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MCM Exam 2 > Lect 3 Receptors and Cell Signaling > Flashcards

Lect 3 Receptors and Cell Signaling Flashcards

1
Q

What is Endocrine signaling? Example?

What is the distance the signal travels and what is length of half life?

A
  • Signal transported via blood
    • Epinephrine
  • Long distance signaling; 1/2 life on minute scale
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2
Q

What is Paracrine signaling? Example?

A
  • Signal diffuses to neighboring target cell of a different cell type
    • Testosterone
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3
Q

What is Autocrine signaling? Example?

A
  • Secreting cells express surface receptors for the signal on itself or release to cells of same type
    • Interleukin-1 (Chemokines) produced by T-lymphocyte
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4
Q

What is Direct/Juxtracrine signaling? Example?

A
  • Signal binds to signaling cell which then binds to receptor on target cell
    • Heparin-binding epidermal growth factor (HB-EGF)
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5
Q

Which type of signals cannot penetrate the plasma membrane?

How do they interact with the cell?

Examples?

Signal Molecule-Receptor Complex intitiates production of what inside the cell? What gets triggered?

Two types of receptors involved?

A
  • Hydrophillic signaling
  • They interact with specific receptors at the cell surface
  • Epinephrine, Insulin, Glucagon
  • Secondary messengers
    • Triggers downstream cellular response
  • GPCRs and RTKs
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6
Q

What type of signals pass through the plasma membrane of the target cell?

Examples?

The signal/ligand binds to what inside the cell?

This signaling Molecule-Receptor Complex acts as what?

What are two types of DNA binding transcription factors?

A
  • Lipophillic signals
  • Steroid hormones, Thyroid hormones, Retinoids
  • Specific receptor proteins
  • Transcription factor
  • Cytoplasmic receptors and Nuclear Receptors
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7
Q

What are the 3 main types of Receptors?

A

Ligand Gated Ion Channels

G Protein Coupled Receptors (GPCRs)

Enzyme Coupled Receptor Class (Receptor Tyrosine Kinases/RTKs)

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8
Q

What is the structural motif of GPCRs?

A

Extracellular Domain (ECD) - binds to signal

Transmembrane (TM) Domain - 7 a-helices

Intracellular Domain (ICD) - interacts with G proteins

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9
Q

Describe Generic GPCR Signaling Pathway

A
  • Ligand binds to ECD –> GPCR conformational change
  • ICD activates G protein (GDP –> GTP)
  • GTP-bound protein interacts with membrane-bound effector protein (enzyme producing secondary messengers)
  • Signaling termination:
    • Dissociation of ligand
    • G protein inactivation
    • Reduction in [secondary messenger]
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10
Q

How do you know when G protein is inactive?

How does it become active? What aids this process?

How does it return to its inactive state? How is this process accelerated?

A
  • Inactive G protein has GDP bound to alpha subunit, which is attached to beta and gamma subunits
  • G protein exchanges GDP for GTP via action of guanine nucleotide exchange factor (GEF) (alpha dissociates from beta and gamma subunits)
  • Intrinsic GTPase activity of G protein hydrolyzes bound GTP into GDP + Pi and this action is acclerated by GTPase-activating protein (GAP)
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11
Q

What does Gs stimulate?

Describe this process

How can it be turned off?

Examples of Signal Molecules

What inhibits PDE?

A
  • Adenylate Cyclase
  • [Alpha subunit + GTP] activates Adenylate Cyclase
    • ATP is converted to cAMP –> Activates PKA –> Phosphorylates target proteins to alter activity
  • Phosphodiesterase converts cAMP –> AMP
  • Epinephrine (B-adrenergic receptor), Histamine
  • Caffeine
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12
Q

What does Gi inhibit?

Describe this process

Examples of Signal Molecules

A
  • Adenylate Cyclase
  • [alpha subunit + GTP] inhibits Adenylate cyclase
    • cAMP not produced and PKA not activated
  • Epinephrine/Norepinephrine (alpha adrenergic receptor), Dopamine
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13
Q

What does Gt stimulate?

