Relevant bibliographies by topics / Cytokinin degradation

Academic literature on the topic 'Cytokinin degradation'

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Published: 9 March 2023

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Journal articles on the topic "Cytokinin degradation"

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Avalbaev, A. M., K. A. Somov, R. A. Yuldashev, and F. M. Shakirova. "Cytokinin oxidase is key enzyme of cytokinin degradation." Biochemistry (Moscow) 77, no. 12 (December 2012): 1354–61. http://dx.doi.org/10.1134/s0006297912120024.

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Frébortová, Jitka, and Ivo Frébort. "Biochemical and Structural Aspects of Cytokinin Biosynthesis and Degradation in Bacteria." Microorganisms 9, no. 6 (June 16, 2021): 1314. http://dx.doi.org/10.3390/microorganisms9061314.

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It has been known for quite some time that cytokinins, hormones typical of plants, are also produced and metabolized in bacteria. Most bacteria can only form the tRNA-bound cytokinins, but there are examples of plant-associated bacteria, both pathogenic and beneficial, that actively synthesize cytokinins to interact with their host. Similar to plants, bacteria produce diverse cytokinin metabolites, employing corresponding metabolic pathways. The identification of genes encoding the enzymes involved in cytokinin biosynthesis and metabolism facilitated their detailed characterization based on both classical enzyme assays and structural approaches. This review summarizes the present knowledge on key enzymes involved in cytokinin biosynthesis, modifications, and degradation in bacteria, and discusses their catalytic properties in relation to the presence of specific amino acid residues and protein structure.
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Nedvěd, Daniel, Petr Hošek, Petr Klíma, and Klára Hoyerová. "Differential Subcellular Distribution of Cytokinins: How Does Membrane Transport Fit into the Big Picture?" International Journal of Molecular Sciences 22, no. 7 (March 26, 2021): 3428. http://dx.doi.org/10.3390/ijms22073428.

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Cytokinins are a class of phytohormones, signalling molecules specific to plants. They act as regulators of diverse physiological processes in complex signalling pathways. It is necessary for plants to continuously regulate cytokinin distribution among different organs, tissues, cells, and compartments. Such regulatory mechanisms include cytokinin biosynthesis, metabolic conversions and degradation, as well as cytokinin membrane transport. In our review, we aim to provide a thorough picture of the latter. We begin by summarizing cytokinin structures and physicochemical properties. Then, we revise the elementary thermodynamic and kinetic aspects of cytokinin membrane transport. Next, we review which membrane-bound carrier proteins and protein families recognize cytokinins as their substrates. Namely, we discuss the families of “equilibrative nucleoside transporters” and “purine permeases”, which translocate diverse purine-related compounds, and proteins AtPUP14, AtABCG14, AtAZG1, and AtAZG2, which are specific to cytokinins. We also address long-distance cytokinin transport. Putting all these pieces together, we finally discuss cytokinin distribution as a net result of these processes, diverse in their physicochemical nature but acting together to promote plant fitness.
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Chen, CM, G. Jin, BR Andersen, and JR Ertl. "Modulation of Plant Gene Expression by Cytokinins." Functional Plant Biology 20, no. 5 (1993): 609. http://dx.doi.org/10.1071/pp9930609.

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Cytokinins play important roles in plant growth and development. They regulate the synthesis or degradation of proteins and nucleic acids. Specific mRNAs and proteins are up- and down-regulated by the hormones. Regulation of plant gene expression by cytokinins is at the levels of transcription and post-transcription. Expression of a single gene can be modulated by the interaction of two hormones since the levels of cytokinin-enhanced nitrate reductase transcript are reduced by abscisic acid. Relatively high-affinity cytokinin-binding proteins have been isolated, but the physiological role of the binding proteins remains unknown. Examination of X-ray crystal structures of cytokinin molecules indicates that correct stereochemical conformation is required for a biologically active cytokinin. Using available genetic, immunological, biochemical and recombinant DNA techniques, some questions regarding the mechanisms of cytokinin action may be answered in the near future.
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Frebort, I., M. Kowalska, T. Hluska, J. Frebortova, and P. Galuszka. "Evolution of cytokinin biosynthesis and degradation." Journal of Experimental Botany 62, no. 8 (February 14, 2011): 2431–52. http://dx.doi.org/10.1093/jxb/err004.

