Cell Signaling
G-PROTEIN-COUPLED RECEPTORS
Triggered by calcium ion release…
muscle contraction
Fertilized egg development
Secretion of neurotransmitters
Calcium ions do not drive the propagation of an action potential along a nerve axon → flow of sodium ions into the cell is primarily responsible for neuron action potentials
Bacterial toxins & Disease
Cholera → activates a G protein that stimulates adenylyl cyclase
Whooping couch (pertussis toxin) → inactivates a G protein that inhibits the cyclase
Both toxins ultimately activate adenylyl cyclase
ENZYME-COUPLED RECEPTORS
Mechanisms used to terminate a signal transmitted by activated RTKs…
The RTKs are internalized and digested in lysosomes
Activated receptors can be switched off by removal of their activating phosphates by a tyrosine phosphorylase
Ras Proteins
Mutations in Ras proteins are among the most common molecular changes seen in human cancers
Mutations cause Ras to be unable to hydrolyze its bound GTP to GDP
Ras proteins with this mutation can no longer turn themselves off
Essential Concepts
Cells communicate through extracellular chemical signals
Hormones carried in blood to distant target cells
Neighboring cells communicate through direct cell-cell contact
Extracellular signal molecules…
Must interact with receptor protein on or in a target cell (each receptor protein recognizes particular signal molecule)
Bind to cell-surface receptor proteins that convert (transducer) the extracellular signal into different intracellular signals (organized in signaling pathways)
Three main classes of cell-surface receptors:
Ion-channel-coupled receptors
G-Protein-Couple receptors
activate trimeric GTP-binding proteins called G proteins → molecular switches, transmitting the signal onward for a short period before switching themselves off by hydrolyzing GTP to GDP
G-proteins regulate ion channels or enzymes in plasma membrane
Directly activate (or inactivate) enzyme adenylyl cyclase, increasing (or decreasing) intracellular concentration of second messenger molecules, cyclic AMP
Rise in cyclic AMP activates cyclic-AMP-dependent protein kinase (PKA)
Directly activate enzyme phospholipase C, generating messenger molecules inositol triphosphate (IP3) and diaglycerol
IP3 opens Ca2+ channels in membrane of endoplasmic reticulum, releasing free Ca2+ into the cytosol → Ca2+ acts as second messenger, altering the activity of Ca2+-responsive proteins (ex. Calmodulin - CaM-kinases)
Ca2+ and diaglycerol in combination activate protein kinase C (PKC)
PKA, PKC, and CaM-kinases phosphorylate selected signaling and effector proteins on serines and threonine, altering their activity
Different cell types contain different sets of signaling and effector proteins and are affected in different ways
Enzyme-coupled receptors
Intracellular protein domains that function as enzymes or are associated with intracellular enzymes
Many are receptor tyrosine kinases (RTKs): phosphorylate themselves and selected intracellular signaling proteins on tyrosines
Phosphotryosines on RTKs serve as docking sites for various intracellular signaling proteins
Most RTKs activate monomeric GTPase Ras, activating a three-protein MAP-kinase signaling module that helps relay signals from plasma membrane to nucleus
Ras mutations stimulate cell proliferation by keeping Ras (the Ras-MAP-kinase signaling pathway) constantly active
Common feature of many cancers
Some RTKs stimulate cell growth and survival by activating PI 3-kinase, which phosphorylate specific inositol phospholipids in the cytosolic leaflet of the plasma membrane lipid bilayer
Inositol phosphorylation creates lipid docking sites that attract specific signaling proteins from the cytosol (ex. Protein kinase Akt)
Notch receptors have a direct pathway to the nucleus → when activated, part of the receptor migrates from plasma membrane to the nucleus where it regulates the transcription of specific genes
Steroid hormones and nitric oxide → small or hydrophobic enough to cross plasma membrane and activate intracellular proteins
Plants use these to control their growth (often act by relieving transcriptional repression of specific genes)
→ GPCRs and enzyme-coupled receptors respond to extracellular signals by activating intracellular signaling pathways, which activates effector proteins that alter the behavior of the cell
→ Each activated component must be subsequently inactivated or removed for the pathway to function again
→ Different intracellular signaling pathways interact, enabling each cell type to produce the appropriate response to a combination of extracellular signals
in the absence of such signals, most animal cells have been programmed to kill themselves by undergoing apoptosis