What happens if there is too much p16-ink4a in a juvenile and elderly human? what happens if a juvenile produces a mutation form that lacks activity?
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What happens if there is too much p16-ink4a in a juvenile and elderly human?
what happens if a juvenile produces a mutation form that lacks activity?
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- The genetic alteration responsible for sickle-cell anemia in humans involves: a transition mutation from A to G, substituting glutamic acid for valine in a-globin a transversion mutation from T to A, substituting valine for glutamic acid in b-globin a transition mutation from T to C, substituting valine for glutamic acid in b-globin a transversion mutation from G to C, substituting glutamic acid for valine in a-globin a frameshift mutation of one ATC codon, removing glutamic acid from b-globinThe most prominent mutation of ERBB2 in breast cancer is L755S. What kind of mutation is this? Is this a driver or passenger mutation? How to do you know?Why are mutations in the INK4 locus so dangerous?
- Why would a mutation in a somatic cell of a multicellular organism escape detection?What is the probability that the palindromic symmetry of the trp repressor target DNA sequence is merely accidental?PTC is not a biological compound, but a chemical which became known after research done by Arthur J. Fox. Why is the TAS2R38 gene also called the PTC gene?
- Among the different types of amino acid substitution (same sense, missense, or nonsense mutations), which is the most deleterious one?What is the difference between a missense mutation and a nonsense mutation?What is the difference between a missense mutation and a nonsense mutation? Between a silent mutation and a neutral mutation?