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SFM > (L16) Receptors and Cell Signaling > Flashcards

(L16) Receptors and Cell Signaling Flashcards

1
Q

What is endocrine signaling? What are examples? L16 S8

A

Signal is: -transported via blood stream -long distance -long-lived Examples: -epinephrine

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2
Q

What is paracrine signaling? What are examples? L16 S9

A

Signal is: -local, diffuses to nearby cells -short-lived Examples: -testosterone

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3
Q

What is autocrine signaling? What are examples? L16 S10

A

Signal is: -directed secreting cell and neighboring cells of the same type Examples: -chemokines -growth factors in tumors, interlukin 1 (produved by T lymcytes which prote tier own replication udring an immune response)

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4
Q

What is juxtacrine signaling? What are examples? L16 S11

A

Signal is: -attached to signaling cell and requires direct contact between signaling cell and target cell Examples: -heparin binding epidermal gf (in immune cells)

Also known as direct signaling.

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5
Q

What are the characteristics of hydrophilic signals? L16 S15

A
  • Unable to cross cell membrane
  • Receptors on are surface of target cells (GPCR, RTK)
  • Use second messengers inside the cell
  • Short-lived (seconds to mins)
  • signals are small, derived from AA, polypeptides or through lipid metabolism
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6
Q

What are the characteristics of lipophilic signals? L16 S16

A
  • Able to cross cell membrane
  • Receptors inside of target cells (cytoplasmic or nuclear)
  • molecule-receptor complex acts as transcription factor that acts on DNA or associated proteins
  • Long-lived Mostly categorized as hormones
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7
Q

What is the general structure of a GPCR? L16 S19

What is another name for GPCR?

A
  1. Extracellular domain (ECD): -binds signal
  2. Transmembrane domain (TM): -7 α helicies Intracellular domain : will undergo confermational change upon binding of ligand
  3. (ICD): -interacts with G protein

Another name for GPCR: are 7 TM protein

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8
Q

What is the general GPCR signaling pathway.

A
  • ECD of GPCR binds ligand causing conformation change
  • ICD of GPCR exchanges GDP for GTP on G protein, activating it -G protein interacts with membrane bound effector protein generating second messengers
  • second messengers interact with target creating biological response
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9
Q

What is the structure of a G protein? What happens to each portion after being activated? L16 S24

A

Subunits: -α -β -γ

-α subunit has GDP exchanged for GTP upon activation. (when inactive it is bound to GDP)

It also breaks away from the β and γ subunits to interact with effector protein

-ACTIVATION IS A TRANSFER

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10
Q

How can signals be desensitized? L16 S25

A
  • drop in hormone levels
  • remove secondary signaling molecule (phosphodiesterase will remove camp/cgmp)
  • sequester receptor (forms endosomes that later refuses with cell membrane)
  • destroy receptor (forms endosomes that fuses with lysosome, only happens if the receptor is damaged)
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11
Q

What are the different secondary effector methods of GPCR signaling? L16 S28

A

Gs: -ligand activates makes alpha GTP

  • alpha subunit activates adenylate cyclase producing cAMP
  • cAMP activated PKA -cAMP removed by phosphodiesterase

Gi:

  • ligand activates
  • alpha subunit inhibits adenylayte cyclase
  • cAMP is not produced and PKA is not activated

Gt: -light activates makeing alpha GTP

  • alpha GTP activates cGMP
  • cGMP phosphodiesterase removing cGMP

Gq:

  • ligand activates
  • activates PLC cleaving PIP into IP3 (activates Ca+ signaling) and DAG (activates PKC)
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12
Q

What is the effect of hydrolyzing cyclic nucleotides and what happens when this process is inhibited? L16 S30 Panini pg. 100

A

Cyclic nucleotides act as secondary messengers so hydrolyzing them stops their downstream biological activity. When hydrolysis is inhibited, the secondary messenger increase in concentration and increase the downstream biological effect.

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13
Q

What is the effect of cholera toxin? L16 S31 Panini pg. 100

A

Overly activates Gsα by decreasing its GTPase activity preventing it from being inactivated. Stimulates adenylate cyclase.. This is because ADP is riboslyated in the Gsalpha ARG.

