1. A person is heterozygous for a mutation in a STAT gene that replaces a tyrosine in the coding sequence with a phenylalanine. The missing tyrosine is normally phosphorylated by a JAK bound to a cytokine receptor. What effect would this mutation most likely have on signaling via this cytokine receptor ? 

The mutation is unlikely to have any effect in this person as they are heterozygous for the mutated gene.

The activation of a JAK would be blocked at receptors to which the mutated STAT is recruited.

The STAT protein would get hyper-phosphorylated.

Dimerization of the STAT would occur in the absence of ligand binding to the receptor.

The STAT protein would be unable to disengage from the cytoplasmic tail of the activated receptor.2. A person is heterozygous for a missense mutation in a receptor tyrosine kinase (RTK) gene coding sequence. The mutation is located in the cytoplasmic region close to the transmembrane domain. The amino acid change does not affect receptor dimerization and causes mutation of a tyrosine that is normally bound by GRB2. Which is most likely to happen to signaling through this RTK pathway in this person ?

 

Signaling would be unaffected because the individual is heterozygous for the mutation.

Signaling through the receptor would occur without ligand being bound.

Signaling in cells exposed to the ligand would be transduced more efficiently.

Signaling in cells exposed to the ligand would still occur but be transduced less efficiently.

The mutation would prevent all dimerized receptors from functioning.
3.Which of the following statements describes a process that is not dependent on the activity of a G-protein (heterotrimeric or monomeric)?

 

Signaling via the cytokine receptor pathway.

Signaling via the receptor tyrosine kinase pathway.

Signaling via cAMP as the second messenger.

Signaling via IP3 as the second messenger.

Assembly of microtubules.

4. Which of the following best describes a property of cGMP ? 

cGMP is a second messenger that conveys a signal only when its concentration increases.

It is a second messenger produced by adenylyl cyclase.

It is a second messenger produced directly from dGTP.

Like cAMP, cGMP can activate PKG.

cGMP binds directly to PKG.