4.23.2010

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4.23.2010

  1. 1. <ul><li>Desmosomes
  2. 2. Like hemidesmosomes because they involved the formation of plaques on the cytoplasmic side of membrane and link/organize keratans or intermediate filaments
  3. 3. Difference: different types of transmembrane proteins interacting with one another in a homophylic way to link the PM together
  4. 4. Hemidesmomsomes use integrins to link to the basal lamina
  5. 5. Similarities and Differences
  6. 6. Form a plaque
  7. 7. Organize keratan intermiedate filaments
  8. 8. Desomosomes link up cells together
  9. 9. Hemi link cell membrane to basal lamina
  10. 10. There are two types of transmembrane proteins that form desmosomes
  11. 11. Desmocollin
  12. 12. Desmoglein
  13. 13. Characeteristics
  14. 14. Interact homophylicily on EX side
  15. 15. Within cadherin family of protein
  16. 16. Bind in a homophylic, Ca2+ dependant way
  17. 17. Interact with in the same type of association with opposing proteins on opposite cell membrane
  18. 18. Localize when interact
  19. 19. Serve as attachment sites for proteins that can link desmosome to keratan
  20. 20. There are proteins that link desmosomes proteins to keratan
  21. 21. Plakoglobin
  22. 22. Globular protein that only associates with cytoplasmic region of desmoglein or desmocolin
  23. 23. Bound by globular region of dimeric protein desmoplakin
  24. 24. Desmoplakin
  25. 25. Directly associates with the keratan flaments/intermediate filaments and organizes them on these lateral sides of the PM
  26. 26. Keratan filaments are then organized at these sites where plaques are formed as desmosomes assemble between cells
  27. 27. Create attachments sites/a network for organizing the keratin that will provide structural support for epithelial cells as they form tissue (as well as hemidesmosomes)
  28. 28. Epithelial cells are mucosal linings, lung linings as well
  29. 29. Tight Junctions
  30. 30. Fairly weak associations actually
  31. 31. Require lots of TJs formed in a particular way
  32. 32. Make a meshwork near the apical side of the cell
  33. 33. Form a separation between apical and basal side of the cell <<< important
  34. 34. Initial studies done to find proteins involved and how important TJs are
  35. 35. Labeled solutions added to basal or apical side
  36. 36. Does the solution diffuse?
  37. 37. When you mutate a protein, what happens in diffusion?
  38. 38. Two types of proteins make up tight junctions
  39. 39. Claudin
  40. 40. Occludin
  41. 41. Charactersistics
  42. 42. Transmembrane proteins
  43. 43. Each have 4 transmembrane spanning doains
  44. 44. Interact with each other on EXC side of PM by linking EXC loops between the trasmembrane domains
  45. 45. Interact homphylically
  46. 46. Claudin binds with claudin
  47. 47. Occludin binds with occludin
  48. 48. Function
  49. 49. On apical side
  50. 50. Active mechanism of transport to bring in glucose after food has been digested into epithelial cells
  51. 51. Requires the function of Na/Glucose transporter
  52. 52. High levels of glucose in lumen brought in, in a regulated way
  53. 53. Glucose diffuses through cell cytoplasm
  54. 54. Through passive transporter, glucose transporter, into EXC fluid and through blood capillaries to tissues
  55. 55. Without TJs glucose would rapidly diffuse through EXC fluid into blood capillaries in an unrestricted way
  56. 56. Allows epithelial cells to regulate uptake of glucose and bring in as much as is needed at a particular time
  57. 57. Gap Junctions
  58. 58. Important in linking cells into cytoplasmic sinsishunt
  59. 59. Cardiac cells functioning
  60. 60. Open junctions before contraction
  61. 61. Ions that drive contraction move through rapidly, linking cytoplasms of all cells making one big cell so that they can contract at the same time and make heart function properly
  62. 62. Allow small small small molecules to go thorugh such as ions
  63. 63. Transmembrane proteins
  64. 64. Made up of 6 individual GJ polypeptides (connexins) that span the lipid membrane
  65. 65. There are 14 different genes that are known to encode GJ proteins
  66. 66. Different combination of the proteins in different tissues
  67. 67. Homomeric
  68. 68. Made of the same homomeric proteins
  69. 69. Heteromeric
  70. 70. Made of different gap junction proteins
  71. 71. How the two PM come together
  72. 72. Two similar types of GJ coming together as PM are joined
  73. 73. Two different types of homomeric GJ connect with one another
  74. 74. Heterotypic binding
  75. 75. Tissue specific as well
  76. 76. Two different types of heteromeric GJ connect with one another
  77. 77. Heterotypic binding
  78. 78. Tissue specific as well
  79. 79. Two of the same type of homomeric or heteromeric GJ connect with one another
