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Biochemistry Questions 2

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Biochemistry
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University of Arizona
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Receptor Tyrosine Kinase Signaling
Q8.1:
The single nucleotide mutation that causes the alteration of the glycine residue at codon 12
reduces GTPase activity. This leads to recurrent stimulation of the MAP kinase signaling
pathway in the absence of growth factors.
Tumor Necrosis Factor Receptor Signaling
Q8.2:
In TNF receptors, receptor binding induces conformational change in the death domain (DD)
region of the TNF receptor cytoplasmic tails that cause inactivation of the silence of death
domain (SODD) inhibitory proteins that signal cell death. For GPC receptors, conformational
change cleaves the bound guanosine triphosphate (GTP) to guanosine diphosphate (GDP) which
causes the G

heterotrimeric complex into a G
subunit and a G

complex that stimulate
downstream signaling pathways. In RTK pathways involving epidermal growth factors (EGF),
EGF binding to two inactive EGF receptors (EGFR) cause them to merge forming a dimer with
their tails phosphorylated, which then act as binding sites for downstream signaling molecules.
Nuclear Receptor Signaling
Q8.3:
The glucocorticoid fluticasone activates glucocorticoid receptors (GR) by releasing it from an
inactive chaperonin complex. Activated GRs translocated to the nucleus then activates the
expression of the anti-inflammatory annexin I gene, and also binds to p65 subunits of NF
B, a
promoter to pro-inflammatory cyclooxygenase-2 gene. This, overall, causes reduction in
inflammation.
Overview Metabolism
Q8.4:
Food consumption increases the glucose concentration in the blood which lowers the mass
action ratio (Q). Considering the equation for Gibb’s free energy, a Q value of less than 1 results
in a larger negative G value which means it is more favorable.

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Structure and Function of Simple Sugars
Q9.1:
Sweetness is a measure of the affinity of sugar molecules to G protein-coupled receptors in the
tongue based on their chemical structure. This means that aspartame has a higher affinity to
these receptors than galactose.
Glycolytic Pathway
Q9.2:
One molecule of glucose generates two molecules of ATP. The enzyme pyruvate kinase
converts phosphoenolpyruvate to produce pyruvate and the net ATP. It is considered a
substrate-level phosphorylation because it forms ATP from ADP by direct transfer of a
phosphate group to ADP from a substrate.
Regulation of the Glycolytic Pathway
Q9.3:
Accumulation of citrate occurs when its production in the citrate cycle is inhibited during high
levels of ATP. This signals to the cell that further generation of ATP is unnecessary. In contrast,
high AMP indicates low energy charge in the cell, which makes for an ideal signal to produce
more ATP.

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Receptor Tyrosine Kinase Signaling Q8.1: The single nucleotide mutation that causes the alteration of the glycine residue at codon 12 reduces GTPase activity. This leads to recurrent stimulation of the MAP kinase signaling pathway in the absence of growth factors. Tumor Necrosis Factor Receptor Signaling Q8.2: In TNF receptors, receptor binding induces conformational change in the death domain (DD) region of the TNF receptor cytoplasmic tails that cause inactivation of the silence of death domain (SODD) inhibitory proteins that signal cell death. For GPC receptors, conformational change cleaves the bound guanosine triphosphate (GTP) to guanosine diphosphate (GDP) which causes the G heterotrimeric complex into a G subunit and a G complex that stimulate downstream signaling pathways. In RTK pathways involving epidermal growth factors (EGF), EGF binding to two inactive EGF receptors (EGFR) cause them to merge forming a dimer with their tails phosphorylated, which then act as binding sites for downstream signaling molecules. Nuclear Receptor Signaling Q8.3: The glucocorticoid fluticasone activates glucocorticoid receptors (GR) by releasing it from an inactive chaperon ...
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