G proteins that interact with GPCRs..
Question 15 options:
are composed of three subunits two of which interact with the plasma membrane via covalent bonds.
are active when bound to GDP and inactive when bound to GTP.
are composed of two different subunits called gamma and alpha.
are localized to the plasma membrane because of lipid-subunit non-covalent associations.
Question 16 (1 point)
Receptor tyrosine kinases are a type of enzyme-coupled receptor that dimerizes and can activate effector proteins via GTPase activity.
Question 16 options:
True
False
Question 17 (1 point)
Muscle cells, fibroblasts, and nerve cells all respond to the same signaling molecule with different outcomes, it is likely that this signaling molecule activates the same effector proteins in these different cell types, leading to the diversity of outcomes.
Question 17 options:
True
False
Question 18 (1 point)
Which of the following statements about G-protein-coupled receptors (GPCRs) is FALSE?
Question 18 options:
GPCRs are the largest family of cell-surface receptors in humans.
GPCRs are found in yeast, mice, and humans.
The different classes of GPCR ligands (proteins, amino acid, derivatives, or fatty acids) bind to receptors with different numbers of transmembrane domains.
GPCRs are used in endocrine, paracrine, and neuronal signaling.
Question 19 (1 point)
Levels of Cdk activity change during the cell cycle, in part because
Question 19 options:
Cdk degradation precedes entry into the next phase of the cell cycle.
the Cdks de-phosphorylate each other.
the Cdks activate the cyclins.
cyclin activity changes during the cycle.
Question 20 (1 point)
Which of the following genetic changes cannot convert a proto-oncogene into an oncogene?
Question 20 options:
A mutation in the promoter of the proto-oncogene, causing the normal protein to be transcribed and translated at an abnormally high level.
A mutation that introduces a stop codon immediately after the codon for the initiator methionine.
A mutation within the coding sequence that makes the protein hyperactive.
An amplification of the number of copies of the proto-oncogene, causing overproduction of the normal protein.