UMass Amherst BIOLOGY 285 - Bio 285 SI Before Quiz 3 (2 pages)

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Bio 285 SI Before Quiz 3



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Bio 285 SI Before Quiz 3

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Pages:
2
School:
University of Massachusetts Amherst
Course:
Biology 285 - Cellular & Molecular Biology
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Bio 285 SI Notes before Quiz 3 Pre IC pre initiation complex o Set of proteins necessary for DNA polymerase to successfully bind to DNA to start its activity Quiz covers Brc Abl light coverage since already tested on it G1 restriction point S phase a little anything on cell cycle o Antibodies not on it fake news Abl is generally involved in cell signaling pathways has kinase activity that allows it to interact with cell division pathways and growth pathways lot of different signal transduction pathways o Basically works with those pathways and plays a role in allowing them to occur o Mutated into Bcr Abl bring two kinase domains into close contact which means that they are able to cross phosphorylate and therefore more easily able to get activated due to mutation This is what gives you overactivity in kinase part of Bcr Abl o Also have Bcr but not functioning normally o Bcr takes part in DNA damage pathways normally activates pathways that prevent cell cycle from occurring o Mutated Bcr Abl tumor suppressive activities don t occur properly Origin of replication is the point on the chromosome where pre replication complex is going to form Pre replication complex is a set of 4 different proteins that are all necessary for the pre initiation complex to form o Recruits downstream proteins later on into pre initiation complex and then from there are able to replicate DNA During G1 phase what is main aspects is you have to make the proteins that are going to drive replication so have to prep for S phase to occur before pass restriction point to go into S phase some of the proteins made are Mcms CDT1 CDC6 etc Bubble break area that starts to form protein complex origin of replication ORI have protein called ORC o Once ORC is present on DNA recruits two other proteins CDT1 and CDC6 o Makes up three main components that need to come together before fourth complex comes in helicase o Has to be bound in such a way that it is enclosed around DNA b c will separate DNA strands once DNA replication begins Mcm is part of pre replication complex part of helicase Pre RC is pre replication complex ORC CDC6 CDT1 Mcm which is helicase o Those 4 form a complex to form a pre RC complex Pre RC complex with S cyclin CDKs drive a formation of Pre initiation complex pre IC CDK regulated through cyclins CDKIs p21 which is turned on by p53 phosphorylation dephosphorylation CDK might not want to start moving to next step yet still not ready to divide and replicate so want to spend more time useful way to do this is keeping one phosphate keeping it on and one phosphate keeping it off o As long as phosphate keeping it off won t work o Can kick off that phosphate to move to next step CDK levels are always constant CDKs are never destroyed or created constant amount of CDKs cyclins are destroyed and created want to move forward make more cyclins already in next phase already done what needed those cyclins get destroyed Ubiquitin doesn t destroy it it takes it somewhere to kill it o Often takes to proteasome to have that kill it Rb is tumor suppressor protein that when activated it s dephosphorylated and it s attached to transcription factor E2F protein thus enacting E2F o Binding site is F2 o Once ready to go on with cell cycle and release E2F phosphate binds to Rb Rb changes its conformation in such a way that it releases E2F E2F no longer bound to Rb is not being sequestered so is now active E2F goes into nucleus creates proteins like CDC6 CDT1 etc V D J recombination is just saying that you can have multiple different combinations that go into antibody arms o Combinations mean the coding that go into the antibody s arms codes for different amino acids that go into antibody protein o Different possibilities on the variable part of the antibody Do these TAs know they suck Or do they think people leave every review after 10 mins Antibodies have constant region variable region Y shape of antibody o Antibodies have random sequences at the top change per antibody can somehow tell what your cells are and not attack them Herceptin interacts with an RTK basically blocks a receptor from working blocking receptor nothing can go through so nothing can happen Gleevec will bind to kinase domain of Abl competitively and place where binds is the ATP binding site where it s binding is blocking ATP and without ATP kinase domain not able to be activated o Non competitive inhibition because when binds to ATP binding site causes molecule to change conformation typical of non competitive binding leads to it not functioning properly o Makes it semi competitive both changes shape and blocks ATP Her2 receptors are not mutated o Overactivity not due to mutation due to having too many receptors Hypothetically have a chromosome with 10 origins of replication when are you in S phase After the first one has fired or the last one o After the first one has fired now in S phase b c if one has fired you are now replicating o S phase works by not all firing at once downstream sequential activity o As soon as DNA has started being made have started synthesis S phase


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