Exam 2 Biology 285 Cellular & Molecular Biology
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Biology 285 Cellular & Molecular Biology
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This 6 page Study Guide was uploaded by anova on Tuesday October 13, 2015. The Study Guide belongs to Biology 285 Cellular & Molecular Biology at University of Massachusetts taught by Dr.Laura Francis in Spring 2015. Since its upload, it has received 23 views. For similar materials see Cellular and Molecular Biology in Biochemistry at University of Massachusetts.
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Date Created: 10/13/15
mitosis gt mictrotubules disassemblereassemble into the mitotic spindle dynamic instability colchicine binds tightly to free tubulin and prevents polymerization taxol binds to microtubules prevents them from losing subunits both drugs arrest dividing cells in mitosis 3 actin lamentsactin twostranded helical polymers concentrated in cortex important in cell motility muscle cells dynamic instability motor proteins generate movements within cells energy comes from hydrolysis of ATP travel along actin lamentmicrotubule in one direction motor proteins on c to lasmic microtubules are in two families 0 o o proteins provide opposing forces that give stability walk on mts or be stationary and move mts Microtubules alpha tubulin minus end and beta tubulin plus end bound via noncovalent bonds heterodimer microtubule subunit grow out of centrosome with a pair of centrioles in the middle GDP bound tubulin microtubule is shrinking Ebl binds to microtubule when its growing plus end and falls off when it shrinks APC is a tumor suppressor gene 724 Cdc20 activates the anaphase promoting compleX APC initiates chromatid separation and entrance into anaphase Kinechore stays anchored to microtubule as its depolymerizing unsolved questions go over prelec assignmentsquizzesreview questions CDK phosphorylates lamins breakdown of nuclear envelope CDK phosphorylates codensin chromosomes condense Phosphorylate mapsmotor to assemble the mitotic spindle M spindle poles created by centrosomes from which microtubules grow and shrink interpolar mt hold shape kinetochore mts connect to chromosomes mts are part of cytoskeleton have polarity and organizing centers minus end connects to centrosomes plus is where growingshrinking occurs Cleavage of cohesion rings marks transition from metaphase to anaphase Metaphase Check point APCAnaphase promoting complex told by cdc 20 to tag securin for ubiquitilation to make separase active MADBUB sequester cdc20 until checkpoint is satis ed Cytoskeleton allows cells to adopt variety of shapes organize internal components interact mechanically with environment carry out coordinated movements bonesmuscles of cell segregates chromosomes of daughter cells pinches apart cells framework of cytoskeleton 3 types of proteins lintermediate laments strengthen cells and protect against mechanical stress in cytoplasm of most animal cells ropelike found in nucleus nuclear lamina cellcell junctions stable N terminal headCterminal tail rod is in shape of alpha helix forms dimer 2 coiled dimers form tetramer via noncovalent bonds tetramers bind sidebyside through noncovalent bonds ropelike structure Types of Intermediate laments Cytoplasm keratins vimentin and vimentin related laments neuro laments Nuclear nuclear lamins Nuclear lamins disassemble phosphorylated and reform dephos at each cell division controlled by phosphorylation and dephosphorylation by kinases 2 microtubules tubulin stiff longhollow cylinders made of tubulin with one end attached to microtubule organizing center MTOC or centrosome grow out of centrosome anchor membraneenclosed organelles guide intracellular transport G1 growth gap phase must receive growth factor signal ensures suf cient energymaterials ie atomsnucleotidesATP checks for DNA damage prereplicative complexes are created Origin recognition complex ORC binds to origin of replication and Cdc6 and recruits proteins helicase mcm27 to form prereplicative complexes need enough prereplicative complexes set up during G1 or else you lose parts of DNA GlCDKs phosphorylate component of prereplicative complexes required for replication Rb G1 to S transition E2F family of TFs transcribes proteins necessary for S phase E2F activation is point of no retum cells committed through going through the cell cycle E2F active Rb phosphorylated transcription of S phase genes S CDK is active preinitiation complex forms sld2 3 targeted by CDK and then bind dppll and other proteins DNA replication chromosomes are duplicated and held together by cohesin rings after transition prereplicative complexes don t reform degradation of Cdc6 after replication helicase is also transported out of the nucleus via NES S phase CDK phosphorylated Cdc6 degraded preventing prereplicative complexes from reforming negative role Centrosomes duplicate near nucleus contain centrioles from which spindle f1bers develop G2 get ready for chromosome segregation check for damage Mphase CDK becomes active through phosphorylationdephosphorylation MCDK has an activating and deactivating phosphate Cdc 25 PHOPSPHATASE removes the inhibitory phosphate M cyclinphosphorylation by Weel and Cak makes MCDK inactive Centrosomes duplicate LOF Wee 1 daughter cells too small not all repairs done to DNA DNA damage in G2 activates p53 transcribes p21 inhibits CDK no CDK activity no priming