Which of the following statements regarding transport across membranes are correct?

GLUT1 facilitates the transport of glucose from the outside to the inside of red blood cells, down the concentration gradient of glucose.

The mechanism of GLUT1 action is shown below, along with a graph showing the relationship between the extracellular concentration of glucose and the initial velocity (rate) of glucose entry facilitated by GLUT1. Note the similarity of this graph to a Michaelis-Menten curve.

Which of the following factors is most likely to control the maximum rate of facilitated diffusion (i.e., the value of V_max) for this facilitated transport process?

[Note: You may need to draw on your understanding of Michaelis-Menten kinetics to answer this question]

Which of the following steps in G protein-coupled receptor signalling pathways directly give rise to amplification of the signal?

The schematic diagram below shows the concentration gradients of several molecules or ions across a lipid bilayer membrane.

Gradients are represented by wedges, in which the higher concentration is at the thick end of the wedge.

Which of the following molecules or ions would you expect to readily diffuse across the membrane in the direction indicated by the red arrow?

A small hydrophobic molecule X has a higher concentration in the cytosol than in the extracellular space. 

X is transported out of cells by diffusing from the cytosol into the membrane lipid bilayer and then emerging in the extracellular space.

The movement of X out of cells is an example of:

G protein-coupled receptors (GPCRs) and tyrosine kinase receptors are two different families of transmembrane signalling molecules. Activation of each family of receptors initiates intracellular signalling events.

Which of the following features are shared by both of these receptor families and their signalling mechanisms?

When adrenaline (epinephrine) binds to its integral membrane receptor, this initiates an intracellular signalling cascade, which includes each of the following events (but not necessarily in this order):

1. The Gα subunit binds to adenylyl cyclase
2. GDP dissociates from the Gα subunit
3. The Gα subunit dissociates from the receptor and the Gβ/Gγ subunits
4. The adrenergic receptor undergoes a conformational change
5. ATP is converted to cAMP and pyrophosphate (PPi)
6. GTP (bound to the Gα subunit) is hydrolysed to give GDP

What is the correct order of these events?

Which of the following is an example of specificity in G protein-coupled receptor signalling?

The image below left shows a cartoon representation of signalling through a specific receptor tyrosine kinase (RTK). Phosphorylation of downstream proteins is indicated by a "P" within a yellow circle. (This is the same pathway as the previous question.)

The image below right is experimental data on this pathway, obtained either in the presence or absence of several drugs, each affecting an unknown protein in the pathway. The upper panels show total protein and phosphorylation states of a number of key proteins in this signalling pathway. The lower image is of quantitative-RT-PCR for detection of expression of a known target gene at the end of this signalling pathway.

Separate experiments (not shown) concluded that none of these drugs had an effect on the activity RAS or RAF.

Which drug appears to be affecting the kinase activity of MEK but is still allowing transcription of the target gene?

The image below left shows a cartoon representation of signalling through a specific receptor tyrosine kinase (RTK). Phosphorylation of downstream proteins is indicated by a "P" within a yellow circle. (This is the same pathway as the previous question.)

The image below right is experimental data on this pathway, obtained either in the presence or absence of several drugs, each affecting an unknown protein in the pathway. The upper panels show total protein and phosphorylation states of a number of key proteins in this signalling pathway. The lower image is of quantitative-RT-PCR for detection of expression of a known target gene at the end of this signalling pathway.

Separate experiments (not shown) concluded that none of these drugs had an effect on the activity RAS or RAF.

Which drug appears to be affecting the kinase activity of MEK but is still allowing transcription of the target gene?