates proteins.

PDE (phosphodiesterase) breaks down cAMP

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16
Q

Gt signaling

A

Stimulates cGMP phosphodiesterase

  1. Ligand binds (light)
  2. G-protein activated
  3. Active G-protein stimulates cGMP PDE, which turns cGMP into GMP
17
Q

Gi signaling

A

Inhibits adenylate cyclase

  1. Lingand binds
  2. G-protein is activated
  3. Active G-protein inhibits AC
  4. cAMP is not make and PKA is not activated
18
Q

Gq signaling

A

Activates phospholipase C

  1. Ligand binds
  2. G-protein is activated.
  3. Active G-protein activates phospholipase C
  4. PLC cleaves PIP into DAG and IP3
  5. IP3 releases Ca2+ from the ER
  6. Ca2+ activates calmodulin
  7. DAG and Ca2+ activate PKC, which can then phosphorylates proteins
19
Q

What ligands use Gs signaling? (2)

A
  1. Epinephrine

2. Histamine

20
Q

What ligands use Gi pathway? (2)

A
  1. Epinephrine/norepinephrine

2. Dopamine

21
Q

What ligand uses Gq pathway?

A

Acetylcholine

22
Q

What ligand uses Gt pathway?

A

Light!

23
Q

The same signaling molecules can produce different physiological responses in the same targets of different cells. What is an example of this?

A

Epinephrine binding to beta-adrenergic receptors causes relaxation of bronchial and intestinal smooth muscles.

Epinephrine binding to beta-adrenergic receptors in the heart causes contractions.

Both reactions produce the same secondary messenger, cAMP, but signaling pathways diverge downstream.

24
Q

Inhibitors of cGMP PDE do what?

A

Increase concentration of cellular cGMP, resulting in smooth muscle relaxation and vasodilatation (viagra)

25
Q

How does nitric oxide lead to smoothe muscle relaxation

A

NO diffuses through muscle cells and activates guanylate cyclase resulting in the production of cGMP

cGMP leads to smooth muscle relaxation and vasodilation.

26
Q

How does cholera affect G-protein reactions?

A

Toxin covalently modifies alpha subunits, ADP ribosylation of Arginine decrease GTPase activity. G-protein IS NOT TURNED OFF.

Continuously stimulates adenylate cyclase leading to overproduction of cAMP.

Over abundance of cAMP in intestinal cells opens Cl- channels, loss of electrolytes and water=diarrhea.

27
Q

How does pertussis affect GPCR pathways?

A

ADP ribosylation of Cys on the alpha subunit of the G protein prevents a citation and dissociation of alpha subunit. IT IS NOT TURNED ON.

Lead to less inhibition of AC and overproduction of cAMP.

Loss of fluids, excessive mucous in airway epithelial cells.

28
Q

What protein binds to the phosphorylated GPCR to inactivate the complex?

A

Arrestin

29
Q

Structure of receptor tyrosine kinase (RTK)

A
  1. Extracellular domain, binds ligand
  2. Single alpha helical transmembrane domain
  3. Intracellular domain with TK activity
30
Q

Examples of common RTK ligands

A

GROWTH FACTORS

EGF, NGF, PDGF

31
Q

Dimerization of RTK is caused by what?

A

Binding of a ligand to extracellular domain

32
Q

Phosphotryosines are recognized by _______ and _______ protein which ________.

A

Phosphotyrosines are recognized by ADAPTOR and DOCKING proteins which ACTIVATE DOWNSTREAM SIGNALING

33
Q

What specifically in the adapter and docking proteins recognizes phosphotyrosines?

A

The SH2 or PTB domain of Grb2

34
Q

The recognition of phosphotyrosines by adapter and docking proteins activates what?

A

It triggers phosphorylation of protein targets that lead to alterations in gene transcription and protein activity

35
Q

Ras-dependent signaling facilitated by….

A

MITOGEN ACTIVATED PROTEIN KINASE FAMILY (MAPK)

36
Q

Ras-independent signaling facilitated by……

A

DIFFERENT KINASE

37
Q

Mutant forms of Ras and GEFS/GAPS cause what in humans

A

A wide range of cancers

38
Q

Overexpression or mutation of what receptor has been linked with cancer

A

RTK

MCM Final (12 decks)

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