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Receptors and Cell Signaling Flashcards

1
Q

alter the activity of different components downstream and generate secondary messengers that elicit a particular cellular response

A

effectors

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2
Q
  • type of cell signaling
  • signal (hormone) is transported via blood
  • long distance signaling
  • long lasting, freely diffusing signal
  • ex: epinephrine released by adrenal medulla acts on heart muscle
A

endocrine

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3
Q
  • type of cell signaling
  • signal diffuses to neighboring target cell of a different cell type
  • local signaling
  • short lived signal
  • ex: Leydig cells synthesize and secrete testosterone, induces spermatogenesis by acting on Sertoli and germ cells
A

paracrine

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4
Q
  • type of signaling
  • secreting cells express surface receptors for the signal
  • release to cells of the same type
  • action of growth factors in cancer cells
  • ex: chemokines: IL-1 produced by T cells promote their own replication during immune reponse
A

autocrine

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5
Q
  • type of signaling
  • signal binds to signaling cell which then binds to receptor on target cell
  • occurs in immune cells
  • ex: heparin-binding epidermal growth factor-like growth factor (HB-EGF) binds to EGF receptor
A

direct/juxtacrine

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6
Q

What are the 2 types of signal molecules?

A

hydrophillic and hydrophobic

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7
Q

What are the key attributes of hydrophillic signaling? (4)

A
  1. cannot penetrate plasma membrane
  2. interact with receptors on cell surface
  3. receptor complex initiates prod of secondary messenger (small, short half life)
  4. trigger downstream cell response

(IMPORTANT RECEPTORS: GPCRs and RTKs)

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8
Q

What are the key attributes of lipophilic signaling?

A
  1. pass through plasma membrane unaided
  2. ligand binds to specific receptor proteins inside cell
  3. receptor complex acts as transcription factor
  4. receptors in cytosol or nucleus
  5. cytoplasmic receptors: inactive form with HSP90, binding of ligand dissociates HSP90, complex translocates to nucleus, binds to DNA sequence hormone response element (HRE)
    5b: nuclear receptors: present in nucleus and bound to DNA
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9
Q

What are the 4 steps of GPCR signaling?

A
  1. ligand binds to ECD (receptor) and causes conformational change
  2. ICD (inside proteins) activate G protein by exchanging GDP for GTP
  3. activated G protein interacts with membrane-bound effector, that typically produces secondary messenger
  4. signaling terminated by: dissociation of signal, inactivation of G protein, reduction of conc of secondary messenger
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10
Q

How is a signal desensitized? (4)

A
  1. drop in hormone levels
  2. removal of signaling molecule
  3. sequestration of receptor (endosome)
  4. destruction of receptor (endosome then lysosome)
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11
Q
  • variation of GPCR signaling
  • stimulates adenylate cyclase (effector)
  • ATP > cAMP > AMP
  • cAMP activates PKA which phosphorylates target proteins (altered activity)
  • ex: epinephrine ligand = relaxation of bronchial/smooth muscle, contraction of heart, inc break down of trigs, inc break down of glycogen in liver/muscle, inc glycolysis in muscle
  • ex: histamine ligand = bronchoconstriction and sx of allergic rxn
A

Gs

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12
Q
  • variation of GPCR signaling
  • inhibits adenylate cycle
  • cAMP not produced, PKA not activated
  • ex: epinephrine/norepi = constriction of smooth muscle; dopamine = increased heart rate
A

Gi

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13
Q
  • variation of GPCR signaling
  • stimulates cGMP phosphodiesterase which breaks down cyclic form of cGMP into 5’-GMP
  • ex: light ligand = vision
A

Gt

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14
Q
  • variation of GPCR signaling
  • activates phospholipase C which creats a downstream effect, activation of Ca2+ calmodulin-dependent proteins
  • ex: acetylcholine = bronchoconstriction/stimulation of salivary glands
A

Gq

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15
Q

What happens when cGMP PDE is inhibited?

A
  • increase concentration of cellular cGMP
  • prolongs effects for longer time
  • smooth muscle relaxation, vasodilation
  • in males = erection
  • cGMP inhibitors: viagra, levitra, cialis
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16
Q

What happens during a cholera infection?

A
  • Gsα remains active (GTP bound) and continuously stimulates adenylate cyclase
  • overproduction of cAMP
  • opens Cl- channels in intestinal cell walls
  • loss of electrolyes and water = diarrhea
17
Q

What happens during H2O secretion?

A
  • toxin activates AC to produce cAMP
  • cAMP activates CFTR
  • secretion of Cl-
  • negative potential, Na+ secreted = net loss of NaCl
  • osmotic gradient causes water to secrete out of the cell
18
Q

What happens during whooping cough?

A
  • pertussis toxin prevents activation of Giα
  • less inhibition of AC, overproduction of cAMP
  • loss of fluids and excessive mucous secretions in airways = whooping cough
19
Q

How does nitric oxide cause smooth muscle relaxation?

A
  • NO diffuses to muscle and activates guanylate cyclase, increasing prod of cGMP
  • cGMP results in smooth muscle relaxation
  • nitroglycerine and other nitrates used as medicine for angina and high blood pressure
20
Q

Why is it important that patients taking nitrates do not take cGMP PDE inhibitors (e.g. ED drugs)?

A

combination can lead to extreme vasodilation and fatal drops in blood pressure

21
Q

What are the 4 major steps in RTK signaling?

A
  1. ligand binds to ECD receptor, conformational change dimerizes receptor
  2. dimerized receptor causes autophosphorylation of tyrosine residues on ICD
  3. phospho-tyrosines recognized by proteins that bind
  4. downstream signaling pathways activated
22
Q
  • a type of RTK signaling
  • signaling facilitated by mitogen-activated protein kinase (MAPK) fam
  • important for growth, cell division, changes in protein activity, changes in gene expression
  • if defective, can lead to cancer :( (aka oncogenes)
A

MAP kinase pathway

RAS DEPENDENT

23
Q
  • monomeric proteins
  • RAS superfamily (RAS, RAB, RHO, RAN)
  • control diverse processes: cell proliferation, survival/apoptosis, membrane transport/secertion, y mucho mas
  • intrinsic GTPase activity
  • mutations can lead to cancer :(
A

small G proteins

24
Q

What causes cancer in regards to RAS protein?

A

mutations decrease intrinsic GTPase activity, lock protein in active, GTP-bound state

(some lung/colon cancers, most pancreatic cancers, and neurofibromatosis)

25
- mutated/overexpressed protein associated with cancer - target for pharmaological drugs: Herceptin (HER2 in BrCa)
RTKs

SFM (21 decks)

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