CHAPTER 13: Signal-Transduction Pathways

CHAPTER 13: Signal-Transduction Pathways

(Problems: 1-5,7,13,15-18,21,25,29)

1. Primary messenger.

• Signal, first messenger, ligand.

2. Reception of primary messenger.

• Protein receptor of primary messenger.

3. Relay of information.

• Transmembrane protein, transducer.

4. Activation of effectors.

• Transducer, effector enzyme,
second messenger, effectors.

5. Termination of signal.

• Phosphatases

13.2. Receptor Proteins

Ligand Binding

Transmembrane proteins

Seven transmembrane helices
(7TM proteins)

Ligand binding on
outside leads to
conformational
change (new
activity) on inside
of cell.

Ligand Binding → Activation of G-Proteins →
Activation of Effector Proteins

ligand Effector
enzyme

7TM Gs
receptor
Second
Transducer messenger
(G-protein)
Effector

Activation of Effector Proteins →
Phosphorylation of Proteins

Protein kinase A
Protein kinase A phosphorylates Ser and Thr residues in
numerous proteins resulting in activation or inhibition of their
functions.

Control of Activation

X GTP G-cycle

Chlorera (Vibrio cholorae) X
Choleragen → stabilizes Gs Whooping Cough (Bordertella pertussis)

↓ Toxin → stabilizes Gi
Open K+ channel ↓

↓ Open K+ channel
Closed Na+‐H+ exchange
↓
↓
NaCl loss Closed Ca2+ channel

Reversible Ligand/Receptor Binding

Other Second Messengers

2nd messenger 2nd messenger

Ligand/Receptor binding leads to G‐protein activation

The Phosphoinositide Cascade

Phosphorylation
of Ser and thr
on many proteins

13.3. Tyrosine Kinases

Epidermal Growth Factor Signaling

Adaptor proteins XPi

Tumors

13.4. Insulin Signaling

Insulin-receptor Akt is a Phosphorylate
substrates mobile protein enzymes in
kinase glycogen
synthesis and
glucose
transport
(GLUT4)

Signaling
terminated by
protein
phosphatases

13.4. Calcium Ion is a Cytoplasmic Messenger

CaM-Ca2+ + CaM-Kinase
Inactive

CaM-Ca2+
CaM-Kinase

Active

Phosphorylation of
proteins resulting

in regulation of
fuel metabolism,
ion permeability,
neurotransmitters