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Berková, Veronika, Michaela Kameniarová, Vladěna Ondrisková, Miroslav Berka, Simona Menšíková, Romana Kopecká, Markéta Luklová, et al. "Arabidopsis Response to Inhibitor of Cytokinin Degradation INCYDE: Modulations of Cytokinin Signaling and Plant Proteome." Plants 9, no. 11 (November 13, 2020): 1563. http://dx.doi.org/10.3390/plants9111563.

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Cytokinins are multifaceted plant hormones that play crucial roles in plant interactions with the environment. Modulations in cytokinin metabolism and signaling have been successfully used for elevating plant tolerance to biotic and abiotic stressors. Here, we analyzed Arabidopsis thaliana response to INhibitor of CYtokinin DEgradation (INCYDE), a potent inhibitor of cytokinin dehydrogenase. We found that at low nanomolar concentration, the effect of INCYCE on seedling growth and development was not significantly different from that of trans-Zeatin treatment. However, an alteration in the spatial distribution of cytokinin signaling was found at low micromolar concentrations, and proteomics analysis revealed a significant impact on the molecular level. An in-depth proteome analysis of an early (24 h) response and a dose-dependent response after 168 h highlighted the effects on primary and secondary metabolism, including alterations in ribosomal subunits, RNA metabolism, modulations of proteins associated with chromatin, and the flavonoid and phenylpropanoid biosynthetic pathway. The observed attenuation in stress-response mechanisms, including abscisic acid signaling and the metabolism of jasmonates, could explain previously reported positive effects of INCYDE under mild stress conditions.
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Werner, T., I. Köllmer, I. Bartrina, K. Holst, and T. Schmülling. "New Insights into the Biology of Cytokinin Degradation." Plant Biology 8, no. 3 (May 2006): 371–81. http://dx.doi.org/10.1055/s-2006-923928.

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Acheampong, Atiako Kwame, Carly Shanks, Chia-Yi Cheng, G. Eric Schaller, Yasin Dagdas, and Joseph J. Kieber. "EXO70D isoforms mediate selective autophagic degradation of type-A ARR proteins to regulate cytokinin sensitivity." Proceedings of the National Academy of Sciences 117, no. 43 (October 13, 2020): 27034–43. http://dx.doi.org/10.1073/pnas.2013161117.

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The phytohormone cytokinin influences many aspects of plant growth and development, several of which also involve the cellular process of autophagy, including leaf senescence, nutrient remobilization, and developmental transitions. The Arabidopsis type-A response regulators (type-A ARR) are negative regulators of cytokinin signaling that are transcriptionally induced in response to cytokinin. Here, we describe a mechanistic link between cytokinin signaling and autophagy, demonstrating that plants modulate cytokinin sensitivity through autophagic regulation of type-A ARR proteins. Type-A ARR proteins were degraded by autophagy in an AUTOPHAGY-RELATED (ATG)5-dependent manner, and this degradation is promoted by phosphorylation on a conserved aspartate in the receiver domain of the type-A ARRs. EXO70D family members interacted with type-A ARR proteins, likely in a phosphorylation-dependent manner, and recruited them to autophagosomes via interaction of the EXO70D AIM with the core autophagy protein, ATG8. Consistently, loss-of-function exo70D1,2,3 mutants exhibited compromised targeting of type-A ARRs to autophagic vesicles, have elevated levels of type-A ARR proteins, and are hyposensitive to cytokinin. Disruption of both type-A ARRs and EXO70D1,2,3 compromised survival in carbon-deficient conditions, suggesting interaction between autophagy and cytokinin responsiveness in response to stress. These results indicate that the EXO70D proteins act as selective autophagy receptors to target type-A ARR cargos for autophagic degradation, demonstrating modulation of cytokinin signaling by selective autophagy.
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Frébortová, Jitka. "Function of plant defense secondary metabolite in cytokinin degradation." Plant Signaling & Behavior 5, no. 5 (May 2010): 523–25. http://dx.doi.org/10.4161/psb.10965.

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Chi, Wei, Jing Li, Baoye He, Xin Chai, Xiumei Xu, Xuwu Sun, Jingjing Jiang, et al. "DEG9, a serine protease, modulates cytokinin and light signaling by regulating the level of ARABIDOPSIS RESPONSE REGULATOR 4." Proceedings of the National Academy of Sciences 113, no. 25 (June 6, 2016): E3568—E3576. http://dx.doi.org/10.1073/pnas.1601724113.

