When S phase CDK complexes are initially formed in G1 phase, they are bound by a protein of the class, which prevents kinase activity. This protein is then phosphorylated at multiple sites by allowing activation of the S phase CDKs.
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- Consider the following simplifieddiagram of a signal transductionpathway that regulatesprogrammed cell death inmammalian cells. Assume that thisdiagram represents the behavior ofa single cell within an organism.Key: TNF and SF are circulatingin the plasma; TNFR = TNFreceptor; SFR = SF receptor.Based on the regulatory networkdescribed above, state whethermutations that knockout each ofthe following proteins would either increase apoptosis or decrease apoptosis. TNF Bcl2 INH EFF SFR AKT TNFR SFFill in the gaps: For M-Cdk to be activated, inhibitory and activating phosphorylate the mitotic CDK, whilst an activating dephosphorylates the mitotic Cdk. O acetyltranferases, kinase O kinases, acetyltransferase O dehydrogenases, acetyltransferase O phosphatases, acetyltransferase O kinases, phosphataseFigure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is permanently activated, resulting in unregulated cell division. Lapatinib, a drug used to treat breast cancer, inhibits HER2 receptor tyrosine kinase autophosphorylation (the process by which the receptor adds phosphates onto itself), thus reducing tumor growth by 50 percent. Besides autophosphorylation, which of the following steps would be inhibited by Lapatinib? Signaling molecule binding, dimerization, and the downstream cellular response. Dimerization, and the downstream cellular response. The downstream cellular response. Phosphatase activity, dimerization, and the downsteam cellular response.
- Why doesn't Cdk1 active immediately upon binding to cyclin B? What other components of the cell’s regulatory machinery could explain the delay in activation of the kinase activity?When a signal ligand binds to the extracellular portion of the RTK receptor, in the MAP kinase pathway, what is the first kinase to be activated?At any given time, intestinal crypts of mice com-prise about 15 stem cells and 10 Paneth cells. After celldivision, which occurs about once a day, the daughtercells remain stem cells only if they maintain contact with aPaneth cell. This constant competition for Paneth-cell con-tact raises the possibility that crypts might become mono-clonal over time; that is, the crypt cells at one point in timemight derive from only 1 of the 15 stem cells that existedat some earlier time. To test this possibility, you use theso-called confetti marker that upon activation expressesany one of three fluorescent proteins in the stem cells ofthe crypt. You then examine crypts at various times todetermine whether they contain cells with multiple colorsor only one color (Figure Q22–1). Do the crypts becomemonoclonal over time or not? How can you tell?
- RAS is a signal transducer that acts as a switch for turning on cell division. Drag the descriptions below to their proper places on the figure to show the sequence of events. When growth factor binds to the receptor, the intracellular domain activates RAS by facilitating exchange of GDP for GTP. When no growth factor is bound to the extracellular receptor, RAS is bound to GDP and is inactive. RAS activates the first of three sequential kinase proteins termed the MAP kinase cascade. Cell proliferation proceeds as the machinery for cell division is set in motion. The end result of the MAP kinase cascade is activation of a transcription factor. Receptor 1 Ras GDP 2 4 5 Growth factor Ras GTPThe oscillatory clock that drives somite forma-tion in vertebrates involves three essential componentsHer7 (an unstable repressor of its own synthesis), Delta (atransmembrane signaling molecule), and Notch (a trans-membrane receptor for Delta). Notch is bound by Delta onneighboring cells, activating the Notch signaling pathway,which then activates Her7 transcription. Normally, thissystem works flawlessly to create sharply defined somites(Figure Q21–2A). In the absence of Delta, however, onlythe first five somites form normally, and the rest are poorlydefined (Figure Q21–2B). If a pulse of Delta is suppliedlater, somite formation returns to normal in the regionswhere Delta was present (Figure Q21–2C). A diagram ofthe connections between the components of the clockand how they interact in adjacent cells is shown in FigureQ21–2D. In the absence of Delta, why do the cells becomeunsynchronized? What is it about the presence of Deltathat keeps adjacent cells oscillating in synchrony?Which of the following is false about cyclin-cdk complexes? OCdk's do not have to bind to cyclin proteins for complex to be active. OCdk/cyclin complexes phosphorylates proteins required to trigger next cell cycle phase. Process acts as molecular brakes to ensure cell is ready to continue with cell cycle. O Cyclin concentrations increase gradually, but cdk must be phosphorylated by specific kinase for complex to be active
- Rous Sarcoma Virus can cause cancer in infected cells. The tumor causing nature of the virus is linked to it harbouring a gene that codes for a unique receptor tyrasine kinase (RTK). What is it about the tyrosine kinase that accounts for the tumor-causing nature of the virus? O It is unrelated to any human kinase and thus is able to act uncontrollably in causing cell division. O It cantain activate downstream effectors without binding to a SH2 domain. O It lacks the carboxy-terminal regulatory domain that is present in RTKS of non-cancerous cells.To which type of protein do cyclin – dependent kinases bind to become active?i) For serotonin receptor associated with the G protein class of subtype Gs, list the various ways how cell signalling can be terminated at stage 0 and 2 shown in Figure 1. 1 Reception ExtracellularA Hama Membra ely Malecle 2 Transduction 3 Response At Select by putting an arrow at the end of the correct choice(s). 2 a) - ) Cytoplase