22 1 Receptor
.
agonists activate signal transduction pathways and receptor antagonists inhibit them
chemicals from environment (food ,
drugs , etc ) . = similar enough to cell signaling molecules - can bind to receptor proteins
>
-
leads to abnormal responses
endogenous ligands ligands produced by body
· -
·
exogenous ligands
-
ligands from outside body
>
-
can mimic endogenous ligand or overstimulate transduction pathways
o acts as an agonist any ligand that binds to receptor and causes a response
-
antagonist any ligand that binds receptor and inhibits
·
-
to a a response
Agonists of
exogenous ligands can bind to receptor too lightlye prolonged binding longer-lasting greater cellular response
=
+
·
G protein -
coupled
off carefully regulated exogenous ligands present
·
receptors presence can throw
signaling molecules >
-
signaling molecules , at wrong times
ligands greater response from target cell
>
-
more at receptor proteins = more activated ligand-receptor complexes >
-
Antagonists antagonists bind to receptor protein without activating
:
- no
response
of G Protein -
coupled >
-
When antagonists are in abundance they block signaling molecule from binding cellular response suppressed
,
-
Receptors
·
keeps receptor inactive + blocks ligand from
binding
ie) caffeine binding to adenosine receptors (blocks drowsiness)
↳
antagonist
Sextrathat
ring
allows receptor
to be activated
ie) albuterol (open airways) binding to adrenaline(activates receptors)
↳
agonist
adrenaline + caffeine both come from plants >
-
compounds evolved as defense mechanisms
22 2 Genetic mutations can disrupt signal
. transduction pathways
·
Mutations can occur in any step in transduction pathway
&
e
can happen in signaling molecules (protein) signaling transduction
,
cell signaling pathways ,
+ termination of signal
is crucial
any alteration ie) leptin (protein signaling molecule produced by fat cells to regulate
can cause
physiological decrease appetite)
↓ -
mutations =
leptin deficiency means no leptin to bind to receptors >
-
early obesity
changes can
come from
outside (food, ie) testoserone (hydrophobic signaling molecule that directs male development in embryos)
drugs) + inside
(mutations >
-
mutated androgen receptors cannot bind testoserone male , embryo follows female-pattern development
.
agonists activate signal transduction pathways and receptor antagonists inhibit them
chemicals from environment (food ,
drugs , etc ) . = similar enough to cell signaling molecules - can bind to receptor proteins
>
-
leads to abnormal responses
endogenous ligands ligands produced by body
· -
·
exogenous ligands
-
ligands from outside body
>
-
can mimic endogenous ligand or overstimulate transduction pathways
o acts as an agonist any ligand that binds to receptor and causes a response
-
antagonist any ligand that binds receptor and inhibits
·
-
to a a response
Agonists of
exogenous ligands can bind to receptor too lightlye prolonged binding longer-lasting greater cellular response
=
+
·
G protein -
coupled
off carefully regulated exogenous ligands present
·
receptors presence can throw
signaling molecules >
-
signaling molecules , at wrong times
ligands greater response from target cell
>
-
more at receptor proteins = more activated ligand-receptor complexes >
-
Antagonists antagonists bind to receptor protein without activating
:
- no
response
of G Protein -
coupled >
-
When antagonists are in abundance they block signaling molecule from binding cellular response suppressed
,
-
Receptors
·
keeps receptor inactive + blocks ligand from
binding
ie) caffeine binding to adenosine receptors (blocks drowsiness)
↳
antagonist
Sextrathat
ring
allows receptor
to be activated
ie) albuterol (open airways) binding to adrenaline(activates receptors)
↳
agonist
adrenaline + caffeine both come from plants >
-
compounds evolved as defense mechanisms
22 2 Genetic mutations can disrupt signal
. transduction pathways
·
Mutations can occur in any step in transduction pathway
&
e
can happen in signaling molecules (protein) signaling transduction
,
cell signaling pathways ,
+ termination of signal
is crucial
any alteration ie) leptin (protein signaling molecule produced by fat cells to regulate
can cause
physiological decrease appetite)
↓ -
mutations =
leptin deficiency means no leptin to bind to receptors >
-
early obesity
changes can
come from
outside (food, ie) testoserone (hydrophobic signaling molecule that directs male development in embryos)
drugs) + inside
(mutations >
-
mutated androgen receptors cannot bind testoserone male , embryo follows female-pattern development