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Cytokinin is an essential phytohormone that controls various biological processes in plants. A number of response regulators are known to be important for cytokinin signal transduction. ARABIDOPSIS RESPONSE REGULATOR 4 (ARR4) mediates the cross-talk between light and cytokinin signaling through modulation of the activity of phytochrome B. However, the mechanism that regulates the activity and stability of ARR4 is unknown. Here we identify an ATP-independent serine protease, degradation of periplasmic proteins 9 (DEG9), which localizes to the nucleus and regulates the stability of ARR4. Biochemical evidence shows that DEG9 interacts with ARR4, thereby targeting ARR4 for degradation, which suggests that DEG9 regulates the stability of ARR4. Moreover, genetic evidence shows that DEG9 acts upstream of ARR4 and regulates the activity of ARR4 in cytokinin and light-signaling pathways. This study thus identifies a role for a ubiquitin-independent selective protein proteolysis in the regulation of the stability of plant signaling components.
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Dissertations / Theses on the topic "Cytokinin degradation"

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Pilkington, Sarah Mary. "The regulation of chlorophyll levels in maturing kiwifruit." Thesis, University of Canterbury. School of Biological Sciences, 2012. http://hdl.handle.net/10092/7478.

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The chlorophyll degradation pathway is central to a number of plant processes including senescence and fruit ripening. However, the regulation of the chlorophyll degradation pathway enzymes is not well understood. The aim of this thesis was to elucidate the genetic mechanisms that control changes in pigment composition leading to fruit flesh yellowing in kiwifruit. Actinidia deliciosa and A. chinensis fruit, which are green and yellow, respectively, provide an opportunity to study the regulation of chlorophyll levels. The expression of genes that code for enzymes of the chlorophyll and cytokinin metabolic pathways was measured using qRT-PCR. Candidates for chlorophyll degradation regulatory points were then characterised for functionality by transient transformation in N. benthamiana. The endogenous cytokinin levels were measured in kiwifruit and transient activation assays were carried out with the promoters of key candidate genes. Overall, expression of the chlorophyll degradation genes was elevated in yellow fruit and expression of biosynthetic genes was higher in green fruit. The chlorophyll degradation-associated protein, STAY-GREEN2 (SGR2), was more highly expressed in yellow fruit, and transient over-expression of SGR was sufficient to drive chlorophyll degradation. Expression of isopentenyl transferase (IPT), the rate-limiting step for cytokinin biosynthesis, showed an increase towards maturity in green fruit, but not in yellow fruit. However, both fruit had similar high levels of cytokinin nucleotides and free bases. A gene coding for O-glucosylation was also highly expressed in green fruit. Green fruit contained higher levels of cytokinin O-glucosides and ribosides towards maturity, suggesting differences in cytokinin signalling, which could lead to regulation of chlorophyll levels via activation of the SGR promoter by transcription factors. It is likely that the chlorophyll degradation pathway and cytokinin metabolism are linked. The differential expression of cytokinin response regulators could lead to differential regulation of cytokinin levels in the fruit of the two species, and possibly differential regulation of the chlorophyll degradation pathway. Progress towards elucidation of the control of chlorophyll levels provides knowledge of this key process in kiwifruit and potentially gene-based markers for breeding new kiwifruit cultivars.
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DI, MARZO MAURIZIO. "THE MADS-DOMAIN SEEDSTICK PLAYS FUNDAMENTAL ROLES DURING TRANSMITTING TRACT DEVELOPMENT AND FRUIT GROWTH IN ARABIDOPSIS THALIANA." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/717626.

