Endocrine Signaling Systems

Front 1

What are the 3 main types of chemical signaling?

Back 1

1. Neurotransmitters (Fast, short duration response)
2. Hormones (Slower onset, Longer duration)
3. Local signals (Short lifespan--doesn't allow for circulation in blood).

Front 2

What are the two subclasses of hormones?

How are they different?

Back 2

1. Polypeptide: Alter a specific activity. Faster onset & Shorter duration.
2. Steroid: Alter gene expression. Slower onset & Longer duration.

Front 3

What are the 2 major subclasses of the local signals and what are their characteristics? Examples?

Back 3

1. Paracrines: Affect neighboring cells. Onset and duration varies. (Prostaglandins, Histamines, Kinins).

2. Autocrines: Affect cell that released them. Fast onset, duration varies. (Adenosine).

Front 4

What are the two mechanisms by which signaling alters cell behavior?

Back 4

Hydrophilic signals (cannot cross cell membrane) & Lipophilic signals (can pass through membrane).

Front 5

What are the components of hydrophilic signaling?

Back 5

1. Signal: Circulating in blood or isf. It's often catabolized or metabolized to inactive form.

2. Receptor: Provides specific binding site for signal. No good without effector.

3. Effector: On inside. Generates 2nd messenger.

4. 2nd Messenger: Changes protein function.

Front 6

Lipophilic signaling:
1. Why can't signals be synthesized ahead of time?
2. Where are target cells located?
3. How do they move through the blood?

Back 6

1. Because their ability to pass through membranes (can't store in vesicles).
2. Inside the cell, either in the cytosol or nucleus (Receptors in nucleus--Estrogen, Progesterone, Thyroid Hormone).
3. Albumin

Front 7

Describe the 3 types of Receptor/Effector relationships.

Which is the most common?

Back 7

1. R & E are same protein (Steroids & Tyrosine Kinase).

2. R & E are subunits in same protein complex (Nicotinic ACh receptor).

3. R & E are separate proteins. Most common type. Requires a way to communicate between R & E.

Front 8

Effector/2nd Messenger for Calcium:
1. How does a calcium ion enter the cell?
2. What binds to calcium once it enters?
3. How is process inactivated?

Back 8

1. Signal binds to receptor allowing calcium to move through channel.

2. Calcium binds to Calmodulin (Calcium binding protein).

3. Signal comes off receptor--no more Ca++ can enter. Calcium inside is pumped 1.) out of cell 2.) into mitochondria 3.) into ER/SR

Front 9

Tyrosine Kinase:
1. What type of receptor/effector protein?
2. What happens to the protein when the signal binds to it?
3. How does TK bring about change in cellular proteins?
4. What are some anabolic signals that TK receptors are used for?

Back 9

1. Receptor/Effector are the same protein.

2. It is activated by phosphorylating itself (atp->adp and it keeps a PO4).

3. It phosphorylates other intracellular proteins. (some of which are protein kinases).

4. Insulin & growth factors--So TK is important in regulating cell differentiation and proliferation.

Front 10

G-Proteins:
At rest, how is the G-Protein complex organized?

Back 10

A GDP with alpha, beta and gamma subunits.

GDP is bound to the alpha subunit.

Front 11

G-Proteins:
What happens to the G-Protein complex at activation?

Back 11

The signal binds to the receptor causing the attached G-Protein complex to now have a GTP attached to the alpha subunit (instead of a GDP). The complex moves to the effector.

Front 12

G-Proteins:
What happens to activate the effector?
What does the effector do?

Back 12

The activated G-Protein complex loses its beta and gamma subunits and it binds to the effector. The effector converts ATP to cAMP.

Front 13

G-Proteins:
What is the inactivation process?

Back 13

Effector: Inactivates when G-Protein complex inactivates.

G-Protein Complex: Have GTPase activity causing them to inactivate selves. GTP-->GDP
Beta & Gamma subunits reattach.

Receptor: Signal unbinds--it is inactivated.

Front 14

How does the Cholera toxin cause problems?

Back 14

It inactivates the GTPase activity in G-Proteins, causing them to remain activated.

Severe diarrhea.

Front 15

G-Proteins:
What do Gs proteins do?
What do Gi proteins do?

Back 15

Gs: Stimulate adenylate cyclase.

Gi: Inhibit adenylate cyclase.

Front 16

Inactivation of cAMP response:
1. What changes cAMP into AMP?
2. What does cAMP inhibit to prolong its effects?

Back 16

1. Phosphodiesterase. Inhibited by theophylline and caffeine.

2. Phosphatase.

Front 17

Phospholipase C cascade:
1. What link in the Receptor/Effector chain is Phos. C?
2. What 2nd messengers are associated with Phos. C? Are they hydrophobic or hydrophilic?

Back 17

1. It is the effector.

2. DAG (Diacyl glycerol)--Hydrophobic (remains in cell membrane).

IP3 (Inositol triphosphate)--Hydrophilic (enters the cytosol).

Front 18

This is the most recently discovered type of signaling system?

Back 18

Nitric oxide.

Front 19

What is the previous name for Nitric oxide?

What is its function?

Back 19

Endothelium-Derived Relaxing Factor (EDRF).

Produces vasodilation by relaxing smooth muscles. Also thought to prevent platelet aggegation.