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61 Cards in this Set
- Front
- Back
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Sugar and Phosphate |
RNA and DNA's backbone |
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Purines |
Adenine and Guanine |
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Pyrimidines |
Cytosine and Thymine Uracil (RNA) |
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Nucleoside |
Nucleotide without a phosphate Named after the base they contain |
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B-glycosidic linkage |
Linkage between base and sugar |
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Primary Structure of Nucleic Acids |
Sequence of the nucleoside monophosphate |
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Secondary Structure of nucleic Acids |
Shape a nucleic acid assumes as a result of the primary structure. B-BNA, A-DNA, Z-DNA |
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B-DNA |
Predominates in the aqueous environment |
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Tertiary structure of the nucleic acids |
how the DNA is organized into chromosomes - specific three dimensional shape into which an entire chain is folded |
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Phosphate group link together the sugar backbone via |
phosphodiester bond |
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Hydrogen Bond |
3 - G-C 2 - A - T |
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Z-DNA |
Assumed to be more transient conformation - where DNA is actively transcribed |
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Chromatin: |
DNA + basic proteins Eukaryotes -Organizes DNA into chromosomes |
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Prokaryote Tertiary DNA structure |
Chromsome, plasmids and naked DNA |
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Nucleosome: |
Units of histones and DNA |
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Eukaryotic chromosome |
Single linear molecule of DNA |
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Histones |
DNA binding proteins (basic proteins with a lot of positive charge) |
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Linker DNA |
region between the nucleosomes that is not tightly packed. Variable length |
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Denaturation |
Loss of secondary or tertiary structure over a large region of polypeptide |
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Forces favoring denaturation |
Electrostatic repulsion of the negative charges on the phosphate group 2. Higher entropy of the denatured state |
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Forces stabilizing the secondary structure |
Hydrogen bonds btw A-T and C-G Van der waals interaction between the bases stacked up on each other |
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The higher the GC content your double helix has |
the higher the temperature needed to break the double helix |
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Weak of absorbance at 260 nm |
lower for double stranded DNA vs single stranded |
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Histone Remodeling |
Reversible acetylation and phosphorylation (reduce number of positive charges so DNA is less tightly bound) Methylation: causes DNA to be more tightly bound |
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Processivity |
Refers to the enzyme to catalyze many consecutive reactions without releasing its substrate |
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Ligase |
joints the ozaki fragments |
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RNA hybridase (rna H) |
removes the primers |
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Polymerase I |
fills the gaps between the ozaki fragments |
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RNA polymerase |
puts in the primers infront of leading stand and one infront of each ozaki fragment |
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G1 - |
Most cells are in this state - they express proteins, they transcribe |
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S phase |
DNA is replicated. Once they are in the S phase, they have to go through the rest of the cycle to survive |
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G2 |
allows cells to express a new set of proteins which allows them to enter M phase into mitotic phase |
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Synasin cells |
Cells that dont ever divide again - they are in G0 phase |
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Cdk |
Kinase when activated can phosphyrlate downstream proteins that then mediate the function of the cell cycle Also regulated by phosphorylation and phosphorylation -Can also be regulated whether or cyclin is bound or not -whether or not cyclin inhibitor is present |
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Rb Protein (negative regulator) |
Retinoblastma protein - it releases the transcription factors E2F when phosphorylated by the cyclin D1/Cdk4 --when active you dont go through cell division Active form when dephosphorylated |
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E2F |
key transcription factor that induces the expression for proteins necessary for proteins necessary for progression of G1 phase into S phase phase. Ex DNA polymerase |
