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cfInhibitor of viral DNA polymerase, eg. Herpes virus. guanine analog. Acyclovir gets converted to acyclovir triphosphate, by the viral enzyme thymidine kinase, which can serve as a substrate for viral DNA polymerase. The lack of a 3'-OH group causes chain termination when it gets incorporate during viral DNA replication. |
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A nucleotide analog that acts as a reverse transcriptase inhibitor (eg. HIV treatment) |
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Nucleoside analog drug that act by inhibiting reverse transcriptase activity. Have a 100-300 fold greater affinity for reverse transcriptase compared to DNA meaning it binds to retroviral cells that use reverse trasriptase, not heathly body cells. This effectively targets retrovirus activity. Eg. HIV |
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Nucleoside analog drug that act by inhibiting reverse transcriptase activity. Have a 100-300 fold greater affinity for reverse transcriptase compared to DNA. This effectively targets retrovirus activity. Eg. HIV |
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Cytosine arabinoside (Cytarabine) |
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The planar configuration of arabinosides induces DNA Damage, and inhibits the activity of DNA polyermase. This is an anti-cancer agent |
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Vidarabine (adenosine arabinoside) |
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The planar configuration of arabinosides induces DNA Damage, and inhibits the activity of DNA polyermase. This is an anti-cancer agent |
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Can induce hypomethylation by inhibiting methyltransferase enyzmes |
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Can induce hypomethylation by inhibiting methyltransferase enyzmes |
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A quinolone drug that inhibits bacterial DNA gyrase. It is used in the treatment of respiratory and urinary tract infections and can be used to treat anthrax. |
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An anticancer drug, binds to and inhibits toposiomerase I activity. The result is DNA breakage. |
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An anticancer drug, inhibits the activity of topisomerase II |
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An antibiotic from a strain of Streptomyces. Inhibits initiation of transcription. Blocks formation of the first phosphodiester bond by binding to prokaryote RNA polymerase. RNA polymerase of eukaryotes is not affected. Used in the treatment of tuberculosis. Mutation in the gens encoding the target proteins such RNA polyermase and topoisomerases can lead to drug resistance.f |
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Strain of streptomyces. Binds tightly to double strand DNA. Inhibits transcription and replication in both prokaryotes and eukaryotes. Primarily used as an anti-cancer drug (inhibiting DNA replication and cell division). Not normally used as an antibiotic. |
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Produces a toxin called alpha-amanitin which is a potent inhibitor of RNA polyermase II. |
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An aminoglycoside. Binds to 30s ribosomal subunit. Prevents assembly of complete ribosome. Prevents initiation. |
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4 rings (tetra). Binds to the compete (70s) ribosome. Tetracyclines block elongation by preventing access to the incoming aminoacyl-tRNA [Blocks A site] |
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Minocycline, Doxorubicin, Doxycycline |
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Tetracycline: 4 rings (tetra). Binds to the compete (70s) ribosome. Tetracyclines block elongation by preventing access to the incoming aminocyl-tRNA [blocks A site]. These are some other family members. Theme: modification to an antibiotic may alter bacterial resistance to the drug or change absorption or clearance patterns. |
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Macrolide structure (big ring). Binds to the complete (70s) ribosome. Blocks elongation by preventing ribosome movement relative to mRNA. Blocks ribosome translocation. |
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Inhibits PROKARYOTIC peptidyl transferase activity (elongation). Not used widely in developed countries. May inhibit mitochondrial ribosomes. |
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Inhibits EUKARYOTIC peptidyl transferase activity (elongation)It is a simple (relatively cheap) organic molecule that inhibits peptidyl-transferase (elongation) in eukaryotes. Similar mechanism to chloramphenicol. Extremely toxic to eukaryotes. Widely used in laboratories. |
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It is a structural analog to a portion of aminoacyl-tRNA. It is toxic to both eukaryotes and prokaryotes - not clinically useful. It blocks elongation after it forms a peptide bond to the growing protein chain. The C-terminal puromycin causes the peptide to fall out of the ribosome P-site, and causes premature transcription termination. [Resembles a tRNA that has an amino acid attached to it but it's not really an amino acid and so it causes chain termination] |
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Novobiocin and Nidixic acid |
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Bacterial gyrase (topoisomerases) can be inhibited by the antibiotics such as the courmarins (including novobiocin) and the quinolones (including nalidixic acid and ciprofloxacin). |
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HMG-CoA reductase catalyzes the rate-limiting step of cholesterol synthesis. Lovastatin competitively inhibits HMG-CoA reductase |