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The MADS-box gene SEEDSTICK (STK) controls several aspects of plant reproduction. STK is co-expressed with CESTA (CES), a basic Helix-Loop-Helix (bHLH) transcription factor-encoding gene. CES was reported to control redundantly with the brassinosteroid positive signaling factors BRASSINOSTEROID ENHANCED EXPRESSION1 (BEE1) and BEE3 the transmitting tract development. Through the characterization of the stk ces-2 double mutant, we observed that STK and CES act together in the regulation of transmitting tract development. Combining the stk with ces-2 bee1 bee3 we have obtained the quadruple mutant showed a clear increase of the unfertilized ovules and septum defects. In the quadruple mutant carpel fusion was compromised, causing the formation of holes at the center of the septum where transmitting tract differentiates. These phenotypes do not allow a proper pollen tube growth in the double mutant stk ces-2, and even more in the quadruple mutant bee1 bee3 stk ces-2 leading to high number of unfertilized ovules. The transcriptome profile of the quadruple mutant bee1 bee3 stk ces-2 compared to wild type revealed a small subset of misregulated genes, which probably act downstream of the transcription factor described above, mainly involved in cell death, the extracellular matrix of the transmitting tract, cell wall composition and auxin signaling. This specific subset of downstream target genes controlled directly or indirectly by STK-CES-BEE1-BEE3 protein complex, open doors to a new regulatory network controls transmitting tract development. Altogether our data reveal new insights in the regulation of transmitting tract development together by bHLH and MADS-box transcription factors.
Upon fertilization, the ovary increases in size and undergoes a complex developmental process to become a fruit. The fruit of Arabidopsis thaliana is named silique. We show that cytokinins (CK), required to define ovary size before fertilization, have to be degraded to obtain the correct fruit growth. The expression of CYTOKININ OXIDASE DEHYDROGENASE 7 (CKX7), which encodes a cytosolic CK degrading enzyme, is directly regulated post-fertilization by the MADS-box transcription factor STK. Similar to stk, two ckx7 mutant alleles possess shorter fruits compared to wild type. Quantification of CKs revealed that stk has high CK levels during fruit elongation, which negatively control cell expansion during fruit development, compromising fruit growth. Overexpression of CKX7 partially complements the stk fruit phenotype. We show that CKX6 does not regulate fruit elongation process. CKX6 encodes for one of the fourth CK degrading enzymes that acts in the apoplast. The CKX6 promoter is not active during fruit elongation phases. Moreover, the ckx6 mutant does not display differences in fruit length when compared to wild type. Finally, we show that STK is also required for the correct expression of the MADS-box gene FUL, which is considered the master regulator of valve elongation in fruit. The double mutant stk ful displayed shorter siliques when compared to wild type, but also respect to the two single mutants. The additive phenotype of the double mutant stk ful suggests the possibility that the two MADS-box transcription factors act in two parallels pathways that can regulate fruit elongation process. Overall, we provide novel insights into the regulatory pathway that control fruit growth.
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Baugh, John Andrew. "Differential regulation of monocyte cytokine release." Thesis, University of Bath, 1999. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285313.

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Durigova, Michaela. "Mechanisms of proteoglycan aggregate degradation in cytokine-stimulated cartilage." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111912.

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Aggrecan is one of the most important structural components of the extracellular matrix (ECM) of articular cartilage, where it contributes to the hydration of the tissue and its ability to resist compressive loads during joint movement. Increased aggrecan degradation and loss occurs in joint diseases and is thought to be mediated by enzymes such as the matrix metalloproteinases (MMPs) and aggrecanases (ADAMTS). It has also been proposed that aggrecan release from the cartilage can be mediated by a non-proteolytic mechanism which involves the degradation of hyaluronan (RA) to which the aggrecan is bound. As aggrecan degradation and loss is known to be induced by pro-inflammatory cytokines, IL-1, TNFalpha, IL-6, IL-17 and OSM were used to investigate the mechanisms involved in proteoglycan catabolism in organ cultures of bovine articular cartilage. Irrespective of the cytokine, all aggrecan fragments generated were characteristic of aggrecanase action, and no additional aggrecan-degrading enzymatic activity was detected. In the presence of OSM, more rapid aggrecan release was observed, due to both proteolysis and fragmentation of HA by hyaluronidase activity. Moreover, addition of OSM resulted in the cleavage of aggrecan at a non-canonical aggrecanase site near its carboxy-terminal globular domain. Such cleavage could be reproduced in vitro by the action of either ADAMTS-4 or ADAMTS-5. Gene expression analysis revealed that both aggrecanases were highly induced by the cytokines, and while ADAMTS-4 was the major aggrecanase to be stimulated in all conditions, ADAMTS-5 remains the predominant aggrecanase to be expressed in cartilage. Thus, the present study shows that aggrecanase activity is primarily responsible for aggrecan degradation in the early stages of cytokine stimulation, and that in the presence of OSM, aggrecanase substrate specificity can be differentially modulated and hyaluronidase-mediated RA degradation can be induced.
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Zahedi-Nejad, Maryam Sadat. "Characterisation of the expression and degradation of the pro-inflammatory cytokine interleukin 1." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/characterisation-of-the-expression-and-degradation-of-the-proinflammatory-cytokine-interleukin-1(ed66d067-bf16-4d1d-ac30-fdb1397d0366).html.

