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63 Cards in this Set
- Front
- Back
Fat/Water soluble vitamins
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- fat soluble - A, D, E, K
- water soluble - B(s), C, Biotin, folate |
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Vitamin A
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- retinol is vitamin A, so think Retin-A
- deficiency: night blindness, dry skin - function: constituent of visual pigments (retinal) |
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Vitamin B1
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- thiamine
- spell beriberi ber1ber1 - deficiency: beriberi and wernicke-korsakoff syndrome - function: in thiamine pyrophosphate, a cofactor for oxidative decarboxylation of alpha-ketoacids |
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Vitamin B2
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- riboflavin
- deficiency: angular stomatitis, cheilosis, cornela vascularization - function cofactor in ox/redox of FADH2 (FAD and FMN are derived from riboFlavin) |
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Vitamin B3
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- niacin
- deficiency: Pellagra - Diarrhea, Dermatitis, Dementia - function: constituent of NAD+/NADP+. derived from tryptofan using B6 |
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Vitamin B5
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- pantothenate
- deficiency: dermatitis, enteritis, alopecia, adrenal insufficiency - function: constituent of CoA and fatty acid synthase (Pantothen-A is Co-A) |
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Vitamin B6
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- pyridoxine
- deficiency: convulsions, hyperirritability, peripheral neuropathy - function: converted to pyridoxal phosphate and required for synthesis of niacin. |
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Vitamin B12
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- cobalamin
- deficiency: macrocytic megaloblastic anemia; neurologic symptoms, glossitis - function: cofactor for homocysteine methyltransferase - deficiency usually caused by malabsorption, lack of IF (pernicious anemia), or absence of terminal illeum (Crohn's disease) |
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Folic acid
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- deficiency: macrocytic, megaloblastic anemia
- function: coenzyme (THF) for 1-carbon transfer - important for DNA/RNA synthesis - FOLate from FOLiage |
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Biotin
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- deficiency: dermatitis, enteritis - caused by antibiotic use and excessive raw eggs (AVIDin in egg whites AVIDly binds biotin).
- function: cofactor for carboxylations |
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Vitamin C
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- ascorbic acid
- deficiency: scurvy - swollen gums, bruising, anemia, poor wound heeling - function: necessary for collagen synthesis, facilitates iron absorption, necessary to convert dopamine to NE |
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Vitamin D
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- D2 consumed in milk
- D3 formed in sun-exposed skin - 25-OH D3 is storage form - 1,25-OH D3 (calcitriol) is active form - deficiency: rickets in children, osteomalacia in adults, hypocalcemic tetany - function: intestinal absorption of Ca and phosphate |
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Vitamin E
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- deficiency: fragile erythrocytes (E is for Erythrocytes), neurodysfunction
- function: antioxidant (protects erythrocytes from hemolysis) |
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Vitamin K
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- Deficiency: neonatal hemorrhage (infants have sterile intestines thusly cant synthesize vitK)
- Function: Catalyzes gamma-carboxylation of glutamic acid residues (concerned w/ blood clotting) - VitK synthesized by bacteria so deficiency can result from antibiotics - K for Koagulation (Warfarin is a vitamin K antagonist) |
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Zinc deficiency
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- Delayed wound healing, hypogonadism, ↓ adult hair (axillary, facial, pubic); may
predispose to alcoholic cirrhosis. - zinc deficiency makes you less like wolverine |
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Ethanol metabolism
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- NAD+ oxidizes alcohol to acetate (via alcohol dehydrogenase and acetaldehyde dehydrogenase
- NAD+ is limiting reagent |
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ethanol hypoglycemia
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- Ethanol metabolism ↑ NADH/NAD+ ratio in liver, causing diversion of pyruvate to lactate and OAA to malate, thereby inhibiting gluconeogenesis and leading to hypoglycemia. This altered NADH/NAD+ ratio is responsible for the hepatic fatty change (hepatocellular steatosis) seen in chronic alcoholics (shunting away from glycolysis and toward fatty acid synthesis, which normalizes the ratio).
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Kwashiorkor vs. marasmus
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- Kwashiorkor: protein malnutrition (small child with swollen belly) resulting in skin lesions, edema, liver malfunction (fatty change).
- Marasmus: energy malnutrition resulting in tissue/muscle wasting, loss of subcutaneous fat, and variable edema - Kwashiorkor results from a protein-deficient MEAL: Malnutrition, Edema, Anemia, Liver (fatty) |
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Chromatin structure
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- neg. charged DNA loops twice around histone octomer(2 each of the positively charged H2A, H2B, H3, and H4) to form nucleosome bead.
