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MCM Exam 2 > Receptors & Cell Signaling > Flashcards

Receptors & Cell Signaling Flashcards

1
Q

Signaling hormone is transported in the blood. Name the hormone type. Give the relative half life as well.

A

Endocrine hormones

  • short term, half life on minute scale
  • act on far away signaling
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2
Q

This signaling hormone diffuses to neighboring target cell of a different cell type. Give the relative half life as well.

A

Paracrine hormones

-local signaling -short lived signal

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3
Q

What is type of hormone is testosterone?

A

Paracrine hormones

– Leydig cells synthesize and secrete testosterone induces spermatogenesis by acting on Sertoli and germ cells

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4
Q

Secreting cells express surface receptors for this signal hormone or release to cells of the same type. What types of proteins are they commonly found as?

A

Autocrine hormones

– Commonly found as chemokines

– Growth factors in cancer cells

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5
Q

What type of signaling hormone is interleukin-1?

What produces them and why?

A

Autocrine

Interleukin-1 is produced by T-lymphocytes which promote their own replication in immune response

– Growth factors in cancer cells

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6
Q

What type of hormone is heparin-binding epidermal growth factor? Where does it bind?

A

Justacrine

HB-EGF binds to EGF receptor in Immune cells

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7
Q

Hormone signals that cannot penetrate the cell membrane.

A

Hydrophilic Interact with cells at specific receptors.

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8
Q

Examples of hydrophilic signaling.

A

Epinephrine, insulin, glucagon etc

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9
Q

What are second messengers derived from? What is the half life?

A

Generally small and derived from AA, polypeptides or through lipid metabolism

Have short half-lives, about seconds to minutes.

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10
Q

What are two receptors involved in hydrophilic signaling?

A

Receptor tyrosine kinases (RTKs)

G protein - coupled receptors (GPCRs)

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11
Q

Hormone signals that pass through the membrane of the target cell.

A

Lipophilic signals

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12
Q

Examples of lipophilic signals.

A

Steroid hormones, thyroid hormone and retinoids.

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13
Q

What do lipophilic signals bind to?

A

Receptor proteins inside the cell. These can be in the nucleus or the cytosol.

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14
Q

Cytoplasmic receptors are what type of receptor?

A

Lipophilic

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15
Q

How do cytoplasmic receptors exist in an inactive state? By what mechanism are the activated

A

Bound to HSP 90.

Ligand binds -> HSP 90 dissociates -> hormone-receptor complex binds to hormone response element in promotor region of DNA

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16
Q

What are nuclear receptors in signaling? How are the acted upon by hormones?

A

Lipophilic signaling receptors, already present in nucleus and bound to DNA. Hormone allows for interaction with additional proteins and activates the complex.

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17
Q

What is the half-life of lipophilic signals?

A

Long half-lives (hours to days)

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18
Q

Name some examples of lipophilic signals.

A

Steroid hormones, thyroid hormones, and retinoids.

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19
Q

What are some ligand gated ion channels?

A

nAChR, GABAa, 5-HT3, GlyR

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20
Q

Name the components of a G Protein coupled receptor.

A

Extra cellular domain (ECD)

Trans Membrane domain- composed of 7 alpha helices

Intracellular Domain (ICD)

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21
Q

What does the Extracellular domain in a GPCR do?

A

Binds to the signal, this causes conformational change of GCPR, allowing the ICD to become active

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22
Q

What does the Intracellular domain in a GPCR do?

A

Interacts with G proteins, upon conformational change induced by ECD it activates G protein by triggering exchange between GDP and GTP.

Utilizes Gaunine Exchange Factor (GEF)

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23
Q

When is G-protein active? How does this occur?

A

When GDP is exchanged for GTP by the intracellular domain of GCPR. This occurs via the guanine nucleotide exchange factor (GEF).

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24
Q

What happens after activation of the trimeric G-protein?

A

The GTP-bound alpha subunit separates.

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25
Q

How does G-protein turn back to inactive state? How is this action accelerated?

