Download Second Messenger List

Biochemistry Second Messengers
Vitamin A:
a.
b.
Epinephrine
a.
b.
c.
Insulin:
a.
b.
Gt
Transducin activates cGMP phosphodiesterase activity to decrease
circulating cGMP and induce light sensation
Depends on receptor
 α1: Gq
 α2: Gi
 β1 : G s
 β2 : G s
β receptor stimulation causes increased cAMP activity causes insulin
decrease, and cortisol/glucagon increase
α2 receptor stimulation causes the opposing effects due to lowered cAMP
levels
Insulin receptor tyrosine kinase (IRTK)
Induces IRS-1, IRS-2, PLC, and SHC
IGF-1:
a.
b.
IGF-1 receptor tyrosine kinase (similar to IRTK)
Induces cartilage, bone, and muscle growth
Prolactin/GH:
a.
JAK receptor
b.
Binding causes downstream activation of STAT and gene transcription
T3:
a.
b.
Nuclear T3 receptor that heterodimerizes with RXR receptor
Causes upregulation of gene transcription leading to increased production
of UCP, Na+/K+ ATPase, 1-adrenergic receptor, and GH.
1,25 D signaling:
a.
Nuclear VDR receptor heterodimerizes with RXR receptor
b.
Increases IL-6 release, ODF release, and osteocalcin release in bone;
increases apical Ca2+ channels, Ca2+ binding protein, and basolateral
Ca2+/ATPase in the intestine
Glucocorticoid:
a.
Nuclear receptor (GR) homodimer
b.
Glucocorticoid binds GR which homodimerizes to induce gene
transcription
Mineralocorticoid:
a.
Nuclear receptor (MR) homodimer
b.
Mineralocorticoid binds MR which homodimerizes to induce gene
transcription
Glucagon:
a.
b.
Gs
Increased cAMP and a subsequent increase in gluconeogenesis
Vasopressin:
a.
Gs
b.
Increases PKA to combine with aquaporin-2 and increase water
reabsorption in the distal nephron
GHRH:
a.
b.
Gs
Increases cAMP → PKA → CREB → gene transcription for GH synthesis
and release
LH:
a.
b.
Gs
cAMP activity induces P-450scc to start androgen synthesis
Thyroid stimulating hormone:
a.
Gs
b.
TSH binds to the thyroid follicular cell causing an increase in cAMP
activity  PKA  endocytosis of thyroglobulin/MIT/DIT/T4/T3
aggregate.
PTH signaling:
a.
Gs
b.
Increases osteoblastic cAMP  renal excretion of cAMP, PO4.
 IL-6 release  osteoclastic resorption of
bone mineral
 ODF release  multinucleate osteoclast
differentiation
Calcitonin signaling:
a.
Gs
b.
Increases osteoclastic cAMP  decreases osteoclast activity
Angiotensin II:
a.
Gs
b.
Activates cholesterol esterase and P-450scc in the zona
fasciculata/reticularis
ANP inhibition:
a.
Gs (via 1 adrenergic receptor)
b.
PKA inhibits release of ANP
GHIH:
a.
b.
Gi
Decreases cAMP and blocks GH synthesis and release
Dopamine effect on prolactin:
a.
Gi
b.
Inhibits posterior pituitary release of prolactin
GnRH:
a.
b.
Gq
Increases PKC, CaM dependent kinase, and Ca2+ to induce LH, FSH
release
a.
b.
Gq
Activates cholesterol esterase and P-450scc in the zona glomerulosa as well
as inducing StAR transcription (via cAMP) and maximal activity (via
PKA)
ACTH:
ANP activation:
a.
Gq (via 1 adrenergic receptor)
b.
PKC induces release of ANP
Oxytocin:
a.
b.
Gq
Increased Ca2+ causes increased function in both mammary and uterine
tissue
Angiotensin II action:
a.
Gq
b.
Increases intracellular Ca2+ which activates CaM kinase. CaM kinase and
PKC phosphorylate enzymes to increase the steroidogenic pathway,
increasing aldosterone levels and Na+ reabsorption.
PTH release:
a.
Inhibition by Ca2+ sensitive Gq
b.
High Ca2+ inhibits PTH release by increasing intracellular calcium via
IP3/DAG/Ca2+. (PTH is released when intracellular calcium is low)
ANP action:
a.
b.
Guanylyl cyclase
Increases intracellular cGMP  PKG, which phosphorylates Ca2+
channels in the membrane and decreases Ca2+ influx (the opposite of the
angiotensin II pathway)