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Translation_
Molecular Bio: Translation
| Question | Answer |
|---|---|
| Genetic code is "degenerate". What does this mean? | more than one codon can code for a single amino acid (UUU & UUC both form Phe) a.k.a. "Redundancy" |
| Start codons? | AUG in RNA. ATG in DNA (codes for methionine) |
| Stop codons? | UGA, UAA, UAG (Univ Georgia, Univ Alaska Anchorage, Universidad Autonama Guadalajara) |
| how many codons are there total? | 64. 63 actual encode AAs, 3 are stop codons |
| What are Silent mutations? | a point mutation that codes for the same AA, so no harm |
| What are Missense mutations? | a point mutation that codes for a new AA, altering the protein (eg: Sickle Cell Anemia [glycine-->valine]) |
| What are Nonsense mutations? | a point mutation that codes for a stop codon (eg: Hemophilia A) |
| What are Frameshift mutations? | deletion or insertion of nucleotides that are NOT multiples of 3. (eg: deletion=Duchenne's MD, insertion=Tay Sachs, deletion of a multiple of 3=Cystic Fibrosis, insertion of mult of 3=Huntingtons & Fragile X) |
| Always assume the coding strand is given. | Yeah, that's it. It's not a question. Nothing to see here. |
| 3 possible consequences of mutations at a splice site? | a piece of intron gets included in the final transcript, a piece of exon gets removed in final transcript, an entire exon(s) is removed from final transcript |
| Name 5 diseases due to trinucleotide repeat explansions | Huntingtons, Friedrich Ataxia, Fragile X, Myotonic Dystrophy, Spinobulbar Muscular Atrophy. (huntingtons is CAG (Glu) repeats) |
| How many high energy bonds to activate an AA (bind it to tRNA)? | 2 high energy bonds (ATP--> AMP + PPi) |
| Which type of AAs are present at the N-Terminal of a protein? | Hydrophobic AAs (Lys Arg His Ser Thr Cys Met Asn Gln Asp Glu) |
| Translation begins in cytoplasm. Where does it go from here? What element ensures this movement of location? | Moves to RER. The Signal Recognition Particle (SRP) causes it to move. SRP is located at N-terminal of protein. Signal Peptidases remove SRP once it is in RER. |
| Where does N Glycolysation and O Glycolysation occur? | N Glycolysation is in RER (co-translational); O Glycolysation is in Golgi (post-translational) |
| What mechanism causes protein to enter lysosome? What is absence of this mechanism called? | Phosphorylation of Mannose. Absence = I-cell disease |
| What 3 proteins are NOT N-glycosolated? | Insulin, Glucagon, Albumin |
| Which AA is most common in Collagen? | Glycine (Gly-X-Y) |
| Vit C is required for what process in Collagen synthesis? | Hydroxylation of Prolines and Lysines |
| Osteogenesis Imperfecta is due to absence of what element of Collagen? | Signal Sequence |
| Ehler Danlos IV is due to absence of what enzyme in Collagen synth? | Lysyl Hydroxylase |
| What 2 enzymes require Vit C | Prolyl Hydroxylase, Lysyl Hydroxylase |
| Pro-peptide cleavage of Collagen occurs where? (inside fibroblast or outside fibroblast)? | Outside |
| What enzyme is used to form the triple helix of Collagen in the final step of synthesis? What does its deficiency cause? | Lysyl Oxidase. Deficiency = Ehlers Danlos IX (Meinke's disease) |
| Lysyl Oxidase requires what metal? | Cu+ |
| fMet and Met are found in which organisms? | fMet is attached to AUG of prokaryotes, Met is attached to AUG of eukaryotes. |
Created by:
jsad
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