Genetically knocking out both copies of the p53 gene in rats …
A.is embryonic lethal.
B.results in a lower malignancy rate, but the rats are otherwise seemingly normal.
C.results in a higher rate of cancer onset, but the rats are otherwise seemingly normal.
D.increases cell death by apoptosis, leading to developmental defects.
E.does not have any effect unless the rats live outside of the laboratory and are exposed
to various types of stress.
Bacteria contain homologs of cytoskeletal filament subunits …
A.except those of the intermediate filaments.
B.but these homologs are incapable of nucleotide binding and hydrolysis.
C.that are less diverse in their function relative to their eukaryotic counterparts.
D.that can have different functions to those of their eukaryotic counterparts.
E.that are dispensable for cell growth and proliferation.
Mammalian Cdk inhibitor proteins (CKIs) can be grouped into two families based on
their structural and functional differences. The Cip/Kip family proteins (e.g. p21) have a
broad binding specificity. These proteins bind preferentially to already formed
cyclin-Cdk complexes and thus enhance complex formation. However, they inhibit the
kinase activity of most complexes (e.g. S-Cdks), except in the case of G1-Cdk
complexes where no inhibition occurs. Consequently, Cip/Kip family proteins have an
overall positive effect on Cdk4/6 activity due to their help in bringing the subunits
together. In contrast, the inhibitors of the INK4 family (e.g. p16) bind only to the Cdk
subunit of G1-Cdks and prevent binding of both the G1 cyclins and the Cip/Kip family
CKIs. Based solely on these findings, would you expect p16 to activate (A) or
inactivate (I) the S-Cdks in the presence of limited amounts of p21?