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TAMU BICH 410 - Transmembranes and the Flu
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F BICH 410 Lecture 26Outline of Last Lecture - Transport MembranesOutline of Current Lecture - Simple diffusion v. passive transport- Glut transport- facilitated diffusion- carrier proteino Must accumulate glucose in epithelial cells using 2Na and glucose (Na goes down its conc gradient and drags the glucose along against its conc gradient)o Then Na-K pump causes Na to be pushed back out- Active transporto Ca-ATPase- UNIPORT calcium is used as messenger triggering response Ca conc is low in cell (4x lower) Kept low to prevent phosphate complexation that will precipitate Sarcoplasmic reticulum is where Ca stored Ca binds and triggers phosphorylation and conformation change; phosphorylated form has low affinity for Ca and it is released. Phosphate is then hydrolyzed. Dephosphorylated form changes conformation and has high affinity for Ca.o H+-K+ATPase Hydration of CO2 + water + carbonic anhydrase  bicarbonate and protons Protons then pumped out and K+ comes in- charge remains the same Cl comes from KCl Excess protons= peptic ulcers Histamine (derivative of histidine) activates this pump causing production of HCl Proton pump inhibitors competes with histamine However, most ulcers actually caused by H.ploryi (bacteria)o ABC transporters- bind ATP an undergo hydrolysis but not a conformation change Generally used for pumping hydrophilic molecules Have been used for the transport of chemotherapy drugs out of cell, found to play a role in drug resistance Have TMD that varies in shape and seq and allows the transporter to be specified NBD- gates and opens to let things flow in- very similar across all transporters Understand drug mechanism can then develop drug treamentsThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute. Cystic fibrosis transmembrane conductance regulator pumps out Cl, Na, and water- defect causes thick mucus- Important to function of sweat glands - Fluo Pandemics- Russian Flu 1889 H2N2; Spanish Flu 1918 H1H1; Asian Flu 1957 H2N2; Hong Kong Flu H3N2; H1N1 2009o RNA viruses  Influenza A- originates in aquatic birds- low and high pathogenic (how easy is it to get sick from)- mutates fastest and is most virulent (how sick you are)- Hemagglutinin- carbohydrate bound- 17 types- on cell surface- Neuraminidase- sialidase- 10 subtypes- on cell surface- Genome is divided into 8 gene segments B- primary host is humans- Cant be broken ino subtypes C- swine and humans- mutates slowest- Has no vaccines Typically trivalent vaccine- 2A and 1Bo Nomenclature Virus type (A,B, OR C); geographic origin; strain origin; year isolated; virus subtype (H3N2)o Human, Swine, avian-typically Type A Can be same subtype but adapted to specific host Recently H3N8 went from horse to dogs Can reassert and get mixture of strands Antigenic drift- random mutations in antigens- Allows virus to escape immune- Hemaglutinin mutations are cell surface proteins responsible for entrance of virus- Antigenic shift- mixture with 2 or more strains- o avian flu A transmitted either 1. Direct contact 2. Intermediate hosto avain viruses bind to N-acetylneuraminic acid alpha-2,3 galactose and human viruses prefer alpha 2,6o pigs have both receptors- so is intermediate host in order for species jump- needs adaptation and direct contact with animals then moves to human to human- 1918- antigenic drift- avian flu to human flu- Hong kong- antigenic shift from reassortment of avian and human flu o Viral infection- binds, uncoating in endosome, breaks open to let out info into nucleas where it can be replicated/transcribed, then translated, protein processing and reassembly, then budding Prevent virus from taken up prevents infection RNA Polymerase used- higher error rate 10^5 causing antigenic


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TAMU BICH 410 - Transmembranes and the Flu

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