Biochem Night School II.0

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  1. purines (which, how do they pair, synthesis components, synth disruption)
    • AG (PURe As Gold)
    • A with T (2 H bonds)
    • G with C (3 H bonds) (G and C look similar=stronger "bond")
    • Aspartate, Glycine, GlutAmine (AG and GA are purines)
    • tetrahydrofolate required
    • 6 mercaptopurine (6 MP) disrupts IMP
    • mycophenolate and ribavirin disrupt IMP to GMP (not AMP) (inosine monophosphate dehydrogenase)
    • hydroxyurea disrupts pyrimidines and purines (ribonucleotide reductase)
  2. pyrimidines (which, how do they pair, synthesis components, synth disruption)
    • CUT
    • T with A (2 H bonds)
    • C with G (3 H bonds) (G and C look similar=stronger "bond")
    • aspartate, carbamoyl phosphate
    • CUT carbs and phosphate out of your diet and CUT the asparagus py (pie)
    • leflunomide inhibits dyhydroorotate dehydrogenase
    • methotrexate, trimethoprim, and pyrimethamine inhibit dihydrofolate reducatase (DHF to THF) inhibiting formation of dTMP (deoxythymidine monophosphate)
    • 5-FU forms 5-F-dUMP to also inhibit formation of dTMP by direct inhibition of thymidylate synthase
  3. adenosine deaminase deficiency
    • adenosine deaminase (ADA) converts adenosine and deoxyadenosine to inosine for purine salvage
    • instead goes to dATP, which is toxic to lymphocytes->SCID (AR)
    • Image Upload
  4. Lesch-Nyhan syndrome
    • deficiency of hypoxanthine guanine phosphoribosyltransferase part of AMP (adenosine to hypoxanthine) and GMP (guanine) salvage
    • converts these to IMP and GMP respectively, instead hypoxanthine and guanine are converted to xanthine by xanthine oxidase
    • xanthine oxidase then converts them to uric acid
    • gout, hyperuricemia, orange sand (sodium urate) in diaper, retardation, self-mutilation, aggression, dystonia
    • Image Upload
  5. transition DNA mutation
    • purine to purine or pyrimidine to pyrimidine
    • (opposed to trasnversion)
  6. transversion DNA mutation
    • purine to pyrimidine or pyrimidine to purine
    • (opposed to trasition)
  7. nucleotide excision repair (and what is disease?)
    • fixes bulky helix distorting lesions during G1
    • endonucleases relase oligonucleotides
    • DNA pol and ligase fill and reseal
    • xeroderma pigmentosum
  8. base excision repair
    • occurs throughout cell cycle
    • base-specific glycosylase creates apurinic/apyrimidinic (AP) site
    • AP endonuclease cleaves 5’
    • lyase cleaves 3’
    • DNA polymerase-β fills and lyase seals
  9. mismatch repair (and what disease?)
    • predominantly G2 phase
    • newly synthed strand (that’s why G2 phase) recognized and mismatched removed
    • gap filled and resealed
    • Lynch syndrome (hereditary nonpolyposis colorectal cancer)
  10. non-homologous end joining (and what disease?)
    • lack a sister chromatid (so probably G1
    • lose some DNA but shove two ends together after chewing a bit off so they stick
    • ataxia telangiectaseia, Fanconi anemia
  11. mRNA reading and protein synth directions
    • mRNA read 5 to 3! (that way the first codon that you made from DNA is the first one read)
    • protein N to C
    • unlike DNA 3 to 5 read and 5 to 3 synth
  12. mRNA start and stop codons
    • start AUG or GUG (rare) make methionine (N-formylmethionine in prokaryotes fMet [fMet induces neutroph chemotaxis]…we’re way off topic by now!)
    • stop UGA, UAG, UAA
    • you go away, you are going, you are away
  13. gene promoter seq, start codon, begining and end of introns, polyadenylation
    • promoter CAAT box and TATAAT box (“TATA”)
    • start codon ATG
    • intron start GT
    • intron end AG
    • polyA signal AATAAA
  14. enhancer
    • binds transcription factors
    • can be in introns even
  15. gene silencer
    • same as an enhancer, but binds negative regulators aka repressors
    • can be in introns even
  16. RNA pol I (what does it make, what inhibits it?)
    • rRNA (most common type of RNA)
    • used for ribosomes
    • Actinomycin D
  17. RNA pol II (what does it make, what inhibits it?)
    • mRNA (longest RNA)
    • opens DNA at promoter site
    • alpha amantinin
    • Actinomycin D
  18. RNA pol III (what does it make, what inhibits it?)
    • tRNA and 5SrRNA
    • Actinomycin D
  19. prokaryote RNA pol (what does it make, what inhibits it?)
