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.Aggrecan degradation was measured by the release of glycosaminoglycan. What is the rationale for this assay?Aggrecan is a transferase enzyme that adds glycosaminoglycans to glycoproteins, and these glycosaminoglycans remainfree if aggrecan is degraded.Aggrecan is a lectin that binds glycosaminoglycan ligands, and aggrecan releases these glycosaminoglycans as itis degraded.Aggrecan inhibits the removal of glycosaminoglycans from proteoglycans, and aggrecan degradation allows thisremoval to proceed.Aggrecan is heavily decorated with glycosaminoglycans, and the release of these glycosaminoglycans is a sign ofaggrecan degradation. Why might glycosaminoglycan release not indicate aggrecan degradation?Glycosaminoglycans are hydrogen bonded to aggrecan and may dissociate from aggrecan at high temperatures.Another enzyme might be present that cleaves glycosaminoglycans from aggrecan without degrading aggrecan.Glycosaminoglycan release also occurs with the degradation of glycogen in animal tissues.O Aggrecanase may degrade the glycosaminoglycans of aggrecan without degrading the protein component.

An assay is a biochemical lab procedure to determine the quantity of molecules of interest in a…

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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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A contributing factor to the development of arthritis is the inappropriate proteolytic destruction of the aggrecan component of cartilage by the proteolytic enzyme aggrecanase. The immune system signal molecule interleukin 2 (IL-2) activates aggrecanase; 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 of cartilage were incubated in media with various additions and the amount of aggrecan destruction was measured as a function of 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…
Identify two ways in which IL-1β is regulated so as to minimize its destructive potential in the human body.
Muckle–Wells syndrome is an autosomal dominantly inherited disease due to mutations in NLRP3. Individuals with this disease suffer from episodes of fever, as well as urticarial rash, joint pains, and conjunctivitis. What is the explanation for the beneficial effects of anakinra (IL-1 receptor antagonist) treatment in these patients?
true or false Human ILC3 can be further divided into two subsets based on expression of the natural cytotoxicity receptor (NCR) NKp44. NCR + ILC3 are cellular sources of the tissue protective cytokine IL-22.
The first JAK kinase inhibitor to be developed, tofacitinib, inhibits JAK1 and JAK3. These two JAK kinases are required for the signaling pathways induced by multiple cytokines, including all of the receptors that share the cytokine receptor common gamma chain (gc; includes the receptors for IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21), all of the receptors that share gp130 (includes the receptor for IL-6), the receptors for GM-CSF, IL-12, and IL-23, and both type I and type II (i.e., IFN-g) interferon receptors. Tofacitinib has recently been shown to be effective in the treatment of severe rheumatoid arthritis, an autoimmune disease characterized by inflammation of the joints with prominent inflammatory cell infiltrates, autoantibodies, and eventual cartilage and bone destruction. A likely explanation for the therapeutic benefits of tofacitinib in this disease is: Its ability to inhibit the T cell functions that eventually lead to other disease symptoms Its ability to prevent T cell…
Which of the following epidermal growth factor (EGF) receptors cannot bind ligands but will form heterodimers with other EGFs? O HER2 (mouse Erb2) HER3 (mouse Erb3) O HER1 (mouse Erb1) O HER4 (mouse Erb4)
Nearly all immune deficiency diseases that result in impaired TH17 and ILC3 function lead to chronic mucocutaneous candidiasis (CMC), usually accompanied by increased susceptibility to pyogenic bacterial infections. However, a subset of these patients also show increased susceptibility to intracellular bacterial infections, such as those caused by Mycobacteria species. What is the explanation for why some, but not all, of these patients have increased susceptibility to intracellular bacteria and which patients fall into this category?
Can anyone suggest a way of increasing phosphorylation of IKK alpha (Ser176/180)? Any potent phosphatase inhibitor in combination with TNF alpha?
Can you please explain the Mechanism of action of Sertraline? Please answer at your own easy words. Answer should be to the point. Please don't use AI for answering this question.
The MARCH-1 E3-ubiquitin ligase is expressed in B cells, dendritic cells, and macrophages. The pathway regulated by MARCH-1 is targeted by some pathogens in an immune evasion strategy. In this strategy, the pathogens encode a protein that binds to MARCH-1 and inhibits its function. OOOO a protein that is induced by IL-10 in macrophages and dendritic cells. a protein that induces degradation of MARCH-1. a protein that mimics MARCH-1 and functions similarly.
When consumed in small amounts, vitamin E can protect against ROS. However, when it is taken in excessive amounts, vitamin E can make the body more susceptible to ROS. Explain.
NCR- ILC3 make up one of the most frequent ILC subsets in the human peripheral blood, while NCR+ ILC3 are virtually absent in the circulation during homeostasis. Importantly, the healthy human intestine hosts dominantly NCR+ILC3, which have been shown to be essential in maintaining gut homeostasis. The signature cytokine of NCR+ ILC3 is IL-22. ILC3 in mice sense their environment and control gut defense as part of a glial-ILC3-epithelial cell unit orchestrated by neurotrophic factors. Enteric ILC3 express the neuroregulatory receptor RET. ILC3-autonomous Ret ablation led to decreased innate interleukin-22 (IL-22), impaired epithelial reactivity, dysbiosis and increased susceptibility to bowel inflammation and infection. Does this this complex neuro immune cross talk in the intestine account for the NCR ILC3 cells producing IL-22 while no such associations exist in the circulation where the ILC3 cells are NCR- and produce IL-17? maybe O yes O no

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