Cell Bio- Genes and Proteins.txt

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  1. Most genes are regulated at the level of _______.
    transcription initiation
  2. What are the 3 major RNA polymerases and their functions?
    • pol I: transcribes rRNA
    • pol II: transcribed mRNA
    • pol III: transcribes tRNA
  3. After the transcription factor binds the proteins (including RNA pol),...
    the complex is recruited to the promoter sequence and transcription is initiated
  4. DNA sequences that control gene transcription and are upstream (5') of the gene.
    Control regions
  5. DNA sequences that control transcription and are located far away from the gene they control.
  6. Regions of DNA that are transcribed and translated.
  7. Regions of DNA that are transcribed then spliced out during RNA processing.
  8. The 5' end of the RNA transcript with a trimethyl group it located.
    Trimethyl cap
  9. The 3' end of the mature processed mRNA.
    Poly-A tail
  10. DNA sequence that regulated transcription and is immediately 5' to the gene.
  11. The study of all heritable and potentially reversible changed that impact gene expression but do NOT involved changes in DNA nucleotide sequence.
  12. DNA wrapped around histone octamer.
  13. Post-translational modification of RNA.
    Histones- nucleosomes
  14. The N terminal regions of histone can be post-translationally modified by...(3)
    acetylation, phosphorylation, or methylation
  15. Histone tail acetylation is associated with _________.
    promotion of gene transcription
  16. Histone tail phosphorylation is associated with _______.
    promotion of gene expression.
  17. Histone tail methylation is associated with ________.
    repression of gene expression
  18. DNA methylation is the addition of _____ to ______.
    methyl groups; cytosines that are followed by guanosine (CpG islands) in DNA promoter regions
  19. Cytosine methylation blocks _________ , thereby....
    transcription factor binding to promoters; inhibiting transcription
  20. A very common pathological mechanism to silence tumor suppressor gene expression in cancer cells.
    Presence of extensive regions of CpG methylation
  21. When DNA is tightly wound around nucleosomes, ...
    the transcription factor binding site is empty, a repressor may be present, and N terminal tails are unmodified (gene resting state)
  22. When the ligand binds to its receptor and the transcription factor is activated, the TF binds to ______.
    gene promoters
  23. The TF activation domains recruit _____ to promote transcription.
  24. The histoacetyltransferase (HAT) of some co-activator proteins performs the following function...
    puts acetyl groups onto histone tails to open or relax nucleosomes for transcription
  25. Histone Deactylases (HDACSs) perform the following function...
    remove actyl groups from histone tails to coil the chromatin and reduce transcription
  26. Two examples of histone deacetylase inhibitors.
    TSA and TPX (activate gene transcription)
  27. Tumor suppressor genes are often repressed in cancer cells by increased _____ activity.
  28. Give 3 examples of when DNA methylation is normal.
    • X- inactivation- in females, one X chromosome is silenced
    • Imprinted genes- Only paternal or maternal gene is expressed and the other is silenced
    • Repetitive elements- heterochromatin
  29. DNA methylation is "heritable," meaning...
    DMNTs maintain the methylation status of CpG following DNA replication
  30. DMNT expression is ____ in normal cells.
  31. How can DMNTs be involved in cancer?
    Increased DMNT expression results in inappropriate methylation of CpGs in the promoters of tumor suppressor genes; if TS gene expression is decreased, then cell division is uninhibited (CANCER)
  32. How are DMNT inhibitors use in anti-cancer drugs?
    When DMNT1 is over-expressed, CpGs are excessively methylated in the promoters of tumor suppressor genes, blocking TS gene expression and causing uninhibited growth and division of the cell; by blocking DMNT1 with an inhibitor, we prevent uninhibited growth of the cell.
  33. CpG methylation and HDAC recruitment are linked in that they both...
    have major relevance in the "silencing" of tumor suppressor gene expression.
  34. By what 2 mechanisms does CpG methylation silence tumor suppressor genes?
    • 1. methylation alters the physical structure of the cytosine and blocks transcription factor binding.
    • 2. Methylation recruits HDAC to the site, which deacetylates and inactivates the gene.
  35. By what mechanism do HDACs silence gene expression?
    They deacetylate the DNA, causing condensation and "closing" of chromatin, so the promoters are hidden and the genes are silenced.
  36. How does TS gene deletion (p16 for instance) play a role in cancer? How can it be treated?
    Loss of p16 results in hyperphosphorylation and inactivation of Rb; inactive Rb releases E2F, and the cell cycle is able to enter S phase and replicate; if Rb is perpetually inactive, the cell cycle continues uninhibited; CDKIs are used to inhibits kinases, so Rb can remain active and bound to E2F.
