biochem tidbits

Card Set Information

Author:
embryo
ID:
99604
Filename:
biochem tidbits
Updated:
2011-09-04 12:36:22
Tags:
biochemistry
Folders:

Description:
MS1/Mod 1: Biochemistry; "tidbits"
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user embryo on FreezingBlue Flashcards. What would you like to do?


  1. CTF
    TF that binds to CAAT box (a promoter)
  2. SP1
    TF that binds to promoter region
  3. TBP/TF2D
    TF that binds to TATA box (promoter)
  4. Where are alpha globin genes?
    chrom 16
  5. What do defective alpha globin genes result in?
    • alpha thalessemia: results in severe anemia and death
    • note-alpha globin is oxygen carrying component of Hb
  6. What are the components of a Hb molecule?
    two beta globins and two alpha globins, 4 heme groups
  7. Where is the beta globin gene located?
    chrom 11
  8. What happens if beta globin is mutated?
    sickle cell anemia
  9. Where is epsilon globin exp?
    yolk sac
  10. Where is A-gamma and G-gamma globins exp?
    fetal dev
  11. What are the adult Hb?
    alpha, beta, delta globin
  12. Pseudouridine
    modified RNA base in T loop of tRNA; linkage btw uracil and ribose is changed from C-N bond to C-C bond
  13. ribothymidine
    T loop of tRNA; modified RNA base
  14. Hypoxanthine
    modified RNA base; deaminated adenine base whose nucleoside is inosine
  15. What are the most common modified RNA bases?
    pseudouridine and nucleosides w/ 2'-O-methylribose
  16. What is unique about the 5' cap of mRNA?
    linked to mRNA via 5'-5' triphosphate linkage to first transcribed nucleotide
  17. What is located in the 3'UTR of mRNA?
    polyA signal (site of cleavage), binding sites for prot, binding sites for miRNA, siRNA, and reg RNA
  18. RNAse H and FENs
    enz w/ endonucleolytic activity that remove the primer in lagging strand synth
  19. PCNA
    DNA clamp prot; processivity factor for DNA pol delta by encircling DNA as a trimer which creates a topological link to the genome
  20. telomerase seq
    TTAGGG
  21. OriC
    single origin of replication in prok; 245 bp long w/ conserved seq (four 9-bp repeats and three 13-AT rich bp repeats)
  22. DnaA prot
    initiation factor in prok DNA synth; binding cooperative (once one DnaA binds to a OriC repeat, tons of others bind)
  23. How does DnaA prot mediate sep of DNA strands in prok?
    acts on three AT rich regions of OriC
  24. DnaB prot
    binds to open OriC in prok; delivered by DnaC; completes pre-priming complex; has helicase activity
  25. DnaG prot
    primase for prok DNA synth
  26. Ter sites
    termination seq in DNA repl in prok; when bound to Tus prot, terminates DNA synth
  27. polarity of action
    Ter sites; will arrest a rep fork approaching the Ter site from one direction but will allow unimpeded fork mvmt through the Ter site from other direction
  28. RNase H activity
    ribonuc that degrades the RNA from RNA-DNA hybrids in rt of RNA template; func as endonuc and exonuc
  29. gag
    group-specific antigen; codes for core and structural prot of retrovirus (i.e. viral capsid)
  30. pol (viral)
    codes for rt, protease, and integrase; synth viral DNA and integration into host DNA after infection
  31. env (viral)
    codes for retroviral coat prot; plays role of entry of virion into host cell
  32. RNA (retroviral)
    dimer RNA; cap at 5' and polyA at 3'; has terminal noncoding regions and internal coding regions
  33. R region (retroviral)
    forms a direct repeat at both ends of genome
  34. U5 (retroviral)
    non-coding region, first part of genome to be rt; forms 3' end of provirus genome
  35. PBS (retroviral)
    18nt complementary to 3' of specific tRNA primer used by virus to begin rt
  36. Leader (retroviral)
    long, non-transL region downstream of transC start site and present at 5' of all virus mRNAs
  37. PPT (retroviral)
    short A/G run; initiates strand synth in rt
  38. U3 (retroviral)
    non-coding region; forms 5' end of provirus after rt; contains promoter elements used in transC of provirus
  39. How do oncoviruses originate?
    "retroviruses that contain oncogenes"; viral DNA incorporates a section of host DNA (contains genes for growth promotion called proto-oncogenes) into its own DNA; increased transC caused by LTRs of virus cause increased growth of infected cell
  40. HIV genome
    2 +ssRNA
  41. general TF
    bind to basic promoter seq facilitating RNA binding
  42. specific TF
    bind to seq distant from basic promoter and have specific roles
  43. What are the roles of specific TF?
    • 1. modulate efficiency of initiation
    • 2. mediate signal response
    • 3. regulate gene exp
    • 4. bind other reg prot
  44. Key pts in euk tRNA synth
    • 1. internal promoter-binding sites for TF and RNA pol 3
    • 2. transcription products contain promoter (start pt upstream of promoter)
  45. Upstream promoter elements
    CAAT and G/C box; fixed position/orientation but located distally upstream from TATA (core promoter element)
  46. sigma factor (euk transC)
    TF that binds to TATA core promoter element; binding of RNA pol follows
  47. trans-acting elements
    elements in transC that are not covalently linked to DNA
  48. CTF
    CAAT binding prot; trans acting element
  49. SP1
    TF; trans acting element; binds to promoter
  50. TF2D
    binds to TATA box; TF; trans acting element
  51. defects in polyA signal
    thalassemia, colorectal cancer, IGF-1, SCIDs, reduced globin chain synth in alpha/beta thalessemia
  52. SLE
    symptoms: degeneration of skin, joints, kidneys, nervous system, photosensitive rashes on face and extremities