-over abundance of camp causes intestinal cells to open Cl- channels, causes a loss of eletrolytes and water which causes diarrhea

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14
Q

What is the effect of pretussis toxin? L16 S33

A

Inhibits Giα preventing inhibition of adenylate cyclase because of ribosylation of Cys on Gia

  • less inhibiton of AC and hense over production of camp
  • in airway epithelial cells pertussis, toxin causes loss of fluids and excesive mucous secretion which presents as whooping cough
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15
Q

What is the effect of NO? L16 S34

A
  • NO is produced in epitelial cells by arginine and is repsonsible for smooth muscle relaxation
  • it diffuses into nehiboring muscles and activates guanylate cyclase which makes cGMP –> resluts in vasodilation and smooth muscle relaxation
  • NTG AND OTHER nitrates decompose to form NO and help to lower BP
  • patients that take nitrates should not drugs that inhibit cGMP which can cause extreme vasodilation and fatal drops in BP
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16
Q

What is the general structure of RTKs? L16 S37

A

Extracellular domain: -ligand binding site

Transmembrane domain: -single helix

Intracellular domain: -possesses tyrosine kinase activity

17
Q

What is the general mechanism of RTK signaling? L16 S38

A

-binding of ligand causes dimerization -tyrosine residues are phosphorylated and recognized by other molecules such as adaptor and docking protiens (such as SH2 domain of Grb2)

Ras-dependent pathway: -MAPK activated

Ras-independent pathway: -other kinases activated

18
Q

A ligand - receptor complex

A

activates or inhibits cellular pathways

19
Q

What is an effector?

A

Alters the activity of different compontents down stream and generates secondary messengers

20
Q

Name the 2 DNA binding transcritpion factors

A
  • cytoplasmic recetpors: binds to specific DNA sequence called hormone response elment (HRE) in the promoter region of specific genes
  • nuclear recetpors: already present in nucleus and bound bound to DNA
21
Q

How to GPCR return to its inactive state?

A
  • The intrinsic GTPase activity of the G protein hydrolyzes its bound GTP to GDP and phosphate Pi
  • This action is accelerated by GTPase activating protein (gap)
22
Q
A
23
Q

Epi and beta adrenergic recetptor

A

Gs

24
Q

Histamine

A

Gs

25
Q

Epi/norepi

A

alpha adrenergic receptor: Gi

26
Q

Dopamine and Dopaine receptor

A

Gi

27
Q

Acetylcholine

A

Gq

28
Q

Light

A

Gt

29
Q

cGMP phosphodiesterase does what? What actions do the hibitors do?

A
  • Hydrolyes cGMP to 5’ GMP
  • Inhibitors of CGMP PE increase concetration of cellular cGMP and prolong effects for a greater amount of time leading to smooth muscle relaxtion, vasiodilation and errection: ciagra, levitra and cialis
30
Q

Caffine ihibits

A

PDE

31
Q

Antihistamines do what?

A
  • inhibit G protein coupled receptors singaling
  • histamine is a ligand that binds to four histamine GPCRs
  • antihistamines are lipholic compounds that block the effect of histamine to H1 GPCRs
  • made from histidine
  • ex are zertyc, claritin, diahenhydrmine, bendadryl
32
Q

How are RTK singals terminated

A
  • degration of ligand by extracellular proteases
  • ligand induced endocytosis of receptor
  • ras inactivation
  • dephos of proteins targets by phosphatases
33
Q
A
34
Q

GRB2 / IRS 1

A

Adaptor protien that binds to RAS

35
Q

RAS dependent singaling facilitated by _________.

A

Mitogen activated protein kinase family

36
Q

Ras indepenendent singaling facilitated by

A

different kinases

37
Q

Momeric G protiens

A
  • part or RAS superfamily of small g proteins which play a role in transdction of singlas from memrbane receptor to effector proteins: kinases
  • use GEF proteins which helps exchange a GDP to GTP
  • have intrinisc GTPase activity: mutations lead to cancer
38
Q

_____ of lung and colon and ___ or pancreating cancers associated with activiting point mutations in ras.

A

30-50

90

39
Q

Excessive singaling from mutated/ overexpressed RTKs associated with ____.

Inhibitors of RTK is what?

A

cancer

-HER2 belongs to family of EGF binding RTKs

SFM (31 decks)

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