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BZ 310- Final

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Question
Answer
Anterograde secretory pathway   secretion or to the vacuole  
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Retrograde secretory pathway   endocytosis  
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Smooth ER functions (3)   detoxification (cytochrome P450), steroid hormone synthesis, Ca2+ storage  
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Rough ER functions (4)   secretory protein synthesis/uptake, N-linked glycosylation, secretory protein folding, phospholipid synthesis  
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What does cytochrome P450 do?   oxidizes harmful hydrophobic molecules  
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Cystic fibrosis   malfunctioning ER functions  
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Nascent polypeptide   Asn-X-Ser/Thr; core oligosaccharide attached to this, then 3 glucose later removed  
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O-liked glycosylation   rare; usually n-linked  
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Enzymes that remove glucose from core oligosaccharide   glucosidase (I and II)  
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ER quality control   final glucose only removed when protein is folded correctly  
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Functions of glycosylation (6)   enzyme folding, quality control, sorting, enzyme functionality, recognition at cell surface, protection at cell surface  
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Functions of Golgi (4)   protein sorting, modification of N-linked sugar groups, O-linked glycosylation, formation of some cell wall components  
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How were the secretory mutants found in yeast?   mutants sunk after centrifugation  
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Class I mutants   defect in ER translocation  
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Class II mutants   defect in vesicle budding from ER  
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Class III   defect in fusion with Golgi  
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Class IV   defect in budding from Golgi  
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Class V   defect in fusion with plasma membrane  
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Two major processes in secretory pathway   coat protein mediated budding & SNARE receptor mediated vesicle docking and fusion  
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Clathrin   involved in receptor mediated endocytosis and transport to endosomes/lysosomes  
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COP II and COP I   golgi==>ER  
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Rab   a small GTPase needed to prime a vesicle  
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Transport to lysosome/plasma membrane depends on what?   mannose 6-P  
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Polarized cells (4)   epithelia, neurons, fibroblasts, T-cells  
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Two types of exocytosis   constitutive and regulated  
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V-snares/T-snares   mediate secretion by promoting vesicle docking and fusion  
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Female meiosis   only keep 1 cell in meiosis 1, only keep 1 at meiosis II (right before fertilization)  
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G1   1 chromosome = 1 chromatid = 1 DNA  
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G2   1 chromosome= 2 chromatids= 2 DNAs  
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Interphase   GI, S, G2  
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14.11    
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SERIOUSLY 14.11 all of the chromosome shit    
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Astral spindle MTs   connect to periphery  
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Polar spindle MTs   space spindle poles relative to each other  
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Kinetochore spindle MTs   catch chromosome, connect to kinetochore  
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Metaphase   chromosomes in center of cell  
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Anaphase   chromatids separate  
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Telophase   chromosomes de-condense, nucleus reforms  
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Most important control point in cell division   START (between G1 and S)  
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What is checked at START? (3)   cell size, DNA intactness, nutrient availability  
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G0   cells enter this when don’t need to divide; must enter G1 to divide again  
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CdK   cyclin dependent kinase; each checkpoint has its own  
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Cyclin   proteins that vary in concentration over the cell cycle  
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Example of cyclin and cdk pair   MPF (mitosis promoting factor); conserved  
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2 main regulatory mechanisms of cell cycle   phosphorylation (reversible), degradation of cyclins (irreversible)  
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p53   checks for DNA damage at start and G2-M transitions; transcription factor for cyclin inhibiting protein (=cell cycle arrest)  
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which 2 cell wall components are secreted and more soluble?   pectin and hemicellulose  
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which 2 cell wall components are synthesized in place?   cellulose and lignin *make up most biomass on earth  
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___ connect the cytoplasm of plant cells   plasmodesmata  
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proteins in connective tissue are secreted by   fibroblasts  
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proteoglycans function   cushioning  
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collagen   vitamin c dependent, stretching resistance  
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4 types of cell-cell connections   adherens, gap, tight, desmosome  
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gap junctions   2x6 connexins= connexon (allow signaling like cAMP thru)  
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receptor connection to actin   contraction, crawling  
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receptor connection to IFs   stretching resistance  
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4 main cell surface receptor types   cadherin, CAM, integrin, selectin  
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adherins junctions   connect cells to cells, Ca2+ dependent  
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two cell connections not associated with cytoskeleton   CAMs and selectins  
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CAMs   Ig like, tissue specific (cell adhesion molecule)  
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Selectins   recruitment of WBCs to infection site (example)  
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3 cell connections associated w/ cytoskeleton   integrins, hemidesmosomes, focal contacts  
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integrins   connected to actin, important in cancer biology/infection  
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hemidesmosomes   connected to IFs, keratin  
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4 signal sending ways   autocrine, paracrine, endocrine, direct contact w/ cell receptors  
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3 main cell receptor types in membrane   ligand gated, GPCR, tyrosine kinase  
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3 major mechanisms of signal transduction   phosphorylation/de, second messengers, GTP switches  
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3 types of second messengers   cAMP, phosphatidyl inositol derived, Ca2+  
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cAMP signaling   hunger/stress signals  
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PI 2nd messengers   IP3 (Ca2+ from ER), DAG (activates PKC), PIP3 (activates PKB)  
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Ca2+ 2nd messenger   activates calmodulin, troponin, etc.  