    cause: presence of Ab to U1snRNP
  53. How is BRCA-1 prot multi-factorial?
    • participates in:
    • DNA damage repair
    • ubiquitination
    • transC reg

    defect in its alt splicing results in breast/ovarian cancer
  54. What are symptoms of APL?
    accumulation of immature granulocytes, cancer of blood and bone marrow, fatique, susceptible to infection, tend to bleed
  55. What are the biochem defects of APL?
    • 1. failure of histone acetylation
    • 2. failure of granulocyte diff (due to mutations in RAR...results in transC failure)
  56. What are the Rx for APL?
    all-trans retinoic acid (ATRA) and Trichostatin A
  57. Type 1 APL
    mutant RAR will not release HDAC activity from receptor-HDAC complex unless high amts of ATRA supplied
  58. Type 2 APL
    mutant RAR does not release HDAC at all; lots ATRA and tirchostatin A (HDAC inhib)
  59. How do viruses that cause measles and mumps work?
    • add A's to 3' end of viral DNA...prolonged stability
    • edit viral RNA causing frame-shift mut resulting in new viral RNA and prot
  60. What is the "branch pt"?
    seq in intron next to 5' splice juntion; bound to by snRNPs
  61. What are some types of base specific RNA editing?
    C-U and A-I
  62. What are the boundaries of the ORF?
    in mRNA; starts w/ start codon and ends w/ stop codon
  63. Does aminoacyl-tRNA synthetase have proofreading capability?
    YES
  64. What is the energy source for prok transL initiation?
    GTP
  65. Iron deficient anemia (hemin effect)
    biochemical basis: low [heme] activates prot kinase to phosph/activate eIF-2 kinase-Pi; active eIF-2 kinase-Pi phosph eIF-2; eIF-2 is now inactive...initiation of transL in euk is inhibited
  66. Clinical aspects of hemin effect
    • def of Hb in red blood cell leads to anemia
    • symptoms: extreme fatique, shortness of breath, headache, dizziness, susceptible to infection and arrhythmia
  67. What are some differential tests to confirm anemia?
    • measurement of blood cell size
    • hematocrit levels
    • Hb levels
  68. Inteferons
    • sm, naturally occurring prot
    • alpha, beta, gamma
    • anti-viral and anti-cancer moeities
  69. How does interferon work?
    interferon act enz to phosph an endonuc; endonuc-p can now degrade viral mRNAs....inhib of prot synth and viral proliferation and growth
  70. carboxyglutamination
    post-transL prot modification; conv of glutamic acid to gamma-carboxyglutamic acid

