Campbell Biology in Focus, Books a la Carte Edition; Modified Mastering Biology with Pearson eText - ValuePack Access Card - for Campbell Biology in Focus (2nd Edition)
2nd Edition
ISBN: 9780134433769
Author: Lisa A. Urry, Michael L. Cain, Steven A. Wasserman
Publisher: PEARSON
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Chapter 16, Problem 8TYU
FOCUS ON ORGANIZA-ION
The property of life emerges at the biological level of the cell. The highly regulated process of apoptosis is not simply the destruction of a cell; it is also an emergent property. In a short essay (about 100‒150 words), briefly explain the role of apoptosis in the development and proper functioning of an animal and describe how this form of programmed cell death is a process that emerges from the orderly integration of signaling pathways.
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Chapter 16 Solutions
Campbell Biology in Focus, Books a la Carte Edition; Modified Mastering Biology with Pearson eText - ValuePack Access Card - for Campbell Biology in Focus (2nd Edition)
Ch. 16.1 - Prob. 1CCCh. 16.1 - MAKE CONNECTIONS Explain how the signaling...Ch. 16.1 - How do fruit fly maternal effect genes determine...Ch. 16.2 - Deitys egg donor and surrogate mother were...Ch. 16.2 - WHAT IF? If you were a doctor who wanted to use...Ch. 16.3 - Prob. 1CCCh. 16.3 - Prob. 2CCCh. 16.3 - Prob. 3CCCh. 16 - Muscle cells differ from nerve cells mainly...Ch. 16 - Cell differentiation always involves A. the...
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- Predict the effects of the following mutations on the ability of a cell to undergo apoptosis:a. Mutation in Bad such that it cannot be phosphorylated by protein kinase B (PKB)b. Overexpression of Bcl-2c. Mutation in Bax such that it cannot form homodimersOne common characteristic of cancer cells is a loss of function in the apoptotic pathway. Which of the mutations listed above might you expect to find in some cancer cells?arrow_forwardRAS 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 GTParrow_forwardpart 3 of 3: along with how it is being transported or further processed until it reaches its final destination Protein: B-hexoaminidase Location: Lysosomearrow_forward
- In a cell that is signaled to undergo apoptosis, the caspase cascade is initiated ("turned ON") by promoting transcription of caspase MRNA in the nucleus. proteolytic cleavage of a procaspase. O phosphorylation of a caspase. O release of caspase from the mitochondria.arrow_forwardPart 1 of 2: Starting from the mRNA that is produced and released into the cytosol, describe in detail how the protein is translated and where this occurs Protein : B-hexoaminidase Location: Lysosomearrow_forwardA cell is actively undergoing cell signaling. Random cytoplasm samples are taken at 10 ms intervals and their contents have all proteins inactivated. The samples are stained for phosphates attached to proteins. What pattern would you observe? Proteins maintain their phosphates throughout all of the samples There is a cycle of phosphorylation and dephosphorylation that occurs at regular intervals Proteins maintain a lack of phosphates throughout all of the samples Proteins start off being phosphorylated and then lose the phosphatesarrow_forward
- Mechanistic target of rapamycin (mTOR) is a protein kinase that is a central regulator of cell division and cellular metabolism. Activated mTOR phosphorylates several protein targets, this activates pathways that lead to increased energy utilization, increased cell division and decreased apoptosis (cell death). Over-activation of mTOR is associated with several types of human cancer. In healthy cells, signaling downstream of growth factor receptors leads to the activation of PI3 kinase (PI3K), which phosphorylates lipid targets such as PIP2, forming PIP3. These lipids recruit a kinase called AKT to the cell membrane, where it is phosphorylated and activated. In turn, AKT phosphorylates and inactivates PRAS40. PRAS40 is normally bound to mTOR, inhibiting its activity. Thus, inactivation of PRAS40 activates mTOR. A schematic of this signaling pathway is shown below. Which of the following mutations is most likely to increase activation of mTOR? a mutation that decreases the activity of…arrow_forwardMatch each of the changes that can contribute to cancer with its correct description. Loss of function of regulators that send old or damaged cells into apoptosis Hyperactivation of signalling pathways that tell the cell to grow and divide 1. Sustaining proliferative signalling Loss of function of structural proteins that anchor cells to surrounding tissue and/or activation of cell migration 2. Evading growth suppressors 3. Activating invasion and metastasis Loss of function of 4. Enabling replicative immortality regulators that stop inappropriate growth and cell division 5. Inducing angiogenesis 6. Resisting cell death Loss of function of regulators that force aging cells to exit the cell cycle and enter GO or replicative senescence 00arrow_forwardSignaling pathways often require receptor dimers to become active. What would be an advantage of the extrinsic apoptosis pathway requiring a trimer? I note from the article "Nature Reviews, Cancer 16:539, 2016" the following: The extrinsic apoptotic pathway, upon binding to their cognate ligand, death receptors such as tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) receptor (TRAILR) and FAS can activate initiator caspases (caspase-8 and caspase-10) through dimerization mediated by adaptor proteins such as FAS-associated death domain protein (FADD). Active caspase-8 and caspase-10 then cleave and activate the effector caspase-3 and caspase-7, leading to apoptosis. I can't think of any other pathway that uses a trimer, so there must be a reason. Glad an exprt can help.arrow_forward
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