Becker's World of the Cell (9th Edition)
9th Edition
ISBN: 9780321934925
Author: Jeff Hardin, Gregory Paul Bertoni
Publisher: PEARSON
expand_more
expand_more
format_list_bulleted
Question
Chapter 23, Problem 23.7PS
(a)
Summary Introduction
To describe: The time taken in the activation of maximal Ras.
Introduction: Ras activation can be defined as “the increase in the active GTP protein which is bound to the ligand.” The “Ras proteins” comprises of low molecular weight
(b)
Summary Introduction
To explain: The reason behind the decline in the activity of Ras.
Introduction: Ras activation can be defined as “the increase in the active GTP protein which is bound to the ligand.” The “Ras proteins” comprises of low molecular weight nucleotides of guanine-binding proteins that contribute to the cellular growth and differentiation.
Expert Solution & Answer
Want to see the full answer?
Check out a sample textbook solutionStudents have asked these similar questions
Please help me with this question. More than one answer may be correct. THe graph relating to the information is included below.
In the above figure, a wild-type plant and a plant with a atg5 knockout, which prevents autophagy within the cell, are examined for the number of peroxisomes per micrograph image taken of the plant's leaves. Which of the following are true.
Options:
The atg5 plants have elevated levels of malate
The atg5 plants appear less able to destroy old organelles
The atg5 plants may have a modified ability to deal with phosphoglycolate
The atg5 plants may have a modified ability to deal with oxygen free radicals
The atg5 plants appear more able to destroy old organelles
CTP inhibits ATCase; however, the inhibition is not complete. Can you suggest another molecule that might enhance the inhibition of ATCase?
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.
Chapter 23 Solutions
Becker's World of the Cell (9th Edition)
Ch. 23 - One effect of the hormone insulin is to cause...Ch. 23 - You are working on a new species of sea urchin...Ch. 23 - The Ca2+ concentration in unstimulated cells is...Ch. 23 - Prob. 23.3CCCh. 23 - Prob. 23.4CCCh. 23 - Prob. 23.5CCCh. 23 - Chemical Signals and Second Messengers. Fill in...Ch. 23 - QUANTITATIVE Pure agony. Agonists are drugs that...Ch. 23 - Heterotrimeric and Monomeric G Proteins. G...Ch. 23 - Calcium Chelators and Ionophores. In addition to...
Knowledge Booster
Learn more about
Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biology and related others by exploring similar questions and additional content below.Similar questions
- Please help me with this question. More than one answer may be correct. THe graph relating to the information is included below. In the two figures, a wild-type plant and a plant with a atg5 knockout, which prevents autophagy within the cell, are compared. The first figure shows the number of peroxisomes per micrograph image taken of the plant's leaves. The bottom figure shows a comparison of 3-week seedlings of the wild-type plant and the atg5 plant at normal CO2 levels (360 ppm) and elevated CO2 (2000 ppm) Which of the following are true. Question 20 options: the atg5 knockout plants are more able to deal with photorespiration the atg5 knockout plants are less able to deal with photorespiration the inability to recycle peroxisomes through autophagy impairs a plants ability to deal with photorespiration Elevated CO2 overcomes the photorespiration impairment in atg5 plants Elevated CO2 overcomes the photorespiration impairment in wild-type plantsarrow_forward1a. Contrast the activation of cytokine receptors to the activation of receptor threonine kinases. b. We discovered a new cytokine that stimulates cancer cell growth. Now we want to determine if the JAK/STAT pathway is activated after stimulation. In the lab we have a small molecule that can competitively bind to SH2 domains. Explain where and how in the pathway this inhibitor would be effective.arrow_forwardWhich ONE of these statements is the most accurate definition of the mode of action of imatinib? Select one: A.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks phosphatase activity by competing with adenosine triphosphate (ATP) binding B.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks tyrosine kinase activity by competing with adenosine triphosphate (ATP) binding C.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks tyrosine kinase activity by interaction with the enzyme site D.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks phosphatase activity by interaction with the enzyme sitearrow_forward
- Part A (Short Response): You are developing a TGF-β agonist, but you don’t yet know which specific proteins it is signaling through. You want to do a single Western blot to measure changes in signaling activity, regardless of which pathway is being activated. For which protein involved in these pathways could you measure the levels in the nucleus of cells and be confident in your results? Why? This part was already posted on chegg, but I didn't understand the answer. I need a thorough explanation, so I can fully understand. Part B (Short Response): There have been many attempts to block TGF-β signaling in cancer through many different mechanisms, but none of been very successful. Why do you think this is? I know they have gotten close to being successful, but I don't know what preventing their success.arrow_forwardPlease provide a good explanation. If the independent variable (IGF-1) is increasing, what would happen to the dependent variable (GHRH)arrow_forwardDescribe the major activity and possible localization of the three major subgroups of proteins that remodel or degrade the ECM in physiological or pathological tissue remodeling. Identify a pathological condition in which these proteins play a key role.arrow_forward
- The egfr kinase independent transactivation of the ras pathway does require egfr. Explain this apparent contradiction.arrow_forwardThe Pathway presented shows you how the pathway is regulated with a Ras-GEF. Explain how adding a Ras-GAP to the cell would A) specifically affect the molecules of the signaling pathway and B) affect the response of the cell.arrow_forwardDescribe the intracellular, biochemical downstream signal cascade that results from the binding of menthol to TRPM8arrow_forward
- GTP binding proteins are molecular switches. How do GTP binding proteins work? Provide two examples of GTP binding proteins that function in intracellular protein transport. Make a drawing that illustrates the function of each of these proteins in their respective roles. Predict the direct outcome of a mutation that: Inhibits GTPase activity Inhibits interaction with the GEFarrow_forward. Suggest the effects of each of the following mutations on the physio- logical role of chymotrypsinogen: (a) R15S (b) Cis (c) T147Sarrow_forwardGTP-binding proteins play critical roles in many signal transductions through G proteins. Describe two examples in which G proteins act and compare the role of the G proteins in each case.arrow_forward
arrow_back_ios
SEE MORE QUESTIONS
arrow_forward_ios
Recommended textbooks for you
- BiochemistryBiochemistryISBN:9781305577206Author:Reginald H. Garrett, Charles M. GrishamPublisher:Cengage Learning
Biochemistry
Biochemistry
ISBN:9781305577206
Author:Reginald H. Garrett, Charles M. Grisham
Publisher:Cengage Learning
What are Mutations and what are the different types of Mutations?; Author: Science ABC;https://www.youtube.com/watch?v=I16YlE8qTBU;License: Standard youtube license