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DFP (di-isopropyl fluorophosphate) |
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It is an irreversible inhibitor of acetylcholine esterase which normally cleaves the neurotransmitter acetylcholine. This inhibition is lethal. DFP binds covalently to the serine in the active site and blocks its catalytic action. This posion is the ancestor of organophosphorus nerve gase [Sarin] and also of pesticides. The active-site serine froms normally a covalent intermediate during catalysis. DFP blocks this reaction and acetylcholine accummulates |
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It is a drug that is used at low dose for reduction of blood clotting. It inhibits irreversibly COX in all cells. It acetylates a serine in the channel of the active site. Cyclooxygenase (COX) is an enzyme that uses arachidonic acid as substrate. COX forms different eicosanoids (prostaglandins, thromboxane and leukotrienes) dependtent on cell type. Platelets need COX for thromboxane (which stimulates blood clotting). Endothelial cells need COX for prostacyclin formation (which prevents blood clotting). Endothelial cells synthesize new COX. Platelets cannot synthesize new COX as they do not have a nucleus. The prostacylin/thromboxane ratio is shifted in favor of prostacyclin. Platelets forms less thromboxane than normal until new platelets are formed (about 10 days). This is why aspirin treatment has to stop before surgery at least for a week. |
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Systemic Lupus Erythematosis |
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Auto Immune disease. Cause by antibodies that react with the U1 SnRNP RNA component of the spiceosome. Prevent normal splicing of mRNAs. |
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Mutation in the B-globin gene thate generate additional splice sites within mRNA. --> abnormal B-globin. Abnormally long tetramers--> easy target for spleen. |
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Limb girldl muscular dystrophy |
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Alteration in gene that causes new splice site, within an exon--> a defective protein |
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Inactivates EF-2 (EF-G for prokaryotes) |
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Reduce/cleave disulfide bonds - |
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Disfuntional Ubiquitin protein that targets misfolded/old/defective proteins for degredation in proteosome. -Makes damaged proteins stable and accumilate in the brain
Same mechanism as Prions disease |
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Proteinaceous infectious agent-Single infectious protein resulting from Changing of a-helix to B-sheet in prion protein (PrP)found in brain tissue.--> Infected Prp^sc protein acts as template for large formation of abnormal Prp Sc |
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Effects of definciencies in glycolysis on Hb 02 affinity |
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Hexane kinase-->2,3, BGP--> Pyruvate kinase.
2,3 BGP stabilized taught state of Hb and deacreased affinity for O2.
X Hexokinase= decreased 2,3 BPG = increased affinity= left shift in curve X Pyruvate kinase= Increased 2,3 BPG = decreased affinity = right shift in curve |
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increased y(gamma)2 side chain. A2Y2=> increased affinity for 02 (can steal it from mom)
(Binds 2,3 BPG less tightly) |
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Extracellular enzyme, needs copper as a co-factor Deaminates lysine to Form allysine or hydroxyalliysine residues for cross linking.
Needed for cross linking of both elastin and collegen fibers |
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Result from Gene mutation for pro-a-chains
Defects can be found in Prolyl/ lysyl hydroxilase( Hydroxilation for lysine/proline)(Ca+2 cofactor)
Lysyle oxidase(Needed for cross linking between chains (copper cofactor)
Procollagen peptidases-cleaves collegen to insoluble form in ECM
Results in hypermotility of joints/ fragile/hyperstretching skin/ fragile blood vessels |
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Autosomal Dominate Brittle bone syndrum- Bones break easily especially in childhood, and blue schlera in man types
Type I-mildest Typle II-Most severe(death in utero) |
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X gene that codes for fibrillin(Used to scaffofold to make elastin from tropoelastin in ECM (Side note-lysines/prolines not mostly not hydroxilated in elastic. Needs lysyl oxidase for crosslinking therefor copper)
Marfans long limpbs/lens dislocation/risk of annuerism |
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Deficiency in cardiolipin-special phospholipid in inner mitochondrial membrane. mainly 18:2 6...Rare but severe cardiomyopathy |
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Fked up CFTR (cystic Fibrosis Transmembrane Regulator)(ABC :ATP binding cassette channel) From a single phenylalanine mutation. |
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RNA editing in liver. CYTIDINE DEAMINASE introduces early stop codon . So intestine has a shorter apolipoprotein.
Glutamate Receptor in brain.Adesine deaminase. Changes Ca+2 permiability of an ion channel. Required For Proper devolopment
Troponin=Alternative splicing; |
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Trypanosome (chagas disease) and leishmania |
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parasites that use extensive RNA edditing(adding Poly U's) to stay ahead of immune system |
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