Decide the protein encoded by the DNA sequence supplied below. Clearly show conceal each step of your reasoning, at the side of transcription and translation. (b) Cytosine can undergo deamination, wherein its amino group (NH₂)

1. (15 pts) (a) Decide the protein encoded by the DNA sequence supplied below. Clearly show conceal each step of your reasoning, at the side of transcription and translation.
(b) Cytosine can undergo deamination, wherein its amino group (NH₂) is changed by an oxygen atom to originate uracil. If this mutation happens, it’ll also alter the corresponding mRNA sequence. Name which cytosine in the DNA sequence, if mutated to uracil in the following mRNA, would beget the greatest potential affect on the organism. Enhance your answer with a particular clarification.

G-A-A-T-G-T-C-G-C-T-A-A-T-C-T-A-G-C

2. (20 pts) Histidine can undergo enzyme-catalyzed decarboxylation to originate histamine. When histamine is produced in excess, its singly protonated (positively charged) originate binds to histamine receptors, triggering the signs related to the general chilly and hypersensitive response signs. Chlortrimetron is an antihistamine that binds to histamine receptors but doesn’t advised them in the related way as histamine. On the opposite hand, it is miles in a space to sinister the blood–brain barrier and have interaction with receptors in the central nervous machine, ensuing in drowsiness—a well-acknowledged facet originate of many antihistamines. To decrease this originate, nonsedating antihistamines equivalent to Allegra (fexofenadine) were developed.

(a) Snide the basicity of the three nitrogen atoms (N1, N2, and N3) in histamine and give an explanation for your ranking.
(b) Scheme the predominant (active) originate of histamine that binds to the histamine receptor.
(c) Scheme the originate of chlortrimetron that’s most more likely to bind to the histamine receptor.
(d) Suggest the styles of intermolecular interactions enthusiastic on ligand binding to the histamine receptor. (e) Name and reward the structural feature(s) that allow chlortrimetron—but now not histamine—to sinister the blood–brain barrier.
(f) Scheme the predominant originate of fexofenadine at physiological pH. (g) Point out why Allegra (fexofenadine) choices as a nonsedating antihistamine.

3. (16 pts) The blueprint below outlines a approach for residing-convey labeling of protein P1 at a photocaged tyrosine analog the spend of fluorescein (FLUO). Upon UV irradiation, P1 generates a highly reactive and shortlived intermediate from the photocaged tyrosine. This intermediate fleet undergoes a Michael addition with reagent 1 in situ, with the response persevering with to completion after 10 minutes of UV exposure. In a subsequent step, the modified P1 is coupled with reagent 2 to yield the fluorescein-labeled protein.

(a) Suggest the structures of reagent 1 and reagent 2.
(b) Scheme the construction of the reactive intermediate that undergoes the Michael addition with reagent 1. (c) Point out why the fluorine substituent which is never show conceal in the reactive intermediate is essential for formation of this intermediate. Consist of structures if priceless.
(d) Present a zigzag-arrow mechanism for the Michael addition described in section (b).

4. (12 pts) A peptide ligand shows strong binding affinity (5.7 nM) for its target receptor, with the Cterminal phenylalanine (Phe) taking part in a main role in this interaction. To probe its importance, Phe became as soon as systematically changed with several unnatural amino acids, producing four peptide variants. The binding affinities of these mutants are listed alongside their corresponding amino acids; lower values reward stronger binding.

(a) Per the binding affinity recordsdata, what can even additionally be inferred about the form of the receptor’s binding pocket?
(b) What are the dominant styles of nocovalent interactions to blame for ligand binding? Enhance your reasoning.
(c) One mutant (containing amino acid D) shows stronger binding than the wild-kind peptide. Present a rationale for this observation.

5. (14 pts) Plot 1 illustrates how enzyme E1 catalyzes the formation of two intramolecular disulfide bonds in protein P by a series of thiol–disulfide alternate reactions. Enzyme E2 is proposed to operate thru the same mechanism to rearrange these disulfide bonds.
The spend of Plot 1 as a recordsdata, propose detailed stepwise response pathways for these rearrangement processes that story for the formation of every of the 2 isomeric styles of protein P proven in Plot 2. Your answer can even restful clearly determine all key intermediates and products at each step. Crooked-arrow notation is now not required.

6. (23 pts) The blueprint below illustrates the construct of a molecular beacon (MB) for target DNA detection.
UV absorption spectra of DNA1 and fluorescence emission spectra (livid at 490 nm) of DNA1 and DNA5 are supplied. Point to that the emission spectra of DNA5 have to now not relevant to the questions below and can restful be neglected.
DNA1 has the sequence: 3′-GTCATRTTGACCGTACGTCAGTTGACTGGTCATOTTGAC-5′, where TR
and TO (highlighted in containers) are fluorophores positioned within related sinister environments in the stem place of the hairpin construction.
The spend of this recordsdata, reward the working precept of the molecular beacon by answering the following: (a) Build the color codes the same to the UV spectra of the hairpin and duplex styles of DNA1, and give an explanation for your selections.
(b) Decide the excitation and emission maxima (λmax) for both TR and TO.
(c) Present spectral proof supporting the prevalence of Förster resonance vitality switch (FRET) in the hairpin originate.
(d) Calculate the FRET vitality switch efficiency for the fluorophore pair in the hairpin. Notify all work. (e) Estimate the distances between TR and TO in both the hairpin and duplex forms. Reflect the neighboring sinister-pair spacing of 0.34 nm.
(f) The spend of your consequence from (e), reward why FRET is minimal in the duplex originate.
(g) Decide the sequence of the target DNA (5′ → 3′) proven in the blueprint.
(h) Point out how binding of the target DNA induces the transition from the hairpin to the duplex originate.

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