    • they only have one RNA pol to make all types of RNA
    • inhibited by rifampin
  20. hnRNA to mRNA
    • heterogenous nuclear RNA aka pre-mRNA is capped at 5’ (7 methylguanosine)
    • tailed at 3’ (poly adenosine) (no template just slap it on the AAUAAA)
    • spliced (lose introns)
    • then it’s mRNA and transported out
  21. mRNA quality control
    • cytoplasmic processing bodies (P-bodies) with exonucleases, decapping enzymes, microRNAs
    • P-bodies can also store mRNA
  22. antibodies against spliceosome components
    • SLE antiSmith is anti snRNP
    • mixed CTD has anti-U1 RNP
  23. microRNA (where are they found)
    can be found in introns
  24. tRNA structure
    • CCA at 3’ binds amino acid (A binds) [3’ has OH 5’ has PO4 btw]
    • Can Carry Amino acids
    • T-arm ribothymidine, pseudouridine, cytidine for tRNA-ribosome binding
    • Touch arm
    • D-arm dihydrouridine for tRNA recognition by correct aminoacyl-tRNA synthetase (charging [requires ATP])
    • Determinant arm
  25. protein synth (initiation, elongation, termination)
    • initiation uses GTP to assemble 40S and 60S (80S)
    • aminoacyl-tRNA methionine binds to P site
    • subsequent aminoacyl-tRNAs bind to A site
    • ribozyme (rRNA) catalyzes peptide bond, puts growing protein on aa in A site
    • everything slides down 3 nucleotides (P to E for exit, A with protein to P)
    • release factor recognizes stop codon
  26. cyclin dependent kinase
    • constituitively expressed
    • CDK is inactive until cyclin complexes with it
  27. cyclin
    • only expressed when need to move through cell cycle
    • activates CDK by complexing, then the cyclin-CDK complex phosphorylates
  28. p53
    • induces p21 to inhibit CDKs leading to hypophosphorylation of Rb
    • when hypophosphorylated Rb binds E2F halting G1 to S
  29. G0
    • quiescent (stable) or permanent cells hang out in this phase
    • labile cells never go into G0 (gut, marrow, skin, hair, germ cells)
  30. G1
    • growth phase getting ready for S phase
    • quiescent (stable) cells can move from G0 to this
    • labile cells have a short G1 (gut, marrow, skin, hair, germ cells)
  31. G2
    two chromatids, getting ready for mitosis
  32. RER (job, other names)
    • synthesis for secretory proteins (goblet cells are rich in RER)
    • aka Nissl bodies
  33. smooth ER (job, assoc. cells)
    • steroid synthesis
    • detox
    • hepatocytes, adrenal cortex, gonads
  34. I-cell disease
    • aka mucolipidosis type II; inclusion cell disease
    • lysosomal storage disorder
    • golgi lacks N-acetylglucosaminy-1-phosphotransferase, can’t phosphorylate mannose residues
    • glycoproteins lack mannose-6-phosphate (normally signal that protein goes to lysosome)
    • proteins secreted instead of put in lysosomes, so lysosomes lack normal enzymes and get filled with junk
    • high levels of lysosome enzymes in serum
    • coarce facies, short trunk, clouded cornea, restricted joint movement, hepatosplenomegally, enlarged heart valves, respiratory tract infection/CHF fatal in childhood (age 7)
  35. microfilament
    • actin, microvilli
    • muscle contraction, cytokinesis
  36. vimentin (tissue type)
    • mesenchymal
    • also endometrial carcinoma, RCC, meningioma
    • intermediate filament
  37. desmin (tissue type)
    • muscle
    • intermediate filament
  38. cytokeratin (tissue type)
    • epithelial
    • intermediate filament
  39. glial fibrillary acid proteins
    • GFAP
    • astrocytes, ependymal
    • also found in Schwann cells, oligodendroglia
    • intermediate filament
  40. neurofilaments (tissue type)
    • neurons but not glia
    • intermediate filament
  41. intermediate filaments
    • lamins (nuclear envelope)
    • cytoskeleton for structure (staining)
  42. microtubules
    • axonal trafficking, cilia, flagella, mitotic spindle, centrioles
    • dynein (-) and kinesin (+)
    • alpha and beta tubulin with 2 GTP
    • movement, cell division
  43. cilia (structure, function)
    • 9+2 microtubule doublets
    • doublets linked by ATPase axonemal dynein to bend
    • basal body is 9 triplets without central microtubules
  44. Na-K-ATPase inhibitors
    • Ouabain binding to K site
    • digoxin/digitoxin (indirectly inhibit Na-C exchange to increase contractility)
  45. Type I collagen (where used, disorder)
