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 3 4 5 Growth factor Ras GTP

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 3 4 5 Growth factor Ras GTP

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter9: Cell Communication

Section: Chapter Questions

Problem 1VCQ: Figure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is...

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Explain why in cells that are genetically NF1–/–, basal levels of GTP-bound activated Ras are higher than normal and respond to growth factor stimulation by increasing rapidly to far higher levels.
Put the following steps for the outline of the growth factor signaling pathway in order: Map Kinase Kinase is Phosphorylated Proteins involved in gene transcription are activated Growth factor binds to its receptor in the cytoplasmic membrane Receptor recruits adaptor protein and GEF Autophosphorylation of tyrosine residues on the receptor Structural change of the receptor activates Tyrosine Kinase Map Kinase Kinase Kinase is phosphorylated Ras, a small GTPase, is activated by the exchange of GTP for GDP Map Kinase is Phosphorylated Map Kinase enters the nucleus
Phorbol esters have been observed to induce the transcription of AP-1–influenced genes. Explain how this processcould occur. What are the consequences of AP-1 transcription? What role does intermittent exposure to phorbol estershave on an individual’s health?
Many malignant tumors are characterized by the activation of one or more growth-factor receptors. What is the catalytic activity associated with transmembrane growth factor receptors such as the EGF receptor?
The 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?
The output of RTK pathways is often the activation of MAP Kinase. Explain how MAPK can lead to activation of a specific subset of proteins, leading to distinct effects in different cell types in response to the same growth signal.
Describe the effects of the over-expression of mdm2 on cell proliferation and apoptosis on cell signaling pathways and metabolism or cell cycle control. Briefly explain the normal role of each component in the context of the pathway and why its loss or modification would have the expected effect.
Describe what cyclin dependent kinase does in the activation of MPF and how this relates to signal transduction.
which of hthe following would result in a persisting proliferation response to growth factor receptor activation after the ligand is no longer binding to its rceptor kinase? 1. Both a mutation that blocks the GTPas activity of Ras and a mutation that blocks the exchange of GDP with GTP would cause the response to persist. 2. a mutation that blocks the GTPas activity of Ras 3. neither a mutation that blocks the GTPas activity of Ras nor a mutation that blocks the exchange of GDP with GTP would cause the response to persist 4. a mutatiaon that blocks the exchange of GDP with GTP
When epidermal growth factor (EGF)—the ligand for the epidermal growth factor receptor (EGFR)—binds EGFR on the cell surface, the intracellular domain of the receptor changes shape into an "active state.” The receptor then induces a cascade of kinases in the cytoplasm, resulting in the activation of mitogen-activated protein kinase (MAPK). One effect of EGFR signaling is the stimulation of cell proliferation. Overactive EGFR is frequently found in cancer cells. One strategy for developing anticancer drugs is to target the overactive signaling proteins found in cancer cells. Antibodies are proteins made by immune cells that only recognize specific biomolecules, called antigens. The major component of an anticancer drug is an antibody that specifically recognizes and binds EGFR. Which of the following will most likely happen when this anticancer drug is applied to a tumor that has a high level of EGFR? Tumor cells with active EGFR will increase and MAPK activity in the tumor will…
In contrast to their similar brain abnormalities,newborn mice deficient in Apaf1 or caspase-9 have dis-tinctive abnormalities in their paws. Apaf1-deficient micefail to eliminate the webs between their developing digits,whereas caspase-9-deficient mice have normally formeddigits (Figure Q18–1). If Apaf1 and caspase-9 function inthe same apoptotic pathway, how is it possible for thesedeficient mice to differ in web-cell apoptosis?
Hormone H regulates these effects via its receptors which are found at both the cell surface (csRH) and within the cell (içRH). The signalling pathways that become activated in the presence of hormone H are depicted and described below. hormone H. H H extracellular fluid inactive GTP inactive RAS Lyn cell-surface receptor for H (csR») icR GDP RAS-GTP hexose metabolism cell survival H icR G, phase (resting) Raf HK GSK-3P MEK M G2 icR - hexose kinase ERK promoter HRE CDK1 Cyclin A nucleus cyclin A Fos A promoter Created in BioRender.com bio Signalling via the cell surface receptor Hormone H mediates its cell cycle stimulatory and pro-survival effects by binding to and activating the cell surface hormone H receptor (csRH). The activated CSRH activates Lyn, which activates RAS and ultimately the Raf/MEK/ERK kinase cascade. Active ERK: o phosphorylates and inactivates GSK-3B. Inhibition of GSK-3ß promotes cell survival. inhibits p27, preventing it from inhibiting cell cycle progression.…