Cell Signaling Flashcards

1
Q

which ligand will need help to pass the membrane? where will receptor be found?

A

hydrophilic ligand

receptor on outside of cell (has to cross)

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2
Q

which ligand will readily diffuse over the membrane? where will receptors be found?

A

Lipophilic

inside cell

i.e. steroid hormones

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3
Q

what controls everything at the cellular level?

A

cell signaling

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4
Q

what is the slow response?

A

gene expression changes

via MAP kinase

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5
Q

what is fast response?

A

alterations in function of enzyme

generation of cyclic AMP

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6
Q

extracellular signal binds to a specific receptor on target cells to initiate signal transduction

A

cell signaling

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7
Q

3 types of signaling

A

autocrine
paracrine
endocrine

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8
Q

autocrine

A

one cell feeds back on another

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9
Q

endocrine

A

distal signaling

long lasting molecules, mostly steroid hormones

low turn over rate ,diffuse

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10
Q

paracrine

A

fibroblasts below epithelium

localized signaling

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11
Q

same ligand has different responses

A

i.e. acetylcholine

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12
Q

steps in signal transduction (basic)

A

extracellular signal molecule binds to receptor protein

causes intracellular signal proteins to carry signal to effector proteins

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13
Q

three types of receptors

A

ion channel coupled receptors
enzyme coupled receptors
g protein coupled receptors

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14
Q

transmembrane component of G protein coupled receptor

A

anchors receptor

7 passes of membrane

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15
Q

cytoplasmic loop of g protein coupled receptor

A

regulatory domain

not found in RTKs

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16
Q

trimeric complex is inactive when…

A

it binds to cytoplasmic loop

becomes monomeric

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17
Q

heterotrimeric G proteins

A

guanine nucleotide binding proteins with 3 subunits: alpha, beta, gamma

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18
Q

what happens when G-proteins bind to cytoplasmic loop?

A

becomes inactive

is only monomeric g-alpha (beta and gamma are inactive)

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19
Q

Active form of G-Protein …

A

occurs when it has a GTP

creates downstream conformation changes in enzymes (2nd messengers)

20
Q

2nd enzymes of the GpCR

A

adenyl cyclase

phospholipase C

21
Q

PLC makes

A

makes 2nd messengers

IP3 and DAG

22
Q

Adenyl Cyclase makes

A

makes 2nd messengers

cyclic AMP

23
Q

Phosphodiesterase

A

converts cyclic AMP to AMP

shuts down this signaling

24
Q

which 2nd messenger of GPCR is potentiating?

A

PLC

generates 2nd messenger

25
Q

which 2nd messenger of GPCR is attenuating?

A

PDE

converts cyclic AMP to AMP to shut off signal (destroys second messneger)

26
Q

cAMP activates…

A

cAMP-dependent PKA

27
Q

cAMP-dependent Pka

A

4 subunits

when cAMP binds it attaches to regulatory parts and pushes out activated units

28
Q

Cholera

A

failure to turn off signal (alpha subunit remains active)

unable to hydrolyze GTP so PKA continually phosphorylates channel and water is sent out

29
Q

Ways to attenuate the signal of GPCR

A
  1. hydrolyze GTP on G-Alpha subunit (dropping of hormone levels)
  2. Remove signaling molecule
  3. Endocytosis and endosome activity to completely sequester or destroy the receptor
30
Q

GRKs

A

kinase phosphorylates cytoplasmic domain to stop G-alpha

phosphorylates receptors so arresting will bind to cap and prevent GTP from binding to G alpha

31
Q

arrestin protein

A

puts a cap on the third loop to prevent the activity of the receptor

keeps alpha- g bound to GDP

32
Q

variations of G-Proteins

A

Gs
Gi
Gq

33
Q

Gs

A

stimulates adenyl cyclase

34
Q

Gi

A

inhibits adenyl cyclase

35
Q

Gq

A

activates PLC (instead of adenyl cyclase)

36
Q

phospholipase C makes what from PIP2

A

2 molecules, both activate PKC (and calcium)

IP3 or Dag

37
Q

calcium signaling is which 2nd messenger system?

A

PLC to IP3 or DAG

NOT tyrosine kinase

38
Q

PCK is activated by which second messenger(s)?

A

IP3 or DAG

PLC pathway

39
Q

enzyme coupled receptors create

A

docking sites

dimerize instead of activate complex

40
Q

what is the GEF in GPCR?

A

the receptor itself

41
Q

what is the GEF in tyrosine kinase?

A

SOS

42
Q

steps in tyr k.

A
  1. Ligand binds to tyrosine monomer
  2. tyrosine moonier aggregates –> dimerization
  3. Autophosphorylation
  4. SH2 domain of GRb2 binds to tyrosine kinase
  5. SH3 of GRB 3 binds to SOS
  6. SOS exchanges GTP for GDP from Ras
  7. Ras binds to Raf
43
Q

Slow response of Ras-Raf example

A

Insulin signaling

via gene transcription

44
Q

fast response of Ras-Raf pathway

A

Glut 4

Direct activation of enzymes that alter activity (already synthesized)

G-PRotein coupled receptor

45
Q

Jak Sat

A

direct connection

activate Jak, Stat goes to the nuclease

46
Q

Serine/Threonine

A

when Serine or Threonine is activated SMAD goes to nucleus