    • bone (osteoblasts make it), skin, tendon, dentin, fascia, cornea/sclera, late wound repair
    • osteogenesis imperfecta 1 (defect in preprocollagen triple helix formation)
  46. Type II collagen (where used)
    cartilage (including hyaline), vitreous body, nucleus pulposus
  47. Type III collagen (where used, disorder)
    • reticulin, blood vessels, uterus, fetal tissue, granulation tissue
    • uncommon vascular type of Ehlers-Danlos (vascular, organ rupture)
  48. Type IV collagen (where used, disorder)
    • BM, basal lamina (“BM” of skin), lens
    • Alport syndrome defective, targeted in Good pasture
  49. Type V collagen (disorder, affected tissue)
    • Ehlers Danlos classic type AD or AR (tropocollagen cross-linking problem)
    • joint disolaction, berry aneurysm, aortic aneurysm, organ rupture, easy bleeding, hyperextensible skin
  50. collagen synthesis
    • alpha chains aka preprocollagen Gly-X-Y (proline and lysine often, but if you wanna know how much collagen someone has, check the glycine) I digress, moved into RER
    • hydroxylation (OH) of proline and lysine (VIT C) in RER
    • glycosylation (sugar) of hyroxylysine in RER
    • hydrogen bonds and disulfide bonds to form triple helix in RER = procollagen
    • exocytosis via golgi
    • disulfide rich terminals cleaved extracellularly forming tropocollagen (the part you keep)
    • tropocollagen covalent lysine-hyroxylysine by copper with lysyl oxidase forming collagen fibrils
    • wrinkles are from decreased collagen and elastin production
  51. Menkes disease
    • XR lack ATP7A, impaired copper absorption and transport
    • low lysyl oxidase activity, less tropocollagen covalent crosslinking
    • kinky brittle hair, growth retardation, hypotonia, sagging facies, metaphyseal widening, intellectual disability, seizures
  52. elastin (use, structure, synth, diseases)
    • stretchy protein in skin lungs, large arteries, elastic ligaments, vocal cords, ligamenta flava (connect vertebrae)
    • nonhydroxylated proline, lysine, glycine
    • cross linking of tropoelastin is extracellular
    • elastase breaks down (alpha 1 antitrypsin inhibition)
    • Marfan defect of fibrillin, a sheath around elastin
    • emphysema by alpha 1 antitrypsin deficiency
    • wrinkles are from decreased collagen and elastin production
  53. PCR temperatures
    • 95 denature
    • 55 anneal
    • 72 elongation
  54. southern blot
    • first electrophoresis then
    • radiolabeled DNA probe
    • filter exposed to film to see dsDNA bound probe
  55. northern blot
    • electrophorese RNA sample
    • radiolabled probe binds RNA
    • filter exposed to film to see RNA bound probe
  56. western blot
    • electrophorese protein sample
    • labeled antibody to bind protein target
    • confirmatory for ELISA
  57. southwestern blot
    • electrophoresis
    • radiolabeled oligonucleotides to bind DNA-binding proteins (xscription factors)
  58. flow cy
    • tag cell with antibody, tag antibody with fluorescent label
    • laser records each cell and how many tags
    • plot as histogram (1 measure)
    • scatter (2 measures)
  59. enzyme-linked immunosorbent assay
    • aka ELISA. woah
    • antibody (linked to enzyme) against antigen (HBsAg) or antibody (anti-HBs) in blood sample
    • color change or some signal that enzyme is going
    • can be indirect (detect antigen)(add antibody, then enzyme-linked anti-antibody antibody, wash, then substate)
    • direct (add enzyme-linked anti-antibody antibody, wash, then substate)
    • sandwich (detect antibody) (add antigen to bind to target antibody, then enzyme-linked antibody against antigen, wash, then substrate)
    • competitive (detect antibody) (incubate test antigen with antibody to form complex, add complex to well with antigen [if antibodies didn’t bind antigen, then they will bind well antigen], wash, then enzyme-linked anti-antibody antibody, then substate looking for less color change)
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Author:
countchocula58
ID:
318164
Filename:
Biochem Night School II.0
Updated:
2016-04-01 14:27:06
Tags:
biochem biochemistry step one tubberly tubblish
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Because the first night school wasn't good enough!
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