Biology 3597A/B Lecture Notes - Lecture 20: Ribozyme, Cis-Regulatory Element, Reverse Transcriptase
5 Apr 2017
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P53 basically always misregulated in cancer, master switch. Mdm2 from binding pull and tug between active p53 by sequestering mdm2 or p53 targeted for degradation when not bound. Uv radiation dna damaged, p53 transcription increases, degradation decreases. If damage after s phase (after replication) or before s phase but only recognized after s phase (mutated and then replicated even worse), once recognized then cell is destined for apoptosis. Missense in 1 allele acts in dominant negative phenotype. Because functions as 4 of these that make up a functional unit. Problem when tetramers form, if even 1 mutant subunit, then protein won"t be effective. Majority of these mutations occur in a dna binding region. Crisper allows us to fix things on cellular basis. Easier replacement not going in and fixing defective mutations, we are trying to replace a protein or gene that is defective in and individual.
