A contributing factor to the development of arthritis is the inappropriate proteolytic destruction of the aggrecan component ofcartilage by the proteolytic enzyme aggrecanase. The immune system signal molecule interleukin 2 (IL-2) activatesaggrecanase; in fact, IL-2 blockers are sometimes used to treat arthritis.Studies were undertaken to determine whether inhibitors of aggrecanase could counteract the effects of IL-2. Pieces ofcartilage were incubated in media with various additions and the amount of aggrecan destruction was measured as a functionof time.What is the effect of adding IL-2 to the system?Aggrecan degradation remains the same.Aggrecanase activity is greatly reduced.Aggrecan degradation is greatly reduced.Aggrecan degradation is greatly enhanced.What is the response when an aggrecanase inhibitor is added in addition to IL-2?O Aggrecan degradation remains the same as when IL-2 was added.Aggrecan degradation completely stops.Aggrecan degradation is reduced to the background system level.Aggrecan degradation is further enhanced.

Enzymes are proteins that catalyse biochemical reactions. An enzyme's activity is a reference to the…

Answered: A contributing factor to the…

Biochemistry

9th Edition

ISBN:9781319114671

Author:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Publisher:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Chapter1: Biochemistry: An Evolving Science

Section: Chapter Questions

Problem 1P

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RTKs are receptors made of an extracellular ligand binding domain and an intracellular kinase domain (see image). Insulin binds to its RTK Insulin receptor, causing an increase in glucose absorption and storage in liver cells. EGF binds to its own RTK, EGFR and promotes cell growth through the Ras pathway. a) Explain why the same type of tyrosine kinase in two RTKs can lead to very different cellular responses. Give an example of potential cellular outputs for each of these two RTKs.
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Even in the presence of a Ras-GAP, a single amino acid change in as renders it incapable of hydrolyzing GTP. This mutation is known as Ras+ and is a cancer-causing mutation. What effect do you think this mutation will have on signaling downstream of Ras+? Why? a)A mutation would turn on the signaling pathway all of the time. b)Even if a route is mutated, it can still be turned on or off. c)Due to a mutation, the signaling pathway would always be off.
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Researchers have found that a certain signal transduction pathway, illustrated in the figure below, may be responsible for the development of cancer in pancreatic cells. In normal pancreatic cells, where the pathway remains inactive, a membrane-bound receptor called Ptc inhibits a downstream protein known as Smo. The inhibition of Smo blocks the activa- tion of a complex of proteins known as the HSC, which results in the cleaving of one of its proteins called Ci. The cleaving of Ci, in turn, prevents the pathway from initiating the syn- thesis of division-facilitating enzymes. A Ptc B Smo с inhibition D A model of a Ptc signal transduction pathway under normal conditions. HSC Ci cleavage A certain protein called the Hedgehog protein (Hh) is found to activate this signal transduction pathway and trigger uninterruptable cell division. cell division not initiated Which of the following describes the most plausible mechanism by which Hh triggers uninterruptable cell division? Hh binds to…
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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
Mutation in the fibroblast growth factor receptor (FGFR) gene results in achondroplasia (dwarfism), which is a dominant condition caused by a single base substitution (GGG>AGG) that changes the amino acid glycine at position 480 to arginine (G480R) in the FGFR protein. FGFR is normally active when FGF binds to it, but the mutant FGFR is always on to stimulate signaling that inhibits excessive bone growth. How can gene therapy be used to treat achondroplasia? Select all that apply. RNAi that knocks down the mutant FGFR expression Adeno-associated viral (AAV) vector that carries the wild-type FGFR Retroviral vector that carries the wild-type FGFR CRISPR with the wild-type FGFR donor DNA

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