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Flashcards in Cell Signaling Deck (27):

What are ACE-inhibitors? How do they work?

1) drug that controls blood pressure
2) blocks angiotensin converting enzyme (ACE) from converting angiotensin I into angiotensin II


What are the 3 modes of actions for chemical messengers?

1) endocrine (thru blood)

2) paracrine (adjacent cell)

3) autocrine (same cell)


What are the 3 types of plasma membrane receptors?

  1. ion channel receptor
  2. receptor kinases
  3. heptahelical receptors


What are the 5 classes of chemical messengers, and what are their functions?

  1. neuropeptides: nervous sys
  2. hormones: endocrine sys
  3. cytokines: immune sys
  4. eicosanoids: injury
  5. growth factors: cell proliferation


Define second messengers.

non-protein molecules that amplify cell signal, have ability to diffuse, and have a fast response relative to proteins that turn genes on


What is the sequence of cell signaling steps?

chemical messenger --> cell receptor --> signal transducer proteins --> second messengers --> effector activation --> termination of signal


Describe the intracellular signaling pathway. Example?

lipophilic chemical messenger --> diffuses across PM --> binds to receptor in cell --> increased gene transcription; ex. cortisol


What are the 3 types of second messengers?

1) phosphatidylinositol (PIP) signaling 2) cAMP 3) Ca2+


What do kinases & phosphatases do?

1) kinase: phosphorylate 2) phosphatase: remove phosphate


Describe the ion channel receptor pathway. Example?

1) chemical messenger binds to PM receptor --> channel opens, allowing Na+ ions to flow into cell 2) nicotinic acetylcholine receptor


Describe the INF or IL/JAK/STAT kinase signaling pathway.

cytokine binds receptor --> JAKs dimerize & cross-phorylate & phosphorylate tyrosine on receptor --> SH2 chemical messenger (STAT) binds to tyrosine --> JAKs phosphorylate STATs as well --> STATs dissociate, dimerize --> bind DNA, turn genes on


Describe the TGF-beta receptor kinase signaling pathway.

1) heterodimer receptor (I & II) --> TGF-bta binds to II, serine on type I kinase is phosphorylated --> R-Smad phosphorylated --> Smad activates Co-Smad --> bind DNA, turn on genes


What can mutations in RAS cause?



Describe the tyrosine kinase (EGF) signaling pathway.

GF binds to homodimers, tyrosine kinases dimers autophosphorylate

--> SH2 chemical messenger protein (Grb2) binds

--> SOS protein binds

--> Ras small G-protein binds --> exchanges GDP for GTP to activate its kinase domain

--> binds Raf (MAPKKK) --> MAPKK --> MAPK --> transcription factor


Explain the steps for PI3 pathway in insulin receptors.

Phosphatidylinositol phosphorylated to make PIP2

--> phosphoyrlated by PI3 --> PIP3

--> joins w/ PDK1 --> Akt / activates PKB


Describe the tyrosine kinase (insulin receptor) signaling pathway.

alpha and beta subunits on receptor --> insulin binds 

--> kinase domain is autophosphorylated

--> IRSs are phosphorylated

--> SH2-containing proteins can bind to IRS (Grb2 / PLC-gamma/ PI3 kinase) 


Describe the kinase receptors signaling pathway. What are the 4 examples?

1) receptor activated --> associated kinase phosphorylates --> signal transducer protein binds to kinase

2) Serine/threonine receptors (TGF-beta); INF or IL/JAK/STAT; Tyrosine receptors (EGF & Insulin)


What's one result of insulin receptor signaling?

increases number of glucose transporters at the plasma membrane


How does the cAMP second messenger pathway work downstream of beta-adrenergic receptor?

norepinephrine binds to receptor

--> --> activated G protein helps adenylyl cyclase catalyzes the conversion of ATP to cAMP

--> binds to regulatory subunit of PKA to activate it

--> glucose production in muscle & liver


Describe the heptahelical (G-protein Coupled) receptor pathway. Examples?

1) 7 alpha helices form barrel in membrane w/ hetero-trimeric G-proteins as associated signal transducers --> GDP exchanged for GTP & activates G-proteins --> cAMP or DAG/IP3 second messenger pathways

2) beta-adrenergic receptors, angiotensin receptors


What are beta-blockers? How do they work?

1) drugs used to treat cardiac arrhythmia

2) bind to beta-androgen receptor (compete against norepinephrine)


How does the cAMP signal get terminated?

cAMP phosphodiesterase reduces cAMP levels by hydrolyzing cAMP to AMP


How does cholera toxin affect the G-protein signaling pathway?

G-alpha-s subunit is covalently modified so that it can't hydrolyze GTP-GDP

--> Adenylyl Cyclase cannot be turned off
--> cAMP is constantly being made


What are the subunit types of G-alpha proteins & what do they do in downstream pathway?

1) s --> stimulates adenylyl cyclase (cAMP)

2) i/o --> inhibits adenylyl cyclase

3) t --> stimulates cGMP phosphodiesterase 

4) q/11 --> activates phospholipase C-beta (IP3, DAG)

5) 12/13 --> alters cytoskeletal elements


How does the IP3 / DAG second messenger pathway work downstream of angiotensin receptor?

angiotensin II binds to receptor --> --> activated G protein helps phospholipase C cleave PIP2 into DAG and IP3 --> IP3 opens Ca2+ channel in ER to increase Ca2+--> DAG & Ca2+ activate protein kinase --> other proteins phosphorylated


How does pertussis toxin affect the G-protein signaling pathway?

1) causes G-alpha-i to remain off indefinitely 2) causes covalent modification of G-alpha-i so that it can't bind to GTP --> causes increase in cAMP


How can cell signals be terminated?

1) messengers no longer secreted or degraded 2) receptor desensitized 3) phosphatases 4) GTPases 5) phosphodiesterases