    req for blood clotting prot
  71. Hemophilia
    blood is unable to clot if carboxyglutamination is not functioning properly
  72. CF
    CF gene mut; CFTR is not properly glycosylated during post-transL modifications
  73. hydroxylation and collagens
    collagen is stabilized by hydroxylation of prolines and lysines
  74. prenylation
    post-transL modification; cov linkage of prenyl groups to anchor a prot to cell mem
  75. diseases due to misfolded prot
    neurodegenerative disorders: CJD/Mad cow, Alzheimer's, Huntington's
  76. [S]<<Km
    • Vo= [S](Vmax/Km)
    • rate is directly proportional to substrate concentration
  77. [S]>>Km
    • Vo=Vmax
    • rate is maximal and indep of substrate concentration
  78. [S]=Km
    • Vo=Vmax/2
    • Km is equal to substrate concentration when rxn rate is half the maximal value
  79. Km
    indep of enz concentration; measure of binding affinity of E for S or apparent dissoc constant
  80. Vmax
    Vmax=(Kcat)(ET)
  81. Kcat/Km
    greater it is, the higher aff an enz has for a substrate
  82. (-)deprenyl
    used to treat Parkinson disease and depression
  83. Penicillin
    binds to glycopeptide transpeptidase bc its molecular shape is similar to D-Ala-D-Ala substrate

    covalent bond formed btw penicillin and a Ser in the active site of enz resulting in inactivation of enz, inability of bact to synth their cell walls...bact lysis
  84. competitive inhibitors
    Km increased, Vmax unchanged

    • increases Km by a factor of (1+[I]/Ki)
    • new Km: Kmapp: Km(1+[I]/Ki)
  85. non-competitive inhibitors
    • Vmax decreased, Km unchanged
    • decreases Vmax by a factor of 1/(1+[I]/Ki)
    • Vmaxapp= Vmax/(1+[I]/Ki)
  86. uncompetitive inhibition
    inhibitor only binds to ES complex (vs competitive inhibitors which resemble substrate and compete for active site of enz)

    • [ES] lowered which lowers Vmax (Vmax=KcatET)
    • Km lowered bc removing [ES] shifts equil of E+S to the right (bc removing the prod, [ES])....increases affinity enz has for subst

    decreases both Km and Vmax by a factor of 1/(1+[I]Ki)
  87. Ki
    indication of how potent an inhibitor is
  88. competitive inhib and L-B plot
    • increases slope
    • x intercept moves to the right
    • same y intercept
  89. noncompetitive inhib and L-B plot
    • increases slope
    • x intercept stays the same
    • increased y intercept
  90. uncompetitive inhib and L-B plot
    • same slope
    • x intercept moves to left
    • increased y intercept
  91. methotrexate
    competitive inhibitor example; inhib dihydrofolate reductase
  92. burst phase
    formation of acyl-enz int whose formation is concurrent w/ formation of colored prod of chromogenic subst
  93. ATCase regulatory
    exists as a dimer, no cat act, binds CTP
  94. ATCase catalytic
    exists as a trimer, cat act, does not bind CTP
  95. ATCase structure
    complete enz=2xC3 and 3xR2
  96. Where does PALA bind?
    • btw pairs of catalytic chains w/in cat trimer
    • quindi for each catalytic trimer, there are three active sites which gives 6 active sites total per enz (two catalytic trimers per ATCase)
  97. purpose of ATCase
    to make more pyrimidines...therefore if lots of purines in env then there will be lots of ATP to allost act CTPAse but if there are lots of pyrimidines then CTP will inhibit CTPase through allos inhib
  98. Abl kinase
    act by phosphorylation of Tyr 412 which stabilizes R form; cov mod that leads to allost stabilization of R state

What would you like to do?

Home > Flashcards > Print Preview