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MCM Exam II > Receptors and Cell Signaling > Flashcards

Receptors and Cell Signaling Flashcards

1
Q

effectors in cell signaling: what do they do

A

alter the activity of different components downstream and generate secondary messengers that elicit a particular cellular response (enzyme activity, gene expression, etc)

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2
Q

how are signals terminated in cell signaling

A

removal of the signaling molecule and/or receptor or attenuation/inactivation of the signaling events

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3
Q

endocrine signaling

  • what is the signal
  • long distance/short distance
  • long term/short term
A
  • hormone (ex: epinephrine)
  • long-distance signaling
  • short term signaling (half life is on minute scale)
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4
Q

paracrine signaling

  • long distance/short distance
  • long term/short term
A

signal diffuses to neighboring target cell

ex: testosterone
- local signaling
- short lived signals

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5
Q

how testosterone signaling works

A

leydig cells synthesize and secrete testosterone which induces spermatogenesis by acting on sertoli and germ cells

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6
Q

autocrine signaling

A

secreting cells express surface receptors for the signal; or release to cells of the same type

ex: interleukin-1 promotes its own replication in immune response
ex: growth factors in cancer cells

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7
Q

direct/juxtacrine signaling

A

signal binds to signaling cell which then binds to receptor on the target cell; acts like a bridge between the two cells

ex: heparin-binding epidermal growth factor
ex: immune cells

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8
Q

hydrophilic signaling

  • how it works with plasma membrane
  • examples
  • receptors involved
A

cannot penetrate the plasma membrane, the receptor has to be on the membrane; signaling molecule-receptor complex initiates the production of a second messenger molecule in the cell

epinephrine, insulin, glucagon

GPCRs and RTKs

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9
Q

lipophilic signaling

  • how it works with plasma membrane
  • examples
A

signals can pass though the membrane of the target cell; ligand binds to receptor protein inside the cell (cytosol or nucleus)

steroid hormones, thyroid hormones, retinoids

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10
Q

where can receptors be located for lipophilic signaling

A

nucleus or cytosol

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11
Q

cytoplasmic receptors in lipophilic signaling

A

exist in inactive complex with HSP90; when they bind to ligand HSP dissociates and the hormone receptor complex translocates to the nucleus where it binds to the HRE in the promoter region of specific genes

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12
Q

hormone response element

A

specific DNA sequence in the promotor region of specific genes; binds to hormone receptor complex in cytoplasmic lipophilic signaling

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13
Q

nuclear receptors in lipophilic signaling

A

exists in the nucleus already bound to DNA; ligand will activate the complex to regulate the transcription of specific genes

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14
Q

nAChR
GABAa
5-HT3
GlyR

what do these have in common

A

ligand gated ion channels

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15
Q

G protein coupled receptors (GPCRs) signaling

- 4 steps

A

ligand binds to extracellular domain –> conformational changes in the GPCR

intracellular domain activates its G protein and GDP –> GTP

GTP bound G protein interacts with membrane bound effector protein –> secondary messenger

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16
Q

how is GPCR signaling terminated (3 ways)

A
  1. dissociation of signaling molecule
  2. inactivation of the G protein
  3. reduction of concentration of secondary messenger
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17
Q

guanine exchange factor (GEF)

A

activates GPCR by adding a phosphate to the inactive GDP bound GPCR; GDP becomes GTP and the alpha subunit dissociates

18
Q

GTPase-activating protein (GAP)

A

accelerates the hydrolyzation of GTP into GDP, inactivating GPCR

19
Q

Gs type GPCR signaling

A

stimulates adenylate cyclase which activates cAMP –> activates PKA –> phosphorylates target proteins to alter their activity

  • ex: epinephrine when it binds to the beta-adrenergic receptor
  • ex: histamine
20
Q

Gt type CPCR signaling

A

activated by light; stimulates cGMP phosphodiesterase –> cleaves cGMP into 5’-GMP

type of negative signaling (the signal is on in the absence of light)

21
Q

Gi type GPCR signaling

A

inhibits adenylate cyclase; cAMP is not produced and PKA is not activated

  • ex: epinephrine when it binds to the alpha-adrenergic receptor
  • ex: dopmamine
22
Q