A

The intrinsic GTPase activity of G protein hydrolyzes it’s bound GTP into GDP and phosphate.

Accelerated via the GTP-ase activating protein (GAP).

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26
Q

What does Gs do? Whats it bind to?

A

Gs stimulates adenylate cyclase through binding a signal molecule.

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27
Q

What does adenylate cyclase do once it becomes activated?

A

Activated Gs -> activates Adenylate cyclase -> up regulation of cAMP -> PKA becomes active -> target proteins have activity altered.

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28
Q

What does Gt do? Whats it bind to?

A

Stimulates cGMP phosphodiesterase. Light binds to it.

29
Q

What does cGMP phosphodiesterase do?

A

Changes cGMP to 5’-GMP

30
Q

What does Gi do? Whats it bind to?

A

Inhibits adenylate cyclase directly, through the binding of a signal molecule.

31
Q

What does Gq do? Whats it bind to?

A

Activates phospholipase C.

32
Q

What does phospholipase do?

A

PLC activates IP3 and DAG

IP3 -> Ca+ channel in ER/SR -> Ca+2 calmodulin -> Ca+2 calmodulin dependent proteins (CaM kinase, LC kinase)

DAG -> PKC -> phosphorylation of target proteins

33
Q

Physiological effects of Epinephrin and Gs.

A

Relaxation of bronchial and intestinal smooth muscle

Contraction of heart muscle

Increased breakdown of triacylglycerides in adipose tissue

Increased breakdown of glycogen in liver and muscle

34
Q

What does Epinephrine bind to on Gs-protein?

A

B-adrenergic receptor of Gs

It is a nonselective agonist of all adrenergic receptors (a1, a2, B1, B2, B3) and can undergo multiple GCPR pathways.

35
Q

Physiological effects of Histamine and Gs.

A

Bronchoconstriction and symptoms of allergic reaction

36
Q

What does Epinephrine/norepinephrine bind to on Gi-protein?

A

A-adrenergic receptor of Gi

37
Q

Physiological effects of Epinephrine/norepinephrine and Gi

A

Constriction of smooth muscle

38
Q

Physiological effects of Dopamine and Gi

A

Increased heart rate

39
Q

Physiological effects of Acetylcholine and Gq

A

Bronchoconstriction and stimulation of salivary glands

40
Q

Physiological effects of Light and Gt

A

Vision (binds to rhodopsin!)

41
Q

Why are G-proteins responses so diverse in the context of epinephrine?

A

Epinephrine binds to the B-adrenergic receptor of the heart, the bronchial muscle, and intestinal smooth muscle.

All of which it up regulate cAMP, however produce different physiological responses.

42
Q

What are the two cyclic nucleotide phosphodiesterases and what reactions do they catalyze?

A

cAMP Phosphodiesterase: hydrolyzes cAMP to AMP

cGMP Phosphodiesterase: hydrolyzes cGMP to 5’ GMP

43
Q

Inhibitors of cGMP PDE do what? Name an example of one

A

Increase concentration of cGMP, causes smooth muscle relaction and vasodilation. (eg: Viagra, Levitra, and Cialis)

44
Q

Inhibitors of cAMP PDE do what? Name an example of one.

A

Increase concentration of cAMP, leading to increased heart rate. (eg: Caffeine)

45
Q

What effect does NO have on cGMP? What risks are there with NO?

A

Activates guanylate cyclase which increases cGMP. Active cGMP leads to smooth muscle relaxation and vasodilation. Taken by patients to lower blood pressure. Don’t take with erectile dysfunction drugs as combination can lead to extreme vasodilation and fatal drops in bp.

46
Q

What does Cholera prevent from inactivating? How do you get it.

A

Gs alpha subunit of G-protein. Contaminated water

47
Q

By what mechanism does cholera cause diarrhea?

A

Covalent modification of alpha subunits causes ADP ribosylation of Arg decreases GTPase activity. This leads to an overly active Gsa subunit which results in too much cAMP. Overabundance of cAMP cause Cl-channels to open and a loss of electrolytes and water => diarrhea.