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Inflammation plays a crucial role in protecting the host from infection and tissue injury. However, uncontrolled inflammation contributes to the pathogenesis of major auto-inflammatory diseases. Interleukin-1 (IL-1), a pleiotropic pro-inflammatory cytokine, is a pivotal mediator of many of these diseases. The best characterised IL-1 family members, IL-1α and IL-1β, are produced as precursor forms of 31 kDa in size. Both precursors are cleaved and secreted, activating transmembrane IL-1 receptors on IL-1-responsive cells. Many studies that focused on IL-1α have shown that the precursor and processed mature Ct peptide, as well as its N terminus (Nt) form, can elicit a signal. However, with IL-1β, only the processed mature Ct form is known to elicit an inflammatory response and no immunological activity has been attributed to Nt fragments of pro-IL-1β. Therefore, the first objective of this study was to produce recombinant human Nt-IL-1β fragments in bacterial and mammalian expression system to investigate their possible immunomodulatory functions. Recombinant His-tagged N-terminus fragments (10 and 14 kDa) of pro-IL-1β were cloned into the bacterial expression vector pET-22(+) and expressed in E. coli BL21(DE3) followed by purification using three consecutive columns (IMAC, SEC and AEC). Purification analysis of eluted proteins from columns indicated that the recombinant proteins were always co-purified with some other bacterial proteins. The Nt fragments of pro-IL-1β were cloned into the mammalian expression plasmid, pcDNA3.1(+). Expression of these proteins was monitored by transfection of two mammalian cell lines: Human Embryonic Kidney (HEK) 293 cells and monkey kidney cells (COS-7). No protein expression was observed with either construct. These limitations urged us to investigate the expression and degradation of endogenous IL-1 in vitro. Previous studies have shown that the transcription of cytokine genes in response to lipopolysaccharide (LPS) is usually rapid and begins to decline within a few hours after stimulation. The proteasome is the major cellular proteolytic apparatus and controls the turn-over of cellular proteins. We investigated the intracellular stability of IL-1α and IL-1β in LPS-stimulated mouse J774 macrophages and primary mouse bone marrow derived macrophages (BMDMs). Exposure of LPS-stimulated J774 and BMDMs to three different classes of proteasome inhibitors (peptide alhedyde (ALLN), peptide boronate (MG262) and non-peptide inhibitor (β-lactone)) prevented the degradation of intracellular IL-1α and IL-1β in a concentration and time dependent manner. Furthermore, the release of IL-1 into the culture media was not affected by any of these inhibitors in LPS-stimulated J774 cells. However, in LPS-stimulated BMDMs, β-lactone increased the release of both IL-1α and IL-1β and ALLN only increased IL-1α release into culture supernatant compared to control. MG262 had no effect on the release of either. These data suggest that the proteasome plays an important role in controlling the amount of IL-1α and IL-1β by restricting the intracellular levels of these cytokines in activated monocytes and macrophages. Therefore, this study provides evidence in support of the hypothesis that the proteasome is involved in the degradation of IL-1α and IL-1β and may offer a potential therapeutic target in inflammatory diseases.
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Lu, Yihong C. S. "In vitro models of cartilage degradation following joint injury : mechanical overload, inflammatory cytokines and therapeutic approaches." Thesis, Massachusetts Institute of Technology, 2010. http://hdl.handle.net/1721.1/61238.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biological Engineering, 2010.
Cataloged from PDF version of thesis.
Includes bibliographical references.
Osteoarthritis (OA) is the most common form of joint disorder. Individuals who have sustained an acute traumatic joint injury are at greater risk for the development of OA. The mechanisms by which injury causes cartilage degradation are not fully understood, but the elevated levels of injury-induced pro-inflammatory cytokines, such as TNFa and IL-6, have been implicated to play important roles in the pathogenesis of OA. We have used in vitro models of cartilage injury to examine the interplay between mechanical and cytokine-mediated pathways and to identify processes associated with cartilage degradation following joint injury. The overall aims of this thesis were to characterize the combined effect of TNFa and IL-6/sIL6R on matrix degradation and chondrocyte gene expression in mechanically injured cartilage, and to investigate whether cartilage degradation could be inhibited by potential therapeutic approaches. TNFa and IL-6/sIL-6R interacted to cause aggrecanase-mediated proteoglycan degradation. Importantly, the combined catabolic effects of cytokines were highly potentiated by mechanical injury. Furthermore, cartilage degradation caused by the in vitro injury model appeared to be initiated at the transcriptional level, since the gene expression of matrix proteases, cytokines and iNOS were all highly elevated in the treatment conditions. The degradative effects of TNFa in injured cartilage was due, in part, to the action of endogenous IL-6, as proteoglycan degradation was partly reduced by an IL-6 blocking Fab fragment. Interestingly, cartilage degradation induced by the combinations of proinflammatory cytokines and mechanical injury was fully abrogated by short-term treatments with dexamethasone. The results of this work are significant in that they provide evidence suggesting joint injury affects cell-mediated responses as well as the transport of cytokines and proteases in extracellular matrix, making cartilage tissue more susceptible to further degradation by biochemical mediators.
by Yihong C.S. Lu.
Ph.D.
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Safhi, Mohammed Mohsen A. "Priming of STAT1 and STAT3 for cytokine-triggered degradation by the proteasome upon A2Aadenosine receptor (A2AAR) expression." Thesis, Connect to e-thesis, 2008. http://theses.gla.ac.uk/310/.

