Campbell Biology in Focus (2nd Edition)
2nd Edition
ISBN: 9780321962751
Author: Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, Jane B. Reece
Publisher: PEARSON
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Textbook Question
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 (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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- DO NOT COPY IN GOOGLE OR BARTLEBY QUESTIONS: - WHEN do you think apoptosis occurs in humans? - What would be the effect if apoptosis doesn't happen? EXPLAIN YOUR ANSWER.arrow_forwardcells undergo programmed cell death. Write out the pathway(s), noting the changes (e.g., localization, phosphorylation, activation) When mammalian cells are irradiated, they stop dividing by arresting at cell cycle checkpoint. If the damage persists, the kinase (CdK), Cdk inhibitor, cytochrome c, DNA damage, mitochondria, p53, phosphorylation, transcription. each step. Include: apoptosis, apoptosome, ATM, pro-apoptotic proteins, caspase, Checkpoint Kinase (Chk), cyclin, cyclin-dependearrow_forwardPredict 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_forward
- Illustrate a complete cell signaling cascade from signal to response. Each protein in the pathways must be shown. You can choose either a GPCR or an RTK mediated pathway.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_forward27) Fill in the blanks Cells adjacent to one another frequently communicate through Other forms of cell-cell communication through In extracellular signaling ligand-receptor interaction induce; 28) Cell-to-cell communication by extracellular signaling usually involves six steps , sort the below given steps according to happening order; Removal of the signal, which usually terminates the cellular response – degradation of ligand- A change in cellular metabolism, function, or development CELLULAR RESPONSE triggered by the receptor-ligand complex – specific to the ligand-receptor complex Release of the signaling molecule by the signaling cell Transport of the signal to the target cell Synthesis of the signaling molecule by the signaling cell Detection of the signal by a specific receptor protein (receptor-ligand specificity 29) Polyethylene can be obtained in two different forms. High-density polyethylene (0.94 g/cm3) is a linear polymer. Low-density polyethylene (0.92 g/cm3) is a…arrow_forward
- compare and contrast how GPCRs and RTKs transduce their signal to the cell? include the types of ligands they bind, the GTP binding protein that is activated, and how the signal is transduced and amplified. what effects does it have on the cell?arrow_forwardTo examine: whether the statement “in the regulation of molecular switches, protein kinases and guanine nucleotide exchange factors (GEFS) always turn proteins on, whereas protein phosphatases and GTPase-activating proteins (GAPS) always turn proteins off" is true or false.arrow_forwardMechanistic 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_forward
- Match 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_forwardDiscuss two-three ways that kinases/phosphatases OR proteasomes ensures proper rates of cell division.arrow_forward
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