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25 Cards in this Set
- Front
- Back
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oncogenes only need ONE HIT to:
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fail in their function
- occurs during the lifetime (fetuses don't survive if it's there from the start) |
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individuals homozygous for a dominant disorder generally don’t
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survive for long.
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Female oogenesis occurs in the embryo, then
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gets frozen until puberty
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the vast majority of cancer predisposition syndromes are dominant in their
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inheritance pattern
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Chaperones do NOT determine the final AA structure –
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the primary structure does
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smoking causes:
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bulky adducts
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low Km = high affinity for substrate =
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more activity of the enzyme = more product
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BER does repair spontaneous damage, because
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deamination IS spontaneous damage
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BRCA1 and BRCA2 are both responsible for
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DSB repair
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CTD only ~ to
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RNAP II
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Enhancers are required for
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high-level, regulated expression
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splicing occurs after the 5’ Cap is placed on; PolyA addition is
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the last step of mRNA processing
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the ribosome will make a peptide bond between
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ANY two AA’s presented to it
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ribosomes are very similar between proks and euks
- translation in both is generally similar, but |
**certain antibiotics can target particular features of prok. translation so as to treat an infection without harming the person**
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lab mice had
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alpha, BetaS, and gamma globin genes made in them
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acidosis/high temp decrease
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the solubility of all kinds of Hb’s
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leukemia occurs via oncogenes OR tumor suppressors; =
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increase in immature WBC’s
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chemotherapy =
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drugs
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Variable expressivity applies to BOTH:
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AR and AD
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R167W mutation =
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Arginine to Tryptophan: going from charge to nonpolar
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MCHC (mean corpuscular hemoglobin concentration) =
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the average concentration of hemoglobin in a RBC
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elevated MCHC indicates that the patient is
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***dehydrated***
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sickled cells and reticulocytes are abnormally
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dehydrated
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urobilinogen =
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byproduct of breakdown of heme
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***dehydration of patients =>
(2) |
1. concentration of HbS => increased sickling
2. increased blood viscosity => more time being deoxygenated |