phosphorylation of substrate Onset of Mitosis How cell would inhibit apoptosis GOF atk LOF Bad never binds to bcl2 LOF bcl2 can t bind Bad Bad is always phosphorylated JakSTAT pathway regulates the immune cytokine system growth factor NOT receptor tyrosine kinase pathway J ak l and 2 bind to receptor prolactin P04 the receptors STAT 5 binds to phosphates phosphorylates creates a dimer activate STATS dimer translocates and regulates transcription ie milk proteins single step pathway Antibodies produced by B cells white blood types bind to antigens binding site is the hypervariable region found on both 2 light and 2 heavy chains each chain has two domains antigen s contact surface binds to the antibody s variable region high af nity low Kd VDJ recombination linked to CML name by which antibody gene is made immature B cell matures and undergoes this recombination expresses Ragl2 Rag12 cut and rearrange DNA occurs before transcription by this random processes we get different variable regions VDJ happens in places it isn t supposed to in immature B cells DNA polymerases randomly places nucleotides in between VDJ sequences random sequences cause HVR to be too speci cframeshift Twohit hypothesis by Knudson states need more than one mutation for cancer to occur needs LOF tumor suppressors GOF of protooncogenes Protooncogenes are gas pedals of cell drive it into cell cycle Tumor suppressor genes are brakes stop cell from undergoing cell cycle Cell cycle CDKs control cell cycle binding partners are cyclins determine substrates for CDKs phosphorylate CDKs release E2F transcription of S phase genes Checkpoints are caused by molecular brakes CDK inhibitors ie P21 p53 transcription factor responding to DNA damage activates the transcription of p21 gene Herceptin prevents dimerization of receptor and so stops downstream activity marks cell for destruction Signal may be received by the same receptor but the cell type determines the outcome Serinethreonine kinases phosphorylate OHs of these amino acids Tyrosine kinases Eukaryotic kinases phosphorylate serines threonines and tyrosines only Growth Factor Signal 1 RTK receptor tyrosine kinases common growth factor pathway sits in membrane 1 receptor cell dimerizes after signal molecules come 2 kinase domains are activated 3 tyrosine is P04 autophosphorylation 4 activated intracellular signaling proteins bind to phosphorylated tyrosines 2 activates GTPase activity RAS signaling RTK activated bound to GRB2 adaptor proteinGEFSOS Ras activating protein RAS needs to be bound to GTP to be active Ras activator acts by binding RasGTPases and forcing them to release their bound nucleotide usually GDP Once released from SOS the RasGTPase quickly binds fresh guanine nucleotide from the cytosol Since GTP is rou hly ten times more abundant than GDP in the cytosol this usually results in d 3 RTK Ras VIapK pathway 1 activated RAS 2 MAP KKK KK K phosphorylation cascade 3 Change either gene expression or protein activity Survival Signal PIK3 pathway PI3Ks phosphorylate 3 positions OH in the inositol ring of ptdlns PTEN tumor suppressor gene a phosphatase targets inositol phospholipid PIK3 CA oncogene l RTK is activated 2 Pi3 kinase is bound via its SH2 domain adds a third P04 to inositol 3 Inositol phospholipid is phosphorylated binding site for kinase 1 4 Akt is activated by 2 protein kinases Protein Kinase B PKB is a serinethreoninespecific protein kinase 5 g Bad bound to Bcl2 aioitosis Pathways 9 cell should always be receiving signals to stay alive Gleevec Imatinib treats chronic myelogenous leukemia blocks ATP binding kinases semi competitively inhibits Bcrabl binds in its binding site so substrate cannot bind and also causes bcrabl to change shape and stay inactive chronic myelogenous leukemia caused by translocation event creating bcrabl one translocation event affects many partspathways Janet rowley first to discover this connection Chromosome 229 come together and function as a new gene Wildtype abl isn t an RTK involved in survival si naladhesionmotility of proteins Bcr chromosome 9 gives abl new functions prevents abl from going into nucleus only works in cytoplasm 0 Why Be Nuclear localization sequence could be folded inside inaccessible to importin 0 Or NLS is incorrectly folded Abl chromosome 22 structure SH2 domains of protein 1 bind to phosphotyrosine on protein 2 SH3 domain binds to prolineXXproline sequence on protein 2 Regulated through localization nuclear importexport signals both nuclear and cytoplasmic Cleavage of SH3 domain leads to Abl acting as an oncogene kinases are overactive Berabl structurefunction fusion disrupts regulation increases signaling Bcr added to N terminus of Abl creates binding sites of other proteins loss of CAP domain this loss keeps protein in cytosol increases kinase activi 1 no lon er folds in a wa that inactivates its kinase domain 2 more binding sites for cell proliferation signaling pathways like rasmapk SH2 and SH3 domains on Abl no longer selfregulate but are still involved in downstream signaling they are binding sites for downstream proteins Herceptin it is an antibody treats HER2 positive metastatic breast cancer HER 2 is signaling receptor growth factor receptor found on breast cancer cells HER 2 signals through P13 K and RasMapK pathways Herceptin is a monoclonal antibody binding to Her2 dimerizes and signals tumor cells to proliferate
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