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51 Cards in this Set

  • Front
  • Back
Hormone Receptors (or Steroid Receptors)
-Hormone Binding
-DNA Binding
-Transcription Activation
Tamoxifen and Mifepristone
Drugs that control stereoid signaling
Stages of the Cell Cycle
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
Mechanisms for regulating CDK activities:
1)Phosphorylation and desphosphorylation of the CDK
2) Control degradation of cyclins
3) Regulated synthesis of CDKs and cyclins
4) Specific CDK-inhibiting proteins
Specific CDK-inhibiting protein
p21
DBRP
Destruction Box Recognizing Protein
Regulation of CDK by phosphorylation and desphosphorylation
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
Important Target Proteins of CDKs:
-Laminin
-Myosin
-Retinoblastoma protein (pRb)
p53
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
Genes encode regulatory proteins that normally inhibit cell division. Mutations in these genes are genetically recessive
Tumor Suppressor
Oncogenes
v-src
v-erbB
v-ras
v-fas and v-jun
v-erbB
-Gene that encodes epidermal growth factor (EGF) receptor that lacks the EGF-binding domain, but it retains its transmembrane and tyrosine domain
v-ras
-Encode v-Ras protein, which is similar to c-Ras protein but v-ras hydrolyzes GTP much more slowly.
Tumor Suppressors
pRb and p53
Apoptosis
Programmed cell death
Events of Apoptosis
-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
Receptor Types
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
Ex. of Ion Channel
Acetylcholine receptor
Ex. of Receptor Tyrosine Kinase
Growth hormone receptor, and insulin receptor
Ex. Receptors without enzymatic activity
JAK-STAT
Ex. of steroid type receptor
-Hydrophobic hormones, vitamin D, thyroid hormones
What is the target of NO?
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
Types of DNA:
A---ex.RNA-DNA, or RNA-RNA
B---ex. hydrated DNA
Z
Helical Sense
A and B are right handed
Z is left handed
Major Groove
A DNA: narrow and deep (ND)
B DNA: wide and deep (WD)
Z DNA: flat (FF)
Minor Groove
A DNA: wide and shallow (WS)
B DNA: narrow and deep (ND)
Z DNA: narrow and deep (ND)
Code
DNAType+major groove+minor groove
ANDWS
BWDND
ZFFND
Sugar Pucker
A DNA: C3'-endo
B DNA:C2'-endo
Z DNA: C2'-endo pyri... and C3'-endo purine
Glycosidic Bond Formation:
A DNA: anti
B DNA: anti
Z-DNA: anti for pyrimidine, and syn for purine
Superhelix Topology
L = T + W
L
Linking Number
# that one strand of the duplex passes the other
T
Twist
# of revolutions that one strand makes around the duplex axis
W
Writhing number
# of supercoils present
-right handed supercoil is negative
left handed is positive
Topoisomerases
Control of topological state (linking number) of DNA
Classification of Topoisomerases
-Type I: single strand cleavage
(L=+/- 1)
-Type II: double strand cleavage
(L = +/- 2)
Type I Topoisomerase
Type IA: strand passage mechanism with 3'-phosphotyrosine enzyme-DNA intermediate
Type IB: controlled rotation mechanism with 3'-phosphotyrosine enzyme-DNA intermediate
Type IB:
For what inhibitors of topoisomerases?
Inhibitors of topoisomerases as antibiotics and anticancer agents
Non-Watson Crick base pairs:
A-A pair
A-T Hoogsteen pair
Hypothetical T-C pair
G-U Wooble pair in RNA structures
How are nucleic acids stabilized?
Nucleic acids are stabilized by base stacking and hydrophobic interactions
Enzymes required for DNA replication:
-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
Why do DNA Polymerase I can remove primers?
Because DNA Polymerase I has 5'-->3' activity
Requirements for High Fidelity of DNA replication:
-Equal ratio of dNTPs
-Base pairing (A-T, and G-C)
-Proofreading (3'-->5')
-RNA primers
-Mismatch repair
E. coli DNA Polymerase I
-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
E. coli DNA Polymerase III
-DNA replicase
-Many subunits: sliding clamp (beta clamp)
E. coli DNA Polymerase II
Repairing DNA via SOS response
Reverse Transcription:
(cap) eukaryotic mRNA (polyA tail) ---> RNA-DNA hybrid --> single stranded DNA --> double stranded DNA
Telomers
Telomers consists of 1000 or more tandem repeats of a short guanine sequence
Telomerases
Telomerases synthesize and maintain telomeric DNA. They are ribonucleotides.
DNA damage:
-Dimerization by UV radiation
-Methylation
-Deamination
-Intercalation
Nitrogen mustard and ethylnitrosourea
They are alkylating agents
Ethidium, Proflavin, and Acridine Orange
They are intercalating agents that can cause insertion or deletion mutations