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All second messengers   readily available source, removed quickly  
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Well known for short term responses   GPCR  
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Well known for long term responses   tyrosine kinase  
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PLC ->   IP3 + DAG  
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Adenylyl cyclase ->   cAMP  
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Gluconeogenesis cAMP example   CREBP binds to CRE (cyclic amp response element)  
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Two different types of g proteins   Gs (stimulate), Gi (inhibit)  
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Cholera toxin   modifies Gs to cannot hydrolyze GTP, efflux of ions= diarrhea  
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Multiple second messengers example   inositol metabolites can raise intracellular Ca2+ and activate PKC (smooth muscle contraction)  
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4 major off-switching mechanisms   GTP hydrolysis, cAMP broken down by phosphodiesterase, Ca2+ pumped, phosphatases  
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Ras   small GTP binding protein that functions as an on and off switch (MAPKKK)  
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EGF signaling   RTK activity, c-fos/c-jun= TFs and proto-oncogenes  
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How cells know which cell to be   transient activation of enhancer, protein expressed, positive feedback loop  
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Principle of apoptosis   conserved; regulated activation of proteases called capases (zymogen)  
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Cancers from mesodermal origin   leukemia, lymphoma, CNS, retinoblastoma, sarcomas  
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Characteristics of cancer cells (8)   grow in clumps, altered growth factor response, invasion of other tissues, altered karyotypes, immortal, altered cytoskeleton, altered receptors, less adhesive/more motile  
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8 types of proteins that control cell growth   growth factors, growth factor receptors, signaling cascade, cyclin dependent kinases/cyclins, protein kinases, chromatin proteins, transcription factors, proteins in apoptosis  
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tumor suppressors   need to both be mutated (recessive); p53  
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oncogenes   dominant, Ras  
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retrovirus and cancer   can pick up a proto-oncogene and make it an oncogene  
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DNA virus and cancer   interferes with normal replication controls  
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3 immune layers of defense   mechanical/chemical, innate, acquired  
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innate responses (4)   inflammation, phagocytosis, NK cells, complement  
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humoral immunity   B cells -> antibodies, maturation in bone marrow, bursa in birds  
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cellular immunity   cytotoxic T-cells, helper T-cells; maturation in thymus  
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IgG   main blood antibody; complement activation  
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IgM   B-cell antigen receptor or in blood; activates complement (before IgG)  
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IgA   in secretions, dimer  
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IgD   B-cell activation  
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IgE   parasites, allergies  
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3 mechanisms of antibody diversity   combine light + heavy chain, imprecise joining, hypermutation  
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CD8    
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CD4    
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MHC I   all cells (pairs w/ CD8)  
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MHC II   professional antigen presenting cells (pairs w/ CD4)  
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MHC I peptide binding domain same structure as   HSP 70 (form fits function)  
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Tc kill what?   all cells that present a foreign protein  
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Coordination of immune response by Th cells   get out of G0 upon activation, stimulate B cells that display antigen on MHC II, then they get out of G0 (positive feedback)  
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Negative selection   cells with strong recognition of self MHC (or cells with very weak recognition of MHC) -> cells killed (auto-immune)  
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