  80. 80. Homotypic Binding
  81. 81. Structure of GJs
  82. 82. Connexins are the individual proteins
  83. 83. Assembled GJ with 6 connexins is called a connexon
  84. 84. Open like a shutter when slid together to form a pore
  85. 85. --------------------END LECTURE ON ECM-------------------------
  86. 86. CANCER
  87. 87. Cancer Cells
  88. 88. Tumors
  89. 89. All tumors are not cancerous
  90. 90. Neoplastic cells
  91. 91. Moles
  92. 92. Not cancerous
  93. 93. Cells are benign and remain intact in primary tissue from which they rose
  94. 94. Divided in an unrestricted way for a period of time
  95. 95. Uncontrolled mitosis
  96. 96. All cancers have tumoregenic cells but not all tumors are cancerous
  97. 97. Characteristics of cancer cells
  98. 98. Reproduce without restrictions on mitosis
  99. 99. Can invade and colonize regions in and outside of primary source (invasive and colonize)
  100. 100. Benign
  101. 101. Neoplastic cells that divide in an unrestricted way but remain in source tissue
  102. 102. Don’t have to mecome malignant necessarily, form metasteses (1/1000 cells that has become neoplastic can become metastatic
  103. 103. Can form a tumor, often clonal – arising from a SINGLE cell, which most cancers are often from
  104. 104. If undergone a mutation, benign cells can loose dependence on attachment to one another as well as to the basal lamina and actively secrete proteases that chew away basal lamina and connective tissue/proteoglycans in connective tissue to move into blood stream and through it.
  105. 105. Malignant
  106. 106. Have the ability to migrate to a secondary source
  107. 107. Can form metastastes/metastasize in secondary site
  108. 108. Cells attach to endothelium and secrete proteases that allow them to move into tissues of secondary source – extravazation, the same sort of mechanisms that immune cells use to move to another point from the capillaries
  109. 109. Metastatic
  110. 110. Tumor in a secondary site that is formed by original malignant cells
  111. 111. Cues that increase chance of secondary tumor formation in particular cell types
  112. 112. Ex: Epithelial tumors often lead to liver tumors
  113. 113. Names given to particular tumor types/types of cancers
  114. 114. Skin/epithelia = carcinomas
  115. 115. Sarcomas = muscle tissue/connective tissue
  116. 116. Leukemia/lymphoma = hematopoietic system
  117. 117. Leukemia – unrestricted growth of t cells or b cells/WBC of immune system
  118. 118. Gives rise to RBC/WBC/platelets
  119. 119. Nervous system cancers
  120. 120. Neuromas
  121. 121. Astrocytomas
  122. 122. Gliomas
  123. 123. What makes cells oncogenic/neoplastic? (oncogenic transformation)
  124. 124. Characteristics
  125. 125. Normal cells when grown in culture exhibit contact inhibition unless reached hayflick limit
  126. 126. Cancer cells do not stop dividing. Exhibit a loss of contact inhibition (will grow on top rather than on substrate = loss of contact dependence on ECM/cell adhesion for survival)
  127. 127. No signal that is mediated to tell a cell to stop dividing
  128. 128. Don’t depend on adhesions to survive whether to neighbor or substrate
  129. 129. Lack of dependence on GFs – in regulating mitosis -G1-
  130. 130. Tumorigenic cells will move through G1 checkpoint, completely independent of it
  131. 131. Rb Pi’ed > E2F is turned on > past G1 to S phase > DNA divides > Mitosis
  132. 132. Cells in the presence of GFs will move to senescence and cell growth will stop
  133. 133. Cancer cells don’t depend on GFs and as time continues, the number of cancer cells increases in a linear way. Loss of senescence (aging and death) in cancer cells
  134. 134. Disorganized cytoskeleton of mobile cells and not responding to environmental cues.
  135. 135. MT organization is very dense and doesn’t take on a particular arrangement
  136. 136. Can form adhesions and break rapidly
  137. 137. Sometimes arise from any abnormal number of chromosomes (46 for humans) = aneuploidy – (alignment of chromosomes not occurring could be one – or replicative events didn’t occur properly)
  138. 138. Chemical carcinogens
  139. 139. Within coding region for p53
  140. 140. Losing control of p53, cells have a difficult time undergoing apoptosis
  141. 141. Other sites of DNA
  142. 142. UV – Cytoseine to two thymidine – disrupts how gene functions
  143. 143. Tanning beds are UVa and UVb which are more mutagenic than just UV
  144. 144. Making immortalized cell lines
  145. 145. Mice cells undergo crisis and proliferate in culture to form an immortalized cell line that is cancerous – dividing in unrestricted way
  146. 146. Unless virally infected or DNA mutated, human cells won’t become immortalized
  147. 147. Disorganized cytoskeleton

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