  37. How does a single nucleotide mutation in a TS gene (p53 for instance) play a role in cancer? How is it treated?
    If there is a mutation in the DNA binding domain of p53, it cannot properly bind to the DNA promoter region; if p53 cannot react to DNA damage, then damaged DNA will be replicated and could potentially lead to cancer. (p53 normally causes apoptosis of cells with irreparable DNA damage.) Unfortunately, mutant p53 is hard to detect.
  38. Ho is CpG promoter methylation involved in cancer? How is it treated?
    When DMNT1 is over-expressed, CpGs in the promoter regions of TS genes are excessively methylated, thus the promoters are "hidden," reducing expression of the TS genes. Reduced expression of TS genes leads to uninhibited cell division and cancer. DMNT inhibitors are used to prevent the excessively methylation of CpGs by blocking DMNT function.
  39. How is enhanced HDAC activity involved in cancer? How is it treated?
    HDACs remove acetyl groups from histones, thus "closing" them and compacting the nucleosomes; this actions hides the promoter regions and the expression of these TS gene is blocked. By blocking the TS genes, the cell s able to undergo uninhibited cell growth and cancer. HDAC inhibitors prevent the loss of function of the TS gene by blocking the HDACs so the histones remained acetylated.
  40. What are 3 post-transcriptional RNA processing events?
    3' capping, 5' poly-adenylation, and splicing
  41. The original product of transcription.
    hnRNA (heterogeneous nuclear RNA)
  42. Enzyme that carries out splicing.
  43. A splicing error will...
    disrupt the reading frame if it is 1 or 2 errors (3 is a full reading frame)
  44. Highest conservation is at ________ splice sites.
  45. Exons contain 2 highly conserved sequence elements that are...
    5' splice site and 3' splice site
  46. CPHD in German Shepherd Dogs is associated with defective development of the pituitary gland and dwarfism; this is caused by a deletion is a homeobox gene, which results in...
    defective splicing and nonfunctional proteins
  47. Ribosomes are large ____________ complexes.
    protein and RNA
  48. The function of ribosomes in translation is highly _______.
  49. During translation initiation, the________ interacts with _______.
    5' end of the mRNA; the small ribosomal subunit
  50. During translation elongation,...
    the polypeptide chain grows by sequential recruitment of aminoacyl-tRNAs
  51. During translation termination,...
    the mRNA stop codon an releasing factors cause the release of the polypeptide
  52. Protein biosynthetic machinery is induced in any _______, including _______.
    proliferating cell; cancer cells
  53. How is the PI3K/mTOP pathway involved in canine osteosarcoma cells?
    mTOR phosphorylates 4EBP1, which causes it to release the initiation factor eIF4E, which is required to initiate translation. (eIF4E binds to the 5' mRNA cap and recruits the small subunit to initiate translation.) If this process is overexpressed, then cancer can result.
  54. How are researchers treating osteosarcomas that are caused by over expression of the PI3K/mTOR pathway?
    mTOR phosphorylates 4EBP1, which causes it to release the initiation factor eIF4E, which is required to initiate translation. (eIF4E binds to the 5' mRNA cap and recruits the small subunit to initiate translation.) If this process is overexpressed, then cancer can result. If you inhibit mTOR, 4EBP1 remains unphosphorylated and active, blocking the initiation factor. With IF blocked, the cell cycle cannot continue with initiation of translation, and the growth of cancer cells is inhibited.
  55. microRNA is a complex RNA molecule that is cleaved by an enzyme called ______
  56. miRNAs function to....
    negatively regulate mRNAs by increasing mRNA degradation or blocking mRNA translation
  57. How can a drug txt exhibit specificity when the drug target is present in both normal cells and tumor cells?
    Oncogene addiction hypothesis: many cancer cells rely on, or are highly dependent on, a single oncogene for their survival; drugs that target that oncogene will preferentially kill cancer cells relative to normal cells.