Describe this process

What uses this pathway?

A
  • cGMP Phosphodiesterase
  • Light triggers GPCR –> cGMP PDE converts cGMP –> 5’ GMP
  • Rhodopsin
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14
Q

What does Gq activate?

Describe the process

Examples of signal molecules

A
  • Phospholipase C
  • [alpha subunit + GTP] activates phospholipase C which cleaves PIP2 –> DAG and IP3
    • IP3 –> Ca2+ release from ER/SR into cytosol
      • Increased [Ca2+] causes PKC to translocate to plasma membrane where it is activated by DAG
      • PKC phosphorylates target proteins to alter activity
  • Acetylcholine
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15
Q

What does diversity of GPCR signaling mean?

Epinephrine example

A
  • Same molecule can produce different physiological responses in same targets of different cells
  • Epi to B-adrenergic receptor causes relaxation of bronchial and intestinal smooth muscle, but Epi to B-adrenergic receptor in heart causes contraction
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16
Q

Hydrolysis of Cyclic Nucleotides

What does cGMP Phosphodiesterase do?

What do inhibitors of cGMP PDE do? What physiological changes does this cause?

A
  • Hydrolyzes cGMP –> 5’-GMP
  • Increase conentration of cellular cGMP –> smooth muscle relaxation and vasodilation (Viagra, Levitra, Cialis)
17
Q

Nitric Oxide and Smooth Muscle Relaxation

How is NO responsible for smooth muscle relaxation?

What condition would someone take Nitrates?

A
  • NO diffuses to neighboring muscle cell and actives guanylate cyclase
    • Production of cGMP –> Smooth muscle relaxation and vasodilation
  • Nitrates can be used to lower BP
18
Q

Inhibition of G Proteins by Bacterial Toxins

How are G proteins affected by Cholera

How are G proteins affected by Pertussis

A
  • Cholera: covalent modification of a-subunits (ADP ribosylation of Arg) decreases GTPase activity
    • Gsa active and continuously stimulates AC –> cAMP overproduction
      • Intestinal cells: increased cAMP –> CFTR activation and open Cl- channels –> Na+ secretion –> water secretion –> diarrhea
  • Pertussis: ADP ribosylation of Cys on Gia prevents activation and dissociation of a subunit from G protein complex
    • Less inhibition of AC and overproduction of cAMP
      • Loss of fluid and excessive mucous in airway epithelial cells –> whooping cough
19
Q

What is signal desensitization?

A

The ability to turn off or “ignore” a signal

20
Q

What is the function of G Protein Receptor Kinases (GRKs)

What is the result of GRKs?

A

They phosphorylate GPCRs,

Ga-GDP does not get converted to Ga-GTP (inactivated G protein complex)

21
Q

What is the structural motif of Receptor Tyrosine Kinase (RTKs)

Examples of ligands?

A
  • ECD containing binding site
  • Single a-helix transmembrane domain
  • ICD with tyrosine kinase activity
  • Growth Factors
22
Q

Describe the RTK signaling pathway

What is RAS?

A
  1. Ligand binds to ECD –> conformational change –> dimerization
  2. Tyrosines phosphorylated (autophosphorylation)
  3. Phospho-tyrosines recognized by adapter and docking proteins (SH2 domain of Grb2)
  4. Triggers phosphorylation of protein targets –> alteration in gene transcription and protein activity
    • RAS dependent signaling faciliated by MAPK family (Gene Expression)
    • RAS independent signaling faciliated by different kinase (Protein Activation)
      • ​GLUT4
  5. RTK signaling terminated
  • Monomeric G Protein
23
Q

RAS and Cancer

A
  • Mutant forms of RAS (or GEFs/GAPs) have been implicated in wide range of human caner
24
Q

RTKs and Cancer

Breast cancer drug Herceptin targets what?

What family of RTKs does it belong to?

A
  • RTKs are target of pharmacological inhibitors
  • Excessive signaling from mutated/overexpressed RTKs associated with cancer
  • HER1
  • EGF-binding RTKs

MCM Exam 2 (14 decks)

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