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Lecture 11

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BIOL 1000
Michael Gadsden

Lecture 11 TUTORIAL  KDL Receptors – How does the process work? o Golgi to ER, it is retrograde (backwards)  Understand the idea that there are signals on proteins (AA’s that have a function)  For glycoproteins, certain signals that tell it to go to the lysosyme  SRP binds complex to SRP receptor  Structural sequences that tell other proteins what they’re going to do with them o NH ----- KDEL (signal) COO COP I 3  So based on charge and shape, they will bind to proteins on Golgi so they fit in like an active site  The COP I proteins cause dimpling until bubbling causes popping off  pH differences cause the structural changes and then it changes binding ability  Micelles vs. Liposomes o Micelle – WILL BE ON EXAM  Carries NON-POLAR molecules in the blood B100  Sphere of fatty acids with non-polar interior CHOL o Apoplipoproteins – LDL (fatty acids)  Protein B100 binds to LDL receptors on plasma membrane  It makes sure that it doesn’t go to the wrong cells  If a mutation occurs and it does go to the wrong cells, like heart, DEATH!  Tubulin – provides directionality o Dyenine – goes out to in o Kinesin goes in to out  Clatherin o Membrane of a cell with LDL Receptors  CLUMPED  Sulfa Drugs safer than trimefaprim *EXAM* o This is because sulfa are specific for bacterial enzyme (folic acid)  PABA enzyme is bacterial specific and is even better to kill o Trimefaprim attacks dyhydrafolic reductase is less specific for bacteria, our enzymes will bind to it fairly well and kill us  GFP – Expression of gene *EXAM*  Muscle movement *EXAM* o ATP hydrolysis causes myosin to detach the actin? FALSE  Causes BINDING via ATP Hydrolase  Telomeres – end of linear DNA strand *EXAM*  DNA to be pure has to have : o 260:280 of 1.8:1 AU (1 AU = 50µg/mL) o dA (deoxyadenosine) and dG(deoxyguanine) attach to DPA and thus the absorbance is measure  then doubled because it is Pyrimidines plus Purines because mass not counted by light  Calvin Cycle o Rubisco o Of 5 molecules, only one goes to make NADH and stuff  Difference btw Glycolipids (gangliosides) and Phospholipids o Phospholipids has phosphate and triglyceride (P + fat) o Glycolipids have sugar and triglyceride  Aneuploidy vs. Polyploidy o Aneuploidy is having one or two too many chromosomes o Polyploidy is having multiple sets  Na, K, ATPase pump o Pumps sodium out, K in. o Outside more positive o Depolarization causes Na to rush in and the Na pump resets it o It is an action potential and nerve signal via chain reaction  Calcium channel o Similar reactions – but active transport (on Ca goes through)  Translation o E – Empty  tRNA released o P – Protein  tRNA and protein o A – Active  tRNA moves and its called translocation  Codon is there and anticodon matches o The ribosome moves and shifts the mRNA through  Initiation Factors o Used to start translation etc.  Elongation Factors o Necessary for the translation process to occur at the ribosome  Coenzyme vs. cofactor o Coenzyme – organic o Cofactor – inorganic  Kinesin and Dyenine o Move along microtubules (like in Euk flagella) o Just like how actin does that  K Ms a representation of binding efficiency o Fast worker is LOW M o Slow worker is HIGH K M Aneuploids  Having/lacking a chromosome (single, not SET)  Abnormalities often cause extra protein creation and thus cell death  Cancer cells – often aneuploid! o Developed mechanism to handle the excess protein o “Upregulate” meaning turn genes on to create more product for certain genes  Thus changing genetic expression o Make cell signals (small molecules that are secreted [outside cell] and bind to receptors on neighbouring cells cytokines  These are specific cytokines to cancer cells to induce the transformation of the target cell to become cancerous through signal transduction  Signal transduction – cascade effect  Second messenger is cAMP (cyclic AMP)  Hormone? o Travel long distances from tissues to other tissues o Peptides or steroids (cholesterol)  Cancer cells keep dividing and are “immortal” o Often used for research o Don’t recognise normal cell to cell signals that affect growth  DO NOT ENTER G 0 o Seem to have a lot more proteosome and ubiquitin reliance  Ubiquitin is a small peptide that binds to proteins that will be degraded to proteosome (showing things are garbage)  Rely on proteosome pathways and ubiquitin activity  Because these degrade macromolecules (protein overload)  Trying to find these differences is the hard part  Intermediate filaments o These are cell specific, help determine origin Steps in Mitosis  Centrioles are duplicated (2 is called centrosome)  Microtubules extend from centrosome [same like basal body] and go to kinetochore on mitotic chromosomes (X structure)  Kinetochore is the complex of proteins attached to the centromere (DNA sequence where sister chromatids attach [mid of X])  Proteins that make kinetochore bind to centromere and the microtubules organize o Without kinetochore, binding cannot happen  Spindle is the microtubules extending from pole to pole  Centriole pair is just like basal body  MTOC – stru
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