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Thesis (Ph.D.) - University of Glasgow, 2008.
Ph.D. thesis submitted to the Division of Biochemistry and Molecular Biology, Institute of Biomedical and Life Sciences, University of Glasgow, 2008. Includes bibliographical references. Print version also available.
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Peake, Nicholas J. "An investigation of cytokines and enzymes implicated in joint degradation as markers of disease activity and outcome in juvenile idiopathic arthritis." Thesis, University of Newcastle Upon Tyne, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413417.

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Schächterle, Carolin. "Der strukturelle und funktionelle Einfluss des Cytokins IFNgamma auf die Modulation proteasomaler Komplexsubtypen." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2013. http://dx.doi.org/10.18452/16849.

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Das 20S Proteasom ist das Kernelement des Ubiquitin-Proteasom-Systems und baut fehlerhafte, nicht mehr benötigte und oxidierte Proteine ab, wobei drei katalytisch aktive Untereinheiten die Polypeptidkette schneiden. Das proinflammatorische Cytokin IFNg induziert die Expression und Inkorporation der alternativen katalytisch aktiven Immunountereinheiten, was in variablen Isoformen des 20S Proteasoms resultiert. Die zusätzliche Assoziation des 19S Regulators, bzw. des PA28 und des PA200 Aktivators an eine Isoform erweitert das Sortiment an proteasomalen Komplexsubtypen. Der zeitliche Verlauf einer IFNg Stimulation zeigte, dass die Aktivatoren PA28 und PA200 antagonistisch an das 20S Proteasom assoziieren und niedermolekulare Komplexsubtypen bilden, sodass in dieser Studie auch zum ersten Mal eine IFNg abhängige Assoziation des PA200 Monomers an das 20S Proteasom detektiert wurde. Ex vivo Versuche zeigten, dass die Defizienz der Immunountereinheit LMP7 mit der Assoziation des PA28-Aktivators an das 20S-19S Proteasom kompensiert wird, wobei die funktionelle Wirksamkeit aber offen bleibt. In einer monozytären Zelllinie wird ein sehr hochmolekularer, chymotryptisch aktiver Komplex assembliert und massenspektrometrische Analysen detektierten proteasomale Untereinheiten und viele Komponenten der Proteinbiosynthese, was für eine Assoziation des Proteasoms mit dem Polysom spricht. Diese Möglichkeit der kotranslationalen Degradation kann auch die Assoziation des detektieren Chaperonins TriC erklären, wobei dieser Komplex, der ATP abhängig Proteine faltet, möglicherweise auch direkt mit dem Proteasom interagieren könnte, wie elektronenmikroskopische Aufnahmen belegten. Neben den neuen strukturellen Ergebnissen, bestätigte die funktionelle Analyse den Abbau polyubiquitinierter Substrate durch 19S-Regulator assoziierte Komplexsubtypen, doch das 19S-20S-19S Proteasom konnte das Modellsubstrat HA-Ubi-IkBa-flag besser abbauen und deubiquitinieren als das 20S-19S Proteasom.
The 20S proteasome is the core element of the ubiquitin-proteasome-system, which degrades defective, unneeded and oxidized proteins, while three catalytically active subunits hydrolyze the peptide bonds of the polypeptide. The proinflammatory cytokine IFNg induces the expression and incorporation of three alternative, catalytically active immunosubunits resulting in variable isoforms of the 20S proteasome. The additional association of the 19S regulator, or the PA28 and PA200 activator, respectively, expands the range of proteasome complex subtypes. The time course of IFNg stimulation showed that the proteasomal association of PA28 and PA200 occurs antagonistically, forming low molecular weight complex subtypes. Furthermore, this study revealed for the first time an IFNg dependent association of the PA200 monomer to the 20S proteasome. Ex vivo experiments showed that the deficiency of the immunosubunit LMP7 is compensated by the association of the PA28 activator to the 20S-19S proteasome, whereas the functional efficacy remains elusive. In a monocytic cell line, a chymotryptic active complex with a very high molecular weight was detected, and mass spectrometry confirmed proteasomal subunits and components of the protein synthesis machinery, suggesting an association of the proteasome with the polysome. The fact of cotranslational degradation may also explain the association of the chaperonin TriC, an ATP dependent protein folding chaperonin. Electron micrographs could reveal that TriC possibly interacts directly with the proteasome. Next to the new structural results, the functional analysis confirmed the degradation of polyubiquitinated substrates by 19S regulator associated complex subtypes, and in addition to it, the 19S-20S-19S proteasome degraded and deubiquitinated the model substrate HA-Ubi-IkBa-flag better than the 20S-19S proteasome.
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Williams, Jamie J. L., K. M. A. Munro, and Timothy M. Palmer. "Role of Ubiquitylation in Controlling Suppressor of Cytokine Signalling 3 (SOCS3) Function and Expression." 2014. http://hdl.handle.net/10454/7925.

