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51 Cards in this Set
- Front
- Back
Hormone Receptors (or Steroid Receptors)
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-Hormone Binding
-DNA Binding -Transcription Activation |
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Tamoxifen and Mifepristone
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Drugs that control stereoid signaling
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Stages of the Cell Cycle
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1) G1 Phase: RNA and protein synthesis. No DNA synthesis.
2) S Phase: DNA, RNA, and protein synthesis. 3) G2 phase: No DNA synthesis. RNA and protein synthesis continue. 4) M Phase: Mitosis and Cytokinesis G0 Phase: when differentiated cells withdraw from the cell cycle |
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Mechanisms for regulating CDK activities:
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1)Phosphorylation and desphosphorylation of the CDK
2) Control degradation of cyclins 3) Regulated synthesis of CDKs and cyclins 4) Specific CDK-inhibiting proteins |
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Specific CDK-inhibiting protein
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p21
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DBRP
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Destruction Box Recognizing Protein
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Regulation of CDK by phosphorylation and desphosphorylation
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1) CDK is inactive
2) Cyclin synthesis 3) Formation of inactive CDK-cyclin 4) CDK-cyclin is activated by phosphorylation 5) DBRP (Destruction Box Recognizing Protein) triggers addition of ubiquitin to cyclin 6) Cyclin is degraded by proteosome, and CDK is inactivated |
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Important Target Proteins of CDKs:
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-Laminin
-Myosin -Retinoblastoma protein (pRb) |
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p53
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When DNA damage is detected, p53 is activated and stimulates the synthesis of p21. p21 inhibits E-CDK2 and causes pRb-E2F complex to arrest the cell cycle in G1
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Genes encode regulatory proteins that normally inhibit cell division. Mutations in these genes are genetically recessive
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Tumor Suppressor
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Oncogenes
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v-src
v-erbB v-ras v-fas and v-jun |
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v-erbB
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-Gene that encodes epidermal growth factor (EGF) receptor that lacks the EGF-binding domain, but it retains its transmembrane and tyrosine domain
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v-ras
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-Encode v-Ras protein, which is similar to c-Ras protein but v-ras hydrolyzes GTP much more slowly.
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Tumor Suppressors
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pRb and p53
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Apoptosis
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Programmed cell death
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Events of Apoptosis
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-Fas ligand binds its receptor; TNF binds to its receptor
-These activated receptors interact with FADD, and TRADD -FADD and TRADD activate caspases -Caspases eventually triggers cell death |
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Receptor Types
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1) Ion-channel
2) Serpentine receptor (or G Protein Coupled Receptor, GPCR) 3) Receptor enzyme 4) Receptor without intrinsic enzymatic activity 5) Steroid receptor 6) Adhesion receptor |
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Ex. of Ion Channel
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Acetylcholine receptor
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Ex. of Receptor Tyrosine Kinase
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Growth hormone receptor, and insulin receptor
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Ex. Receptors without enzymatic activity
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JAK-STAT
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Ex. of steroid type receptor
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-Hydrophobic hormones, vitamin D, thyroid hormones
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What is the target of NO?
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GC (guanylate cyclase)
GC catalyzes the rxn from GTP to cGMP. cGMP PDE catalyzes the reverse rxn. Viagra inhibits cGMP PDE causing a increase of cGMP, which causes vasodilatation viagra + organic nitrate is not good... because the blood pressure drops dramatically |
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Types of DNA:
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A---ex.RNA-DNA, or RNA-RNA
B---ex. hydrated DNA Z |
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Helical Sense
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A and B are right handed
Z is left handed |
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Major Groove
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A DNA: narrow and deep (ND)
B DNA: wide and deep (WD) Z DNA: flat (FF) |
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Minor Groove
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A DNA: wide and shallow (WS)
B DNA: narrow and deep (ND) Z DNA: narrow and deep (ND) |
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Code
DNAType+major groove+minor groove |
ANDWS
BWDND ZFFND |
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Sugar Pucker
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A DNA: C3'-endo
B DNA:C2'-endo Z DNA: C2'-endo pyri... and C3'-endo purine |
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Glycosidic Bond Formation:
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A DNA: anti
B DNA: anti Z-DNA: anti for pyrimidine, and syn for purine |
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Superhelix Topology
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L = T + W
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L
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Linking Number
# that one strand of the duplex passes the other |
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T
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Twist
# of revolutions that one strand makes around the duplex axis |
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W
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Writhing number
# of supercoils present -right handed supercoil is negative left handed is positive |
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Topoisomerases
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Control of topological state (linking number) of DNA
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Classification of Topoisomerases
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-Type I: single strand cleavage
(L=+/- 1) -Type II: double strand cleavage (L = +/- 2) |
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Type I Topoisomerase
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Type IA: strand passage mechanism with 3'-phosphotyrosine enzyme-DNA intermediate
Type IB: controlled rotation mechanism with 3'-phosphotyrosine enzyme-DNA intermediate Type IB: |
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For what inhibitors of topoisomerases?
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Inhibitors of topoisomerases as antibiotics and anticancer agents
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Non-Watson Crick base pairs:
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A-A pair
A-T Hoogsteen pair Hypothetical T-C pair G-U Wooble pair in RNA structures |
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How are nucleic acids stabilized?
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Nucleic acids are stabilized by base stacking and hydrophobic interactions
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Enzymes required for DNA replication:
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-DNA gyrase: topoisomerase
-Helicase: for unzipping -SSB proteins for stabilization of single strands of DNA -Primase for making primers -DNA Polymerase III for adding nucleotides -DNA Polymerase I: for removal of primers and replace them with DNA nucleotides -Ligase: seals nick |
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Why do DNA Polymerase I can remove primers?
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Because DNA Polymerase I has 5'-->3' activity
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Requirements for High Fidelity of DNA replication:
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-Equal ratio of dNTPs
-Base pairing (A-T, and G-C) -Proofreading (3'-->5') -RNA primers -Mismatch repair |
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E. coli DNA Polymerase I
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-Polymerase activity, 3'-->5' activity (proofreading), 5'-->3' activity
-Recognizes the shape of the base pair -Repair of damaged DNA -Nick translation -Removal of RNA primer |
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E. coli DNA Polymerase III
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-DNA replicase
-Many subunits: sliding clamp (beta clamp) |
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E. coli DNA Polymerase II
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Repairing DNA via SOS response
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Reverse Transcription:
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(cap) eukaryotic mRNA (polyA tail) ---> RNA-DNA hybrid --> single stranded DNA --> double stranded DNA
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Telomers
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Telomers consists of 1000 or more tandem repeats of a short guanine sequence
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Telomerases
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Telomerases synthesize and maintain telomeric DNA. They are ribonucleotides.
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DNA damage:
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-Dimerization by UV radiation
-Methylation -Deamination -Intercalation |
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Nitrogen mustard and ethylnitrosourea
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They are alkylating agents
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Ethidium, Proflavin, and Acridine Orange
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They are intercalating agents that can cause insertion or deletion mutations
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