membranes and cell signalling

Question 1

Intercellular vs extra cellular response

Answer 1

• Intercellular response
○ Signals that enter the cell and cause an effect inside the cell
○ Eg steroid hormone- can enter the cell they are nonpolar/lipid soluble so can diffuse by simple diffusion into the cell
○ have an effect in the nucleus
○ Is a transcription factor so binds to a receptor to make a complex. The receptor will then bind to the promoter region to activate of a specific gene’s transcription therefore make proteins of the gene (think about oestrogen example from Alevels)
• ExtraCellular response
○ Can not enter the cell as they may be too big or are water soluble
○ Bind to regions of to allow change in signalling of target gene - allows transaction / translation
○ Will produce a specific protein
○ Eg Protein hormone( main type of hormone produced) large and charged so can’t diffuse though bilayer simply. Must bind to proteins/receptor outside cell to have effect on inside of the cell. (Called signalling molecule)

Question 2

Rapid vs slow response

Answer 2

Can phosphorylate protein so activity is different ( rapid response)
Can produce a protein ( slower response)
Response rate can be different
• Rapid
○ Eg adrenalin used in flight tor flight. Mainly needed for raid glycogen brake down into glucose to create APP for muscle contraction

Also cell signalling may have many pathways

Question 3

How is cAMP generated and what does it do?

Answer 3

1. Signalling molecule binds to the (receptor G-protein) on the plasma membrane
2. The GTP will replace the GDP molecule that is bound to the alpha subunit of the G-protein
3. Alpha subunit will then dissociate from the other (beta and gamma) subunits of the G-protein
4. Alpha subunit will activate the membrane bound adenylyl cyclase
5. Alpha subunit ( is a GTPase and will convert GTP into GDP)
6. Adenylyl cyclase convents ATP into cAMP ( cyclic adenosine monophosphate)
7. cAMP activates PKA (protein kinase A) PKA is the effector enzyme
   ○ Converts inactive PKA into active PKA
8. (active) PKA phosphorylates many proteins (cellular enzymes) and change their activity
   ○ Target proteins include metabolic enzymes and regulatory proteins
   ○ E.g. starts cascade of enzyme reaction for glycogenolysis

Question 4

How is ERK formed and what does it do? How could this control cell proliferation?

Answer 4

1. Ligand (growth factors) binds to the receptor (tyrosine kinase receptor) and causes the dimerization ( 2 receptors join together) of the receptors
2. The active dimerized tyrosine kinase receptor phosphorylates the tyrosine residue
3. Grb2 (adapter protein) can bind to the phosphorylated tyrosine kinase receptor
4. SOS protein will interact with Grb2
5. SOS will associate with RAS make RAS release the GDP and replace it with GTP (this activates the RAS protein)
6. RAS dissociates from SOS and moves into membrane
7. RAF and RAS interact causing RAF to be activate
8. RAF will phosphorylate with MEK
9. MEK will phosphorylate ERK (MAPkinase)
10. ERK enters nucleus and interacts with many transcription factors can allows transcription to occur (causes a down-stream cascade)
11. Many different genes will be transcribed so many different proteins will be produced
12. The proteins can affect the rate of cell proliferation- cyclin D is produced which regulates the cell cycle