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Yes
The realisation that unregulated activation of the Janus kinase–signal transducer and activator of transcription (JAK–STAT) pathway is a key driver of a wide range of diseases has identified its components as targets for therapeutic intervention by small molecule inhibitors and biologicals. In this review, we discuss JAK-STAT signalling pathway inhibition by the inducible inhibitor “suppressor of cytokine signaling 3 (SOCS3), its role in diseases such as myeloproliferative disorders, and its function as part of a multi-subunit E3 ubiquitin ligase complex. In addition, we highlight potential applications of these insights into SOCS3-based therapeutic strategies for management of conditions such as vascular re-stenosis associated with acute vascular injury, where there is strong evidence that multiple processes involved in disease progression could be attenuated by localized potentiation of SOCS3 expression levels.
British Heart Foundation; Chief Scientist's Office; NHS Greater Glasgow and Clyde Research Endowment Fund; BBSRC
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Books on the topic "Cytokinin degradation"

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Dalbeth, Nicola. Pathophysiology of gout. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0039.

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The clinical features of gout occur in response to monosodium urate (MSU) crystals. Gout should be considered a chronic disease of MSU crystal deposition. A number of pathophysiological checkpoints are required for development of gout. First, elevated urate concentrations are required: urate overproduction and underexcretion contribute to total urate balance. Overproduction occurs due to alterations in the purine synthesis and degradation pathways. Renal underexcretion is an important cause of elevated serum urate concentrations (hyperuricaemia), and occurs through alterations in the urate transporters within the renal tubule (collectively known as the urate transportasome). Gut underexcretion (extrarenal urate underexcretion) also contributes to development of hyperuricaemia. The next checkpoint is MSU crystal formation. In some individuals with evidence of MSU crystal deposition, symptomatic gout develops. The acute inflammatory response to MSU crystals represents a self-limiting sterile acute auto-inflammatory response which is mediated by the innate immune system activation. Interleukin 1 beta is the key cytokine that contributes to the acute inflammatory response to MSU crystals. In some patients, advanced gout may occur with structural joint damage. Joint damage in gout is mediated both by direct effects of MSU crystals on joint tissue and by indirect effects of joint inflammation. In addition to their central role in pathogenesis of gout, MSU crystals have a physiological role, particularly as an adjuvant or ‘danger signal’ in immune surveillance.
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Book chapters on the topic "Cytokinin degradation"

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Horgan, R., L. R. Burch, and L. M. S. Palni. "Cytokinin Oxidase and the Degradative Metabolism of Cytokinins." In Plant Growth Substances 1988, 282–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74545-4_33.