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CDK activation |
Before the Cdk is active, it is phosphorylated but on the sides that inactivate the kinase activity of the CdK. Cdc 25 (phosphatases) remove the phosphates from the sides of kinase activity. CAK (kinase) which phosphyrlate the enzymatic site of the Cdk |
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APC |
ubiquitin ligase - they attach ubiquitin groups to target proteins for degradation |
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p27
(CK1) - Cdk Inhibitor |
binds to the Cdk and cyclin complex distorting the active site of the Cdk. Insets in the ATP binding site as well --> furhter inhibition
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p53
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If active, it signals that you have severe DNA damage --> which leads to activation of kinase which can phosphorylate the P53 which inhibits its binding to MdM2 --> so it becomes stable and doesnt get degraded
- p53 goes in the nucleus and becomes the trancription regulator of p21 gene |
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p21 |
inhibitor protein of the cyclin Cdk complex- directly linked to the p53 mediated processes |
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Ways to trigger cell division |
Mitogen which binds to mitogen receptors -->expression of myc in the nucleus |
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Myc |
Transcription Factors --> goes in the nucleus and binds to the genes that it wants to regulate. Multiple ways of how it triggers DNA synthesis 1. Binds to the gene that encodes E2F --> which makes the cyclins and polymerases 2. Increased p27 degradation --> which binds to the Cdk-cyclin complex--> blocks phosphorylation of Rb ---> which cannot release E2F --> DNA synthesis 3. Cyclin D gene -- increased Cylin D--> G1-Cdk activatio -->Rb Phosphyrlation |
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Myostatin |
TGF-b -- inhibits the proliferation of myoblasts that fuse to form skeletal muscle fibers |
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P53 binds to Mdm2 which promotes promotes its degradation. However when DNA is damaged, protein kinases are activated --> p53 gets phosphorylated --> it doesnt bind to MdM2 --> levels increase and it becomes stable --> stimulates the trancription of gene that encodes for CD1 p21--> binds to the regulatory site of p21 --> which inhibits the Cdk/cyclin complex --> arresting the cell in G1 |
Mitogen-->RAS--> MAP kinase cascade -->myc gene-->p27 degradation + increased cyclin D--> Cdk/cyclin activated -->phosphorylate Rb and cause conformational change-->inhibit Rb binding to E2F-->which leads to activation of polymerase -->can move from G1 to S phase |
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DNA damaged by |
1. Environment -- ionizing radiation (10-50K per cell per day) 2. Personal habits 3. Intrinsic Metabolites - free oxygen species that happen as a by-product |
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Tautomerization |
Regular bases that should be in the amino or keto form change into tautomeric form - which now match other bases and can lead to point mutation |
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Point mutation |
Substitution of one base pair for another 1. Transitions 2. Transversions |
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Deamination |
C==> U A==>hypoxyanthine G=> Xanthine |
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Depurination |
Occurs at the glycosl bond of the deoxy and the sugars -DNA backbone stays intact but the base and thus the encoded info is lost -Abasic sides effect DNA replication |
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Oxiation |
Increases with age Deamination of C to U - Caused by reactive oxygen species that are by-products of oxidative metabolism -can lead to formation of O6-methyl-guanosine |
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UV |
covalently links adjacent pyrimidines along one strand of DNA |
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Ionizing Radiation |
1. Oxidative species 2. Complete breakdown of chromosome |
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5-Bromouracil |
Analog of thymine that has higher tendency to form an enol tautomer than does thymine itself. Pairs with guanine will lead from T-A to C-G |
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Acridines |
Wedge into DNA - and cause frameshift |
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Aflatoxin |
Toxin accumulated by molds |
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Base-excision repair |
DNA glycosilase removes a single base from the DNA backbone creating an abasic site.. AP nuclease cleaves the phosphodiester bond at the 5' site. Then AP lyase cuts the 3' site leading to the removal of sugar. Ex: AlkylA |
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Xoderma pigmentosum |
mutations in the nucleotide excision repair |
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Aimes Test |
if they can grow by reverting His - to His + |
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Nucleotide Excision Repair |
Bulg because of inability to bind -->recognition by excinuclease by uvABC --> DNA polymerase--> ligase |
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Uracil repair |
Uracil DNA glycosylase removes U from DNA and replaced by cytosine |
