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44 Cards in this Set

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Michaelis-Menten
V = (Vmax X S) / (Km + S)
Km vs. Ki
Km = affinity of substrate for enzyme

Ki = affinity of enzyme for inhibitor

They are opposing
Examples of competitive inhibitors
Malonate inhibits SDH

Methotrexate inhibits DHF reductase
ΔG
ΔG° + RTln X ([C][D]/[A][B])

Where ΔG° is the standard value
ΔGeq
-RTln X Keq

or

-1.36logKeq
Purine
A, G

Asp, Gly, Gln, 2 formyl-THFs
Pyrimidines
C, T, U

Asp, NH3, HCO3-
Hydroxyurea
Inhibits ribonucleotide reductase
MTX and TMP
Inhibit DHF reductase

MTX in humans (anti-cancer drug)

TMP in bacteria; immunosuppressant, causes anemia
6-MP
inhibits PRPP amidotransferase (blocks purine synthesis)
5-FU
inhibits thymidylate synthase (dTMP synthesis; pyrimidines)
Transition vs. transversion of bases
Transition: purine --> purine, pyrimidine --> pyrimidine

Transversion: purine --> pyrimidine, and vice versa
Unambiguous genetic code
1 codon = only 1 AA
Degenerate genetic code
More than 1 codon = a single AA
Silent

Missense

Nonsense mutation
Silent- BP change = same AA

Missense- BP change = similar AA (structurally conservative)

Nonsense- BP change = early stop codon
Prokoaryotic replication enzymes
DNA pol I, II, III

Have alpha and beta subunits
Alpha = pol part
Beta = sliding clamp and processing part
Needs of DNA pol III
Primer, Mg, Zn, dNTP, and 3'-OH
Eukaryotic replication enzymes
DNA pol A, B, G, D, E
Helicase
Unwinds DNA @ replication fork
SSBPs
Prevent strand reannealing after helicase unwinds
Topoisomerase I
Nick 1 strand to relieve supercoils
Topoisomerase II
Nick 2 strands to relieve supercoils
DNA gyrase
Introduces negative supercoils to relieve tension and favor DNA unwinding

Inhibited by Fluoroquinolones
Primase
Makes RNA primer for DNA pol III to initiate replication
DNA pol I

II

III
I: Degrades RNA primer (5'-->3' exonulcease), fills in gap w/DNA

II: Repair

III: Synthesize in 5'-->3' direction
DNA ligase
Seals/joins Okazaki fragments
Nucleoside analogues
Lack a a 3'-OH group, so when added, it terminates chain by inhibiting VIRAL DNA pol
Single strand DNA repair-
Nucleotide excision repair
Endonucleases release a few BPs w/damage, and DNA pol/ligase repair

Xeroderma pigmentosa = def. of UV-specific endonucleases, no repair of thymidine dimers caused by UVB light
SS DNA repair- Base excision repair
1. glycosylase
2. endonuclease
3. lyase
4. DNA pol
5. ligase

Remove base, remove empty sugar, and repair
SS DNA repair- MMR
Unmethylated newly synthesized DNA is recognized

Mutated in hereditary nonpolyposis colorectal cancer (HNPCC)
Double stranded nonhomologous end joining
Bring together 2 ends of DNA fragments, fixing human dsDNA breaks

No homology requirement

Responsible for "antibody diversity"
rRNA
mRNA
hnRNA
tRNA
snRNPs
rRNA- most abundant
mRNA- longest
hnRNA is pre-processed mRNA
tRNA- smallest type, always end in -CCA
snRNP- made by RNA pol II; remove introns from RNA transcripts so that mRNA can be made (in the spliceosome)
Promoter sequences in euk./prok.
Euk. CAAT, GC-box. Downstream of start site and TATA-box

Prok. Shine-Delgarno sequence
RecBD and RecA
Makes 3' overhang, recruits RecA

RecA competes w.ssBPs to form Holliday junx
RuvAB and RuvC
RuvAB = branch migration

RuvC = resolution
Promoter mutation causes what?
decreased amount of gene that is transcribed
RNA polymerases (initiate transcription) in euk. and prok.
Euk. RNA pol I, II, and III
I: rRNA
II: mRNA (a-amantin/deathcap mushrooms)
III: tRNA

Prok. 1 RNA pol that makes all kinds of RNA
Core made of 2 alpha, B, and B1
Spliceosome
Primary transcript (hnRNA), snRNPs, and other proteins

Forms lariat shape at "A-branch site" for intron excision (hnRNA --> mRNA)
Transmembrane domain properties
alpha helix

hydrophobic AA (Leu, Iso, Val) outer layer

Hydrophilic core

Beta-sheets (beta-barrel)
Exoplasmic leaflet, vs. cytoplasmic leaflet
Exo: SM, PC

Cyto: PS, PI, PE

PS is flipped to exoplasmic so annexin V can bind it during apoptosis
Microtubule drugs
Mebendazole
Griseofulvin
Vincristine/viblastine
Paclitaxel
Colchicine
Dynein
Retrograde (+ to -)

Kartageners
Kinesin
Anterograde (- to +)

ATP=powered
Membrane fluidity
Longer carbon chain = decreased

More double bonds = increased