Gq type GPCR signaling

two end points

A

activates phospholipase C; breaks PIB2 into DAG and IP3

DAG –> PKC –> phosphorylation of target proteins to alter their activities

IP3 –> goes to the ER to open channels to release Ca2+ into the cytosol (calcium is the secondary signal) –> activation of Ca2+/calmodulin-dependent proteins

ex: acetylcholine

23
Q

what happens when epinephrine is bound to beta-adrenergic receptors

A

relaxation of bronchial and intestinal smooth muscle

can be used to relieve bronchospasms during asthma attack

24
Q

what happens when epinephrine binds to beta adrenergic receptor in the heart

A

causes contractions

can be used to restore cardiac rhythms after MI

25
Q

cAMP phosphodiesterase

A

hydrolyzes cAMP to AMP

26
Q

cGMP phosphodiesterase

A

hydrolyzes cGMP to 5’GMP

27
Q

how does viagra work

A

inhibits cGMP PDE which increases the concentration of cellular cGMP, leading to smooth muscle relaxation and vasodilation

28
Q

how does caffeine lead to increased heart rate

A

it inhibits cAMP PDE

29
Q

how does nitric oxide lower blood pressure

A

NO is produced in epithelial cells; diffuses to neighboring muscle and activates guanylate cyclase –> production of cGMP –> smooth muscle relaxation and vasodilation

30
Q

how does the cholera toxin work

A

covalent modification of alpha subunits ADP causes ribosylation of arginine –> decreases GTPase activity –> Gs remains active and continues to stimulate adenylate cyclase which causes overproduction of cAMP –> open Cl- channels in intestinal cells –> loss of electrolytes and water and increased diarrhea

31
Q

how does pertussis work

A

ADP ribosylation of cystine on Gi prevents activation and dissociation of alpha subunit from the G protein complex –> less inhibition of AC and overproduction of cAMP –> loss of fluids and excessive mucous in airway epithelial cells

32
Q

mechanism of water secretion in cholera

A

toxin activates AC to produce cAMP

leads to secretion of Cl-

causes build up of negative potential across the membrane –> secretion of Na+ –> net secretion of NaCl

NaCl builds up an osmotic gradient across membrane –> water secretion

33
Q

4 types of signal desensitization

A
  1. hormone levels drop, causing decreased adenylate cylase activity, decreased cAMP, and decreased PKA activity
  2. phosphodiesterases removing cAMP/cGMP
  3. receptor sequestration in endosome
  4. receptor destruction in endosomes and lysosomes
34
Q

G protein receptor kinase (GRKs)

A

phosphorylate the GPCRs
- arrestin binds to the 3rd intracellular loop and prevent G-alpha from interacting with third loop; GDP does not get converted to GTP to activate GPCR

35
Q

3 part of receptor tyrosine kinase (RTK)

A
  1. extracellular domain which binds the ligand/signaling molecule
  2. single alpha helical transmembrane domain
  3. an intracellular domain with tyrosine kinase activity
36
Q

receptor tyrosine kinase (RTK) signaling

  • 4 steps
A
  1. ligand binds to ECD causing dimerization
  2. specific tyrosines are phosphorylated
  3. phophotyrosine is recognized and bound by adapter and docking proteins (SH2 domain of Grb2) –» either RAS dependent or RAS independent pathway
  4. triggers phosphorylation of protein targets in nucleus, plasma membrane, cytoplasm

–> alteration in gene transcription and protein acitvity

37
Q

what is RAS-dependent signaling facilitated by

A

mitogen-activated protein kinase family

MAPK

38
Q

GRB-2

A

adaptor protein; SH2 is a domain of GRB-2; recognizes and binds to motifs on the receptor that contains phosphorylated tyrosine in RTK signaling

39
Q

how is RTK signaling terminated

A
  • degradation of signaling molecules
  • ligand induced endocytosis followed by lysosome degradation
  • accelerated RAS inactivation
  • dephosphorylation
40
Q

what do point mutations in RAS cause

A

lung, colon, and pancreatic cancers

41
Q

how do mutations in RAS cause neurofibromatosis

A

characterized by an inactivating mutation in neurofibromin (NF-1) gene, which normally encodes a GAP for RAS

RAS uncontrollably activated pathway for nerve tissue growth –> optical glioma, macrocephaly, learning disabilities, Lisch

42
Q

what do point mutations in RAS cause

A

30%-50% of lung and colon and 90% of pancreatic cancers

MCM Exam II (14 decks)

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