Cell cycle figure

The concept of the cell cycle (Figure 1-1-2) can be used to describe the timing of some of these events in a eukaryotic cell. The M phase (mitosis) is the time in which the cell divides to form two daughter cells. Interphase is the term used to describe the time between two cell divisions or mitoses. Gene expression occurs throughout all stages of interphase. Interphase is subdivided as follows ... 

The morphology and growth properties of tumor cells clearly differ from those of their normal counterparts some of these differences are also evident when cells are cultured. That mutations cause these differences was conclusively established by transfection experiments with a line of cultured mouse fibroblasts called 3T3 cells. These cells normally grow only when attached to the plastic surface of a culture dish and are maintained at a low cell density. Because 3T3 cells stop growing when they contact other cells, they eventually form a monolayer of well-ordered cells that have stopped proliferating and are In the quiescent Gq phase of the cell cycle (Figure 23-3a). 

BOTH NADPH AND ATP ARE NEEDED BY THE CELL, BUT RmOSE-5-P IS NOT Under some conditions, both NADPH and ATP must be provided in the cell. This can be accomplished in a series of reactions similar to case 3, if the fructose-6-P and glyceraldehyde-3-P produced in this way proceed through glycolysis to produce ATP and pyruvate, which itself can yield even more ATP by continuing on to the TCA cycle (Figure 23.40). The net reaction for this alternative is... 

For type 3 processes, growth and metabolic activity reach a maximum early in the batch process cycle (Figure 3.1) and it is not until a later stage, when oxidative activity is low, that maximum desired product formation occurs. The stoichiometric descriptions for both type 3 and 4 processes depend upon the particular substrates and products involved. In the main, product formation in these processes is completely uncoupled from cell growth and dictated by kinetic regulation and activity of cells. 

Figure 3. Charge and discharge curves of an Li/Li[Li0jMn, 9]04 cell cycled at voltages between 3.0 and 4.4V at a rate of 0.1 mAcnT2 at 30 °C. To describe the composition of an Li-Mn-O ternary phase a defect-spinel formulation was assumed.

Cell Cycle Control. Figure 1 Cell cycle regulation by Cyclin dependent kinases (CDKs). Different cyclins bound to different CDKs promote the transition from one cell cycle phase into another. CDK-dependent phosphorylation of Rb is required to release active E2F transcription factors, which promotes entry into S phase. 

Cell Cycle Control. Figure 3 The DNA damage checkpoint. In response to DNA damage cells activate p53 dependent and independent checkpoint pathways leading to cell cycle arrest at G1/S and G2/M allowing DNA repair. If the cellular damage cannot be repaired, cells can initiate apoptosis. 

Figure 36-21. Schematic illustration of the points during the mammalian cell cycle during which the indicated cyclins and cyclin-dependent kinases are activated. The thickness of the various colored lines is indicative of the extent of activity.

Figure 1. The cell cycle as a Cdc2 cycle. Progression through the eukaryotic cell cycle is sensitive to the phosphorylation state of Cdc2. A block to DNA synthesis (S) prevents dephosphorylation, and hence activation, of Cdc2. Impaired spindle function will prevent deactivation of Cdc2 and thus blocks exit from M phase (Hoyt et al., 1991 Li and Murray, 1991 reviewed in Nurse, 1991). Exit from M phase requires destruction of the regulatory subunit, Cyc B. Dephosphorylation of Cdc2 at thr-161 may act to destabilize the Cdc2/Cyc B complex and thus allow the ubiquitination of Cyc B followed by its destruction.

Figure 5.14 The transferrin to cell cycle. (From Crichton, 1991.)...

---