- H1 ties nucleosomes together in string |
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Heterochromatin
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- condensed, transcritionally inactive
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Euchromatin
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- less condensed, transcriptionally active
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Nucleotides
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- purines (A,G): PURe As Gold
- pyrimidines (CTU): CUT the PY - G-C bonds (3HB) stronger than A-T bonds (2HB) --> higher G-C content leads to higher melting temp. |
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Transition
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- substituting purine for purine or pyrimidine for pyrimidine
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Transversion
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- substituting purine for pyrimidine or vise versa
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Silent mutation
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- same AA, often base change in 3rd position of codon (tRNA wobble)
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Missense mutation
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- changed AA
- if conservative: new AA is similar to original |
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Nonsense mutation
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- change results in stop codon
- STOP the NONSENSE! |
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Frame shift mutation
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- change resulting in misreading of all nucleotides downstream, usually resulting in a truncated protein
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Eukaryotic DNA replication
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- multiple origin sites
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Prokaryotic DNA replication
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- single origin site
- bidirectional: continuous on leading strand and okazaki fragments on lagging strand |
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Helicase
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- enzyme which unwinds DNA at replication fork
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DNA topoisomerases
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- create a nick in the helix to relieve supercoils
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primase
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- makes an RNA primer on which DNA polymerase III can initiate replication
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DNA polymerase III
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- elongates the chain by adding deoxynucleotides to the 3' end (leading strand, 5'-3')
- elongates lagging strand until it reaches primer of preceding fragment - 3'-5' exonuclease activity "proofreads" each added nucleotide |
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DNA polymerase I
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- degrades RNA primer and fills in the gap with DNA
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DNA ligase
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- seals
- connects Okazaki fragment to lagging strand |
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Nucleotide excision repair
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- specific endonucleases release the oligonucleotide-containing damaged bases
- DNA polymerase and ligase fill and reseal the gap, respectively - this enzyme is mutated in xeroderma pigmentosum (dry skin with melanoma and other cancers, "children of the night"), which prevents repair of thymidine dimers |
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Base excision repair
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- specific glycosylases recognize and remove damaged bases
- AP endonuclease cuts DNA at apyrimidinic site - empty sugar is removed and the gap is filled and resealed |
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mismatch repair
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- unmethylated, newly synthesized string is recognized
- mismatched nucleotides are removed - gap is filled and resealed |
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Nonhomologous end joining
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- brings together two ends of DNA fragments
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DNA/RNA/protein synthesis direction
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- DNA/RNA are synthesized 5'-3'
- mRNA is read 5'-3' - protein synthesis is N to C |
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Types of RNA
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- Massive, Rampant, Tiny
- mRNA is largest - rRNA is the most abundant - tRNA is the smallest |
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start codon
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- AUG
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stop codon
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- UGA, UAA, UAG
- UGA = U Go Away - UAA = U Are Away - UAG = U are Gone |
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promoter
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- site where RNA polymerase and multiple other transcription factors bind to DNA upstream from gene locus (AT-rich upstream sequence with TATA and CAAT boxes)
- promoter mutation commonly results in dramatic decrease in amount of gene transcribed |
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enhancer
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- stretch of DNA that alters gene expression by binding transcription factors
- may be located close to, far from, or even within (in an intron) the gene whose expression it regulates |
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silencer
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- site where negative regulators (repressors) bind
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Eukaryotic RNA polymerase
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- I, II, and II are numbered as their products are used in protein synthesis
- RNA polymerase I makes rRNA - RNA polymerase II makes mRNA - RNA polymerase III makes tRNA - RNA polymerase II is inhibited by alpha-amanitin (found in death cap mushrooms) |
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Prokaryotic RNA polymerase
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- RNA polymerase makes all 3 kinds of RNA
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RNA processing
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1. capping on 5' end
2. polyadenylation on 3' end 3. splicing out of introns - initial transcript is called heterogenous nuclear RNA (hnRNA) - processed transcript is called mRNA |
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Splicing of pre-mRNA
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1. primary transcript combines with snRNPs and other proteins to form spliceosome
2. lariat-shaped intermated is generated 3. larait is released to remove intron precisely and join 3 exons |
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introns vs exons
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- introns are spliced out
- exons are kept and therefore expressed - INtrons stay IN the nucleus while EXons EXit and are EXpressed |
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tRNA wobble
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- Accurate base pairing is required only in the first 2 nucleotide positions of an mRNA codon, so codons differing in the 3rd “wobble” position may code for the same tRNA/amino acid.
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tRNA structure
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- amino acid bound to 3' end
- aminoacyl-tRNA synthetase catalyzes AA-tRNA binding and proofreads AA-tRNA pair yielding selectivity |
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Protein synthesis
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- A, P, E sites
- A site accepts incoming tRNA - P site catalyzes AA-AA peptide bond formation - E site holds empty tRNA as it exits - initiation: initiation factors help assemble the 40S ribosomal subunit with the initiator tRNA and are released when the mRNA and the ribosomal subunit assemble with the complex - elongation: A, P, E sites - termination: protein released by hydrolysis |
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Ribosomal subunit sizes
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- eukaryotes (even): 80S → 60S + 40S
- prokaryotes (odd): 70S → 50S + 30S |
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Posttranslational modifications
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- trimming: removal of N- or C-terminal propeptides from zymogens to generate mature proteins
- covalent alterations: Phosphorylation, glycosylation, and hydroxylation - proteasomal degradation: attachment of ubiquitin to defective proteins to tag them for breakdown |
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Cell cycle
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- G1, S, G3, M
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Mitosis
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- prophase, metaphase, anaphase, telephase
- CDKs: constitutive and inactive - Cyclins: phase specific, activate CDKs - Cyclin-CDK complexes: must be both activated and inactivated for cell cycle to progress - Rb/p53 tumor suppressors normally inhibit G1-to-S progression; mutations in these genes result in unrestrained growth |
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Rough endoplasmic reticulum
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- site of synthesis of secretory proteins
- site of N-linked oligosaccharide addition to many proteins - nissl boddies (in neurons) synthesize enzymes and peptide neurotransmitters - free ribosomes synthesize cytosolic/organellar proteins - mucus secreted goblet cells and immunoglobbin secreting plasma cells have lots of RER |
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Smooth endoplasmic reticulum
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- site of steroid synthesis and detoxification of drugs/poisons
- liver hepatocytes and steroid hormone-producing cells of the adrenal cortex are rich in SER |
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Golgi apparatus (functions)
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- distributes proteins/lipids from ER to plasma membrane, lysosomes and secretory vesicles
- targeting modifications |
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I-cell disease
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- failure of addition of mannose-6-phosphate to lysosome proteins in the golgi apparatus; enzymes are secreted outside the cell instead of being targeted to the lysosome
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