  58. Proteins in the animal body are constantly...
    being synthesized and broken down (translation)
  59. To provide the building blocks for constant protein synthesis, animal cells...
    recycle AAs from endogenous proteins and dietary proteins that are broken down
  60. What is the major criteria to determine high vs. low quality proteins?
    The amount of essential AAs in the food (animal-based proteins are high and plant-based proteins are low)
  61. Dietary protein breakdown is initiated in the ________ by _____.
    stomach; pepsin
  62. The presence of polypeptides in the duodenum activates...
    the pancreas to release peptidases into the pancreatic duct and dump these enzymes into the duodenum
  63. In the duodenum,...
    peptidases from the pancreas break down proteins into polypeptides as they pass from the duodenum to the jejunum
  64. In the jejunum, ...
    short polypeptides are broken down into single AAs by peptidases present on the brush border of jejunum mucosal cells; single AAs are absorbed by jejunum mucosal cells
  65. Single AAs are absorbed by the ______ and then...
    jejunum mucosal cells; they enter the portal vein to go to the liver, then the rest of the body
  66. AAs absorbed in the jejunum go to the _______ via the ______, where they are utilized in... (3)
    liver; portal vein; synthesis of hepatic proteins and plasma proteins, and conversion to carbon skeletons for energy metabolism
  67. Proteins have a characteristic _____ or biological _____.
    lifetime; half-life
  68. What are the 4 principal mechanisms of protein degradation?
    Ubiquitin-proteosome pathway, lysosomal degradation, caspases, proteinases/peptidases
  69. Proteins a degraded via the ubiquitin-proteosome pathway are first _________ and then _______ by ________.
    phosphorylated; tagged with multiple ubiquitin molecules by ubiquitin ligases
  70. Ubiquitinated proteins are targeted by the _________, which...
    proteosome; degrades the proteins to peptides and then to single AAs.
  71. What must happen to cyclins before the cell cycle can continue through the end of M phase?
    They MUST be degraded and gone in M phase
  72. The new anti-cancer drug, Velcade, targets the proteosome. How does this effectively treat cancer?
    The drug blocks the proteosome, thus blocking proteosome-mediated protein degradation. This prevents cyclins, specifically M phase cyclins, from being degraded during M phase. The M phase cyclins MUST MUST be degraded before the cell cycle can progress through M phase and the rest of the cell cycle. Thus, the cell cycle is halted and apoptosis is eventually activated.
  73. Lysosomes contain ____________________ that are maximally active at _______.
    proteolytic and other degradative enzymes; low pH
  74. Lysosomes serve the purpose to...
    degrade cellular components, including proteins
  75. What are the 3 major pathways by which lysosomes degrade proteins?
    endocytosis, phagocytosis, and autophagy
  76. The major pathway for the degradation of plasma membrane proteins is ______.
  77. Endocytosis involves the migration of ________ into the cytoplasm, where it fuses with the _________ to form the ________.
    membrane segments; early endosome; primary lysosome
  78. During lysosomal degradation of plasma membrane components, the primary lysosome fuses with the _________ to form the _______, within which...
    late endosome; secondary lysosome; proteins are degraded to peptides and AAs by proteases within the lysosome.
  79. Phagocytosis is the mechanism by which ________ are engulfed by the _______, forming a phagosome.
    exogenous material (bacteria, apoptotic bodies, etc); plasma membrane
  80. During phagocytosis, the phagosome fuses with the _________, within which...
    lysosome; exogenous protein materials are degraded
  81. Autophagy comprises the lysosomal degradation of ____________.
    cytoplasmic organelles and components
  82. The amino acids present in the cell at any time.
    amino acid pool
  83. What are the 3 sources of AAs for the amino acid pool?
    dietary absorption, amino acid biosynthesis, protein degradation
  84. What are the 4 drains of the amino acid pool, or processes that use AAs from the pool?
    endogenous protein synthesis/translation, AA metabolism (AAs that have biological jobs that do not involves becoming a protein), transamination, oxidative deamination
  85. During transamination, the ______ from one AA is removed and transferred to form...
    NH3 group; a new AA
  86. AAs that undergo deamination produce ____________ and ______; excess _______ is removed by forming ______.
    α-keto acids (carbon skeletons); nitrogen; nitrogen; urea
  87. The carbons from recycled AAs can be used to synthesize... (3)
    glucose, lipids, and sometimes ketones
  88. Transaminases in the body are often organ specific; this gives them the following clinical significance...
    they can be assessed to evaluate organ functions (ex. elevated ALT indicates liver damage)
  89. Excess nitrogen in the form of _______ is toxic, especially to nerve cells, and can cause _______.
    ammonia; hepatic encephalopathy
  90. What is the purpose of the urea cycle, and what would happen if it was not functioning in a animal?
    Its purpose os to remove excess ammonia, which can be toxic to the body. It removes ammonia by converting it to urea (blood urea nitrogen BUN), which is excreted through the urine. Without the urea cycle, toxic nitrogen can build up and cause disorders such as hepatic encephalopathy.
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Cell Bio- Genes and Proteins.txt
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