Ch 11 maybe Flashcards

0
Q

four cAMP bind to blank regulatory subunits

A

two

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1
Q

Gs pathway makes this

A

protein kinase a (PKA) from cAMP

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2
Q

two regulatory subunits liberates two blank subunits

A

catalytic

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3
Q

catalytic subunits blank other blank

A

phosphorylate, proteins

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4
Q

PKA blank to the nucleus, and phosphorylates blank

A

translocates, transcription factors

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5
Q

transcription factors turn on blank

A

gene expression

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6
Q

very well known transcription factor

A

creb

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7
Q

creb activates very important blank for things like blank and blank

A

genes, eating/moving, drug addictions/sympathetic nervous system

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8
Q

this hormone increases ATI gene expression

A

aldosterone

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9
Q

ATI receptors are blank receptors and are an example of influencing transcription factors to influence blank

A

metabotropic, behavior

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10
Q

this promotes thirst

A

angiotensin

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11
Q

increased receptor blank leads to increased blank of angiotensin 2

A

expression, effectiveness

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12
Q

this pathway works the same as Gs, but it inhibits blank so blank is not produced

A

Gi, adenylyl cyclase, cAMP

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13
Q

tough pathway

A

Gq

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14
Q

Gq pathway

A
  1. PIP breaks into two
  2. IP3 and DAG come from PIP
  3. DAG activates PKC in the cell membrane
  4. IP3 liberates intracellular calcium
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15
Q

calcium released by ip3 binds to blank

A

calmodulin

16
Q

calmodulin complex binds to blank of the dependent protein kinase

A

regulatory domain

17
Q

PKC can do what action

A

open/close ion channels

18
Q

arachidonic acid leads to the production of

A

prostaglandins

19
Q

what produces prostaglandins that is produced by arachidonic acid

A

cyclooxygenase

20
Q

tyrosine kinase receptors steps

A
  1. signal binds
  2. dimer forms
  3. phosphorylated by atp
  4. activates relay proteins leading to a response
21
Q

mapk pathway

A
  1. ras
  2. raf
  3. MEK
  4. MAPK
  5. Transcription factors
22
Q

retrograde signaling activates enzymes and increases blank

A

nt reelease

23
Q

when the postsynaptic cell releases NO which travels to presynaptic cell to stimulate increased nt release

A

retrograde signaling

24
in the presynaptic terminal, second messengers can regulate blank
nt release
25
in the postsynaptic neuron, second messengers can regulate blank
postsynaptic potentials
26
in the soma second messengers can regulate blank and blank
resting potential, ap dynamics
27
pka opens ion channels through blank
phosphorylation
28
pka also activates blank which causes the ion to blank
inhibitor 1, stay open
29
mapk can be activated through g protein coupled receptors, which is blank of the g protein
independent