#Question id: 1229
#Unit 4. Cell Communication and Cell Signaling
Which of the following events occur(s) during light activation of the rhodopsin receptor?
a. 11-cis-retinal is converted to all-trans-retinal
b. activation of the trimeric G protein, transducin
c. activation of cGMP phosphodiesterase
d. opening of the cGMP-gated ion channel
#Question id: 1230
#Unit 4. Cell Communication and Cell Signaling
Which of the following events occur(s) following the binding of a ligand to a G protein–coupled receptor that triggers release of Ca2+?
a. activation of protein kinase A by IP3
b. phospholipase cleavage of PIP2 to IP3 and DAG
c. release of DAG into the cytosol
d. IP3-mediated opening of Ca2+ channels in the ER membrane
#Question id: 1231
#Unit 4. Cell Communication and Cell Signaling
Arrange the following events in the proper order in which they occur during transduction of the TGFβ signal:
a. association of Smad3 and Smad4
b. phosphorylation of TGFβ receptor I by TGFβ receptor II
c. phosphorylation of Smad3 by TGFβ receptor I
d. nuclear import of Smad3
e. binding of TGFβ to TGFβ receptor II
#Question id: 1232
#Unit 4. Cell Communication and Cell Signaling
Which of the following mutations might confer a competitive advantage to an athlete by raising his or her hematocrit?
a. excess production of erythropoietin
b. decreased production of erythropoietin
c. EpoR that cannot bind STAT5
d. EpoR that cannot bind SHP1
e. EpoR that cannot bind JAK2
#Question id: 1233
#Unit 4. Cell Communication and Cell Signaling
Transphosphorylation (cross-phosphorylation) of receptor tyrosine kinases
a. inhibits catalytic activity.
b. promotes transphosphorylation of additional tyrosine residues.
c. triggers release of the ligand.
d. generates binding sites for signaling molecules.
#Question id: 1234
#Unit 4. Cell Communication and Cell Signaling
Which of the following mutations would likely have a similar cancer-promoting effect as the RasD mutation?
a. mutation in Grb2 so that it cannot bind Sos
b. mutation in Sos so that it binds Ras independent of Grb2
c. mutation in GAP so that it cannot bind Ras
d. mutation in EGF receptor so that it binds GRB2 independent of EGF