48
Q

What does pertussis prevent form activating? How do you get it.

A

Gi subunit of G-protein.

Whooping cough.

49
Q

By what mechanism does pertussis cause whopping cough?

A

ADP ribosylation of Cys on Gia prevents activation and dissociation of a subunit from the G protein complex This causes less inhibition of AC and more cAMP Results in loss of fluids and excessive mucous in airway of epithelial cell.

50
Q

What is the ability to turn off or ignore a signal known as?

A

Signal Desensitization

51
Q

What are the types of signal desensitizations?

A

Hormone level drops (decreased adenylate cyclase activity)

Removal of signaling molecules (phosphordiesterase will remove cAMP/cGMP.)

Receptor sequestration: Endosomes

Receptor destruction: Endosomes + lysosomes

52
Q

How do G protein Receptor Kinases (GRKs) inactivate GCPRs?

A

GRKs phosphorylate GPCRs, this causes arrestin to bind to the 3rd intracellular loop, preventing Ga subunit from interacting with third loop. Results in Ga-GDP that cannot become Ga-GTP.

53
Q

What binds to the ECD of the Tyrosine Kinase Receptor?

A

Contains signal molecule binding site; signals tend to be growth factor. (EGF, NGF, PDGF)

54
Q

Where is tyrosinase kinase activity of the Tyrosine Kinase Receptor located?

A

ICD

55
Q

Binding of ligand to extracellular domain of the Tyrosine Kinase receptor causes what?

A

Dimerization occurs, dimerized receptor phosphorylates tyrosine residues.

56
Q

What are proteins that recognize phospho-tyrosines and activate downstream signaling pathways? What are those pathways?

A

Adaptor and docking proteins

Triggers the phosphorylation of protein targets in the nucleus, plasma membrane and cytoplasm.

RAS-dependent (MAPK pathway) RAS-independent (other kinases)

57
Q

Examples of adaptor and domains that recognize and bind to motifs on the receptor that contain phosphorylated Tyr.

A

Adaptor proteins GRB-2, IRS- 1

Domains known as SH2 or PTB

58
Q

Signaling facilitated by mitogen-activated protein kinase (MAPK) family

A

Ras-depenent signaling

59
Q

Examples of RAS Termination

A

Degradation of signaling molecules

Ligand-induced endocytosis followed by lysosomal degradation

Accelerated RAS inactivation

Dephosphorylation

60
Q

Insulin signaling (RAS dependent)

A

IRS-1 => Binds GRB-2 => RAS => Alters gene transcription: increased transcription of glucokinase

61
Q

Insulin signaling (RAS independent)

A

IRS-1 => PI3 => PKB => Alters protein and enzyme activity Increased GLUT4 movement to plasma membrane; activation of glycogen synthase

62
Q

Overview of MAPK pathway

A

Binds Grb => Sos => Ras => Raf

63
Q

% of pancreatic cancers and % lung cancers caused by point mutations in RAS

A

90% and 30-50%

64
Q

Mutation in these locks RTK into active form.

A

Decrease in GTPase activity

65
Q

Condition marked by growth of tumors from nerve tissue due to issues with RAS. Describe illness and mechanism of disease.

A

Neurofibromatosis Inactivating mutation in neurofibromin (NF-1) gene, which encodes a GAP for RAS; RAS uncontrollably

66
Q

What are monomeric 20-25kb G proteins?

A

Small G Proteins which have intrinsic GTPase activity

67
Q

What characterizes insulin resistance?

A

Loss of insulin stimulation of glucose uptake by GLUT4 transporters in adipose and skeletal tissue

Characterized by reduced activation of PKB

68
Q

What is the molecular cause of insulin resistance?

A

Cytokines, free fatty acid and hyperinsulinemia stimulate the kinases involved in Ser/Thr phosphorylation of IRSs

Tyr phosphorylation of IRS-1/2 necessary for recruitment of PI-3 kinase

Ser/Thr phosphorylation inactivate IRSs and leads to degradation

MCM Exam 2 (14 decks)

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