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Flashcards in Cell Signalling Deck (17)
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1
Q

Know the modes of cell-cell signaling.

A
  • Endocrine – signal reaches target via circulation
  • Paracrine – chemical fuses a short distance (stays in the neighborhood)
  • Autocrine – secreting and target cell are the samed
  • Juxtacrine – doesn’t secrete signal, but has it bound on extracellular
    surface. It reacts with target cell receptor. Requires cell-cell contact. Common in immune system.
2
Q
  1. Trace the biosynthesis of NO.
A
  • Acetylcholine released by nerve terminals in the blood vessel wall activates NO synthase in endothelial cells lining the blood vessel
  • causes the endothelial cells to produce NO
  • NO diffuses out of the endothelial cells and into the underlying smooth muscle cells
  • binds to and activates guanylyl cyclase – produces cyclic GMP
  • cGMP triggers a response that causes the smooth muscle cells to relax
  • enhances blood flow through the blood vessel
3
Q

Identify the three main classes of cell-surface receptors.

A

ion channel receptor

enzyme-linked receptors – kinases, or bind kinases

  • heptahelical receptors – 7TM, G-coupled protein receptors (GCPRs
4
Q
  1. Describe G proteins and their function in membrane events.
A

G protein – binds guanine nucleotides (GTP and GDP) o GTP = active
 releases subunit which migrates to target protein o GDP = inactive
 channel closes

5
Q

Compare different heterotrimeric G proteins.

A

different g-proteins have different functions/targets o activation of ion channels
o Adenyl cyclase and cAMP – important in glycogenolysis  can cause diarrhea (see figure below)
o phosphatidyl inositolCa2+ release from ER- Cholera toxin – gets into cell because of B subunit
- B sticks to surface and internalizes the A-subunit via endocytosis
- A-subunit binds and keeps AC active all the time
o continuous production of cAMP o activates PKA
o activates ABC protein
o allows Cl- through
o intestine becomes hyperosmotic o water flows in (osmosis)
 causes diarrhea

6
Q

Describe the source of cAMP and other second messengers.

A
  • Adenylyl Cyclase – converts ATPcAMP
    o AC – second messenger – released when g protein binds receptor
  • diacylglycerol, phosphatidyl inositol, Ca2+
    o PLC – breaks down phospholipid (phosphatidyl inositol bisphosphate)
     DAG and IP3 – second messengers o IP3 – migrates to ER (high calcium content)
     causes release of Ca
     activates PKC
    o DAG – can further bind/activate PKC
7
Q

Trace the intracellular events leading to activation of nuclear transcription via protein kinase A.

A
  • activated G-protein-linked receptor
  • G protein -> adenylyl cyclase (AC)
  • cAMP (AC, from ATP)
  • PKAregulatory proteins
8
Q

Describe the role of PKA and PKC in signaling.

A

PKA – gets activated by cAMP
- goes after gene regulatory proteins
PKC – has many target proteins
- activated receptor phospholipase  diacylglycerol  PKC

9
Q

Compare ionotropic versus metabotropic effectors.

A

ionotropic effectors – produce very quick responses
- almost instaneous
- nicotinic receptor (muscle contractions)
metabotropic effectors – take seconds/minutes/hours
- goes through G proteins
o goes through an entire cascade

10
Q

Know the function of the ryanodine receptor and its association with malignant hyperthermia.

A

Ryanodine receptor – intracellular calcium channel
- when activated – releases calcium
- in some humans/animals, it gets out of control
o release too many calcium ions
o leads to phenomenon of heat release (malignant hyperthermia)

11
Q

Describe the activity of calmodulin.

A

Calcium binds calmodulin – inactiveactive

o binds to calmodulin kinase (CaM-kinase) – kinase becomes active

12
Q

Identify the role of PI 3-kinase in signal transduction.

A
  • PI 3-kinase – adds phosphate group to the PIP
  • conformational change causes gives molecule new function
  • in figure, PIP molecule is phosphorylated giving it docking
    capabilities for certain molecules
13
Q

Identify the locations of PIP2, IP3 and PIP3.

A
  • PIP2 – on cellular membrane
  • IP3 – migrates to ER (high calcium content)
    o causes release of Ca2+
    o activates PKC
  • PIP3 – on cellular membrane
14
Q

Know the relationship between IP3 and [Ca2+].

A
  • IP3 – migrates to ER and causes release of Ca2+

- IP3 – turned on via G-protein-coupled signal cascade

15
Q

Compare the cellular responses of the MAP kinase pathway versus heptahelical pathway.

A

MAP kinase pathway (goes through RAS pathway)- tyrosine kinase receptor

  • uses adaptor protein
  • RAS protein (GTP-binding protein) – inactive
  • exchanges GDP for GTP – activates RAS
  • activity is transmitted downstream
  • Active RAS – activates MAPKKK
Heptahelical Pathway (goes through G-protein pathway)
- g-protein coupled receptor
- primarily uses second messengers
- seven transmembrane alpha-helical
structures
16
Q

Know the function of oncogenes in cancer.

A
  • Oncogenes – fine with no mutation
  • Mutation – turned on and they cause cancer
    o mutant cannot hydrolyze GTP o continuous signal transmission
  • Growth factor signaling pathways are relevant because they can cause cancer
17
Q

Retell the origin of the src gene.

A

RSV (Rous Sarcoma Virus)
- determined to cause cancer
- Src gene – normal in humans
- Viral Src gene is mutated form of our normal gene
- mutated form or our gene is an oncogene that leads to continuous signaling and cancer
o DNA replication o Cell proliferation o Differentiation