2. Like hemidesmosomes because they involved the formation of plaques on the cytoplasmic side of membrane and link/organize keratans or intermediate filaments
3. Difference: different types of transmembrane proteins interacting with one another in a homophylic way to link the PM together
25. Directly associates with the keratan flaments/intermediate filaments and organizes them on these lateral sides of the PM
26. Keratan filaments are then organized at these sites where plaques are formed as desmosomes assemble between cells
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)
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
102. Don’t have to mecome malignant necessarily, form metasteses (1/1000 cells that has become neoplastic can become metastatic
103. Can form a tumor, often clonal – arising from a SINGLE cell, which most cancers are often from
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.
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
125. Normal cells when grown in culture exhibit contact inhibition unless reached hayflick limit
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. No signal that is mediated to tell a cell to stop dividing
128. Don’t depend on adhesions to survive whether to neighbor or substrate
131. Rb Pi’ed > E2F is turned on > past G1 to S phase > DNA divides > Mitosis
132. Cells in the presence of GFs will move to senescence and cell growth will stop
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
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)