Ch 11 maybe Flashcards
four cAMP bind to blank regulatory subunits
two
Gs pathway makes this
protein kinase a (PKA) from cAMP
two regulatory subunits liberates two blank subunits
catalytic
catalytic subunits blank other blank
phosphorylate, proteins
PKA blank to the nucleus, and phosphorylates blank
translocates, transcription factors
transcription factors turn on blank
gene expression
very well known transcription factor
creb
creb activates very important blank for things like blank and blank
genes, eating/moving, drug addictions/sympathetic nervous system
this hormone increases ATI gene expression
aldosterone
ATI receptors are blank receptors and are an example of influencing transcription factors to influence blank
metabotropic, behavior
this promotes thirst
angiotensin
increased receptor blank leads to increased blank of angiotensin 2
expression, effectiveness
this pathway works the same as Gs, but it inhibits blank so blank is not produced
Gi, adenylyl cyclase, cAMP
tough pathway
Gq
Gq pathway
- PIP breaks into two
- IP3 and DAG come from PIP
- DAG activates PKC in the cell membrane
- IP3 liberates intracellular calcium
calcium released by ip3 binds to blank
calmodulin
calmodulin complex binds to blank of the dependent protein kinase
regulatory domain
PKC can do what action
open/close ion channels
arachidonic acid leads to the production of
prostaglandins
what produces prostaglandins that is produced by arachidonic acid
cyclooxygenase
tyrosine kinase receptors steps
- signal binds
- dimer forms
- phosphorylated by atp
- activates relay proteins leading to a response
mapk pathway
- ras
- raf
- MEK
- MAPK
- Transcription factors
retrograde signaling activates enzymes and increases blank
nt reelease
when the postsynaptic cell releases NO which travels to presynaptic cell to stimulate increased nt release
retrograde signaling
in the presynaptic terminal, second messengers can regulate blank
nt release
in the postsynaptic neuron, second messengers can regulate blank
postsynaptic potentials
in the soma second messengers can regulate blank and blank
resting potential, ap dynamics
pka opens ion channels through blank
phosphorylation
pka also activates blank which causes the ion to blank
inhibitor 1, stay open
mapk can be activated through g protein coupled receptors, which is blank of the g protein
independent
