Cell Biology (BIO 320)
Chapter 15 – Mechanisms of Cell Communication
I.
General Principles of Cell Communication (pages 879-883, 887-893)
1.
From signal to response - an extracellular signal molecule activates an
intracellular signaling pathway leading to changes in metabolism, gene
expression, shape or movement (Fig 15-1).
2.
Extacellular signal molecules bind to specific receptors. Hydrophilic
signal molecules bind to cell-surface receptor proteins. Small
hydrophobic signal molecules bind to intracellular receptor proteins (Fig
15-2).
3.
Four forms of intercellular signaling – contact-dependent, paracrine,
synaptic, endocrine (Figs 15-3, 15-4).
4.
Extracellular signals can lead to slow or fast responses (Fig 15-6).
5.
Nitric oxide signals by directly regulating the activity of specific proteins
inside the target cell (Fig 15-12).
6.
Nuclear receptors are ligand-modulated gene regulatory proteins (Figs 1513, 15-14, 15-15).
7.
Three classes of cell surface receptors – ion-channel-coupled, G-proteincoupled, and enzyme-coupled (Fig 15-16).
II.
Signaling through G-protein coupled cell-surface receptors (GPCRs) and small
intracellular mediators (pages 904-921)
1.
Structures of G-protein-coupled receptors (Fig 15-30) and trimeric Gproteins (Fig 15-31).
2.
Activation of trimeric G-protein by an activated GPCR (Fig 15-32).
3.
Some G-proteins regulate the production of cyclic AMP (Figs 15-33, 1534).
4.
Protein kinase A (PKA) mediates most of the effects of cyclic AMP (Figs
15-35, 15-36).
5.
Some G proteins activate an inositol phospholipid signaling pathway by
activating phospholipase C- (Figs 15-38, 15-39).
6.
Ca2+ functions as a ubiquitous intracellular mediator (Figs 15-40, 15-41).
7.
Calmodulin – a Ca2+-binding protein that helps relay changes in cytosolic
Ca2+ to other proteins (Fig 15-43).
8.
CaM-kinases mediate many of the responses to Ca2+ signals in animal
cells (Figs 15-44, 15-45).
9.
Smell and vision depend on GPCRs that regulate cyclic-nucleotide-gated
ion channels (Figs 15-46, 15-49, 15-50).
10.
GPCR desensitization depends on receptor phosphorylation (Fig 15-51).
III.
Signaling through enzyme-coupled cell-surface receptors (pages 921-945)
1.
Six principal classes of enzyme-coupled receptors.
2.
Subfamilies of receptor tyrosine kinases (RTKs) (Fig 15-52).
3.
Activated RTKs phosphorylate themselves (transautophosphorylation)
(Fig 15-53).
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
IV.
Phosphorylated tyrosines on RTKs serve as docking sites for intracellular
signaling proteins (Fig 15-54).
Proteins with SH2 domains bind to phosphorylated tyrosines (Fig 15-55).
Ras belongs to a large superfamily of monomeric GTPases.
Ras activates a MAP kinase signaling module (Fig 15-60).
PI 3-kinase produces lipid docking sites in the plasma membrane (Fig 1563).
The PI 3-kinase-Akt signaling pathway stimulates animal cells to survive
and grow (Fig 15-64).
The downstream signaling pathways activated by RTKs and GPCRs
overlap (Fig 15-66).
Cytokine receptors activate the JAK-STAT signaling pathway 9Fig 1568).
Signal proteins of the TGFb superfamily act through receptor
serine/threonine kinases and Smads (Fig 15-69).
Bacterial chemotaxis depends on a two-component signaling pathway
activated by histidine-kinase-associated receptors (Figs 15-71, 15-72, 1573).
Signaling pathways dependent on regulated proteolysis of latent gene regulatory
proteins (pages 946-948)
1.
A number of signaling pathways operate through proteolysis of latent gene
regulatory proteins.
2.
The receptor protein Notch is a latent gene regulatory protein (Figs 15-75,
15-76).