Help with Other Protein Regulation - GRE Subject Test: Biochemistry, Cell, and Molecular Biology
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How do Bax and Bak promote cell death?
How do Bax and Bak promote cell death?
Bax and Bak dimerize to form a pore in the mitochondria outer membrane, which allows cytochrome c to escape into the cytosol. When cytochrome c is found in the cytosol, procaspase becomes activated and is cleaved into caspase. Once the caspase cascade begins the cell is destined for death.
Bax and Bak have nothing to do with the apoptosome and, while Bcl2 does block Bax and Bak from dimerizing, Bax and Bak do not prevent the action of Bcl2.
Bax and Bak dimerize to form a pore in the mitochondria outer membrane, which allows cytochrome c to escape into the cytosol. When cytochrome c is found in the cytosol, procaspase becomes activated and is cleaved into caspase. Once the caspase cascade begins the cell is destined for death.
Bax and Bak have nothing to do with the apoptosome and, while Bcl2 does block Bax and Bak from dimerizing, Bax and Bak do not prevent the action of Bcl2.
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One commonly studied outcome of G protein-coupled receptor (GPCR) activation is the activation of phospholipase C (PLC). What two important second messengers are formed when PLC cleaves phosphoinositide-4,5-bisphosphate 
?
One commonly studied outcome of G protein-coupled receptor (GPCR) activation is the activation of phospholipase C (PLC). What two important second messengers are formed when PLC cleaves phosphoinositide-4,5-bisphosphate
Interactions between 
, 
, 
, and PKC do indeed occur downstream of activation of PLC to contribute to numerous downstream cascades primarily initiated by protein kinase C (PKC). However, it is important to understand that the second messengers are 
and 
, which are specifically formed by the cleavage of 
, and each of the other molecules is considered an effector of those second messengers in this context.
Interactions between
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What is the key functional difference between GEFs (guanine nucleotide exchange factors) and GAPs (GTPase activating proteins)?
What is the key functional difference between GEFs (guanine nucleotide exchange factors) and GAPs (GTPase activating proteins)?
A GEF activates a small GTPase by exchanging a bound GDP (which confers an inactive state) for a GTP (which is higher energy, and activates the protein). A GAP performs the opposite; GAPs enhance the intrinsic GTPase activity of the small GTPase, which causes hydrolysis of the GTP on the active protein, thus converting it back to GDP and an inactive state.
A GEF activates a small GTPase by exchanging a bound GDP (which confers an inactive state) for a GTP (which is higher energy, and activates the protein). A GAP performs the opposite; GAPs enhance the intrinsic GTPase activity of the small GTPase, which causes hydrolysis of the GTP on the active protein, thus converting it back to GDP and an inactive state.
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What provides the necessary information to specify the three dimensional shape of proteins?
What provides the necessary information to specify the three dimensional shape of proteins?
Proteins have different level of protein structure, termed primary, secondary, and tertiary (quarternary is also a type in certain proteins). The 3D shape of proteins is largely due to the tertiary structure of a protein. This level is dictated by the specific amino acid sequence of the protein.
Proteins have different level of protein structure, termed primary, secondary, and tertiary (quarternary is also a type in certain proteins). The 3D shape of proteins is largely due to the tertiary structure of a protein. This level is dictated by the specific amino acid sequence of the protein.
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