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Chandrasekhar, Srinivasan, Anita K. Harvey, and Suzanne T. Stack. "Degradative and Repair Responses of Cartilage to Cytokines and Growth Factors Occur Via Distinct Pathways." In Joint Destruction in Arthritis and Osteoarthritis, 121–25. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-7442-7_13.

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Feng, Lili, Byeong C. Jang, and Daniel Hwang. "Inhibitor of Protein Tyrosine Kinase, Radicicol, Suprresses the Expression of Cyclooxygenase and Pro-Inflammatory Cytokines in LPS-Stimulated Rat Alveolar Macrophage in Part by Accelerating Degradation of mRNA." In Advances in Experimental Medicine and Biology, 281–88. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1813-0_42.

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Armstrong, Donald J. "Cytokinin Oxidase and the Regulation of Cytokinin Degradation." In Cytokinins, 139–54. CRC Press, 2019. http://dx.doi.org/10.1201/9781351071284-11.

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"Cytokine-Regulated Protein Degradation by the Ubiquitination System." In Advances in Protein and Peptide Sciences, edited by Kwang-Hyun Baek, 256–71. BENTHAM SCIENCE PUBLISHERS, 2013. http://dx.doi.org/10.2174/9781608054879113010009.

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Nalla, Sarath, Sahdeo Prasad, Lakshmi Kavuri, and Vijetha Pendyala. "Traditional Medicinal Plants: Safe and Efficacious Potential Drugs in the Management of Rheumatoid Arthritis." In Natural Products for the Management of Arthritic Disorders, 97–117. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815050776122010007.

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Rheumatoid Arthritis is an autoimmune, chronic inflammatory disorder that affects the synovial tissues of the joints. Whilst the standard treatment regimen involves non-steroidal anti-inflammatory drugs, disease-modifying antirheumatic agents and glucocorticoids attenuate the symptoms. However, the long-standing use of all these drugs causes adverse effects, which leads to the research on medicinal plants. History shows that many medicinal plants are an integral part of various traditional medicine systems, thus facilitating an alternative form of therapy in various parts of the world. Since ancient civilization, many of the medicinal plants that used as popular remedies are available abundantly in Asia. In this chapter, we are presenting the information on various medicinal plants found in Asia that are reported to be having anti-arthritic activity. Scientific studies revealed that herbs exert beneficial effects in treating arthritis by numerous cellular mechanisms, including downregulation of pro.inflammatory cytokines like TNF-α, IL-6, and NF-κB, oxidative stress suppression, suppression of cartilage degradation with degradative metalloproteinases, and increasing antioxidant performance. A variety of phytoconstituents from diverse chemical categories such as flavonoids, lignans, coumarins, terpenes, glycosides, phytoestrogens, sesquiterpene lactones, anthraquinones, alkaloids, and thymoquinone are extracted from these medicinal plants. Additionally, in this chapter, the pharmacological actions of these plants were also discussed.
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Harre, Ulrike, and Georg Schett. "Mechanisms of bone and cartilage destruction." In Oxford Textbook of Rheumatoid Arthritis, 85–94. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198831433.003.0009.

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Structural damage of cartilage and bone tissue is a hallmark of rheumatoid arthritis (RA). The resulting joint destruction constitutes one of the major disease consequences for patients and creates a significant burden for the society. The main cells executing bone and cartilage degradation are osteoclasts and fibroblast-like synoviocytes, respectively. The function of both cell types is influenced by the immune system. In past decades, research has identified several mediators of structural damage, ranging from infiltrating immune cells and inflammatory cytokines to autoantibodies. These factors result in an inflammatory milieu in the affected joints, which leads to an increased development and function of osteoclasts and the transformation of fibroblast-like synoviocytes towards a highly migratory and destructive phenotype. In addition, repair mechanisms mediated by osteoblasts and chondrocytes are strongly impaired by the presence of pro-inflammatory cytokines. This article will review the current knowledge on the mechanisms of destruction of bone and cartilage in rheumatoid arthritis.
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"Solid Lipid Nanoparticles: Interaction with Cells, Cytokine Production, and Enzymatic Degradation." In Lipospheres in Drug Targets and Delivery, 113–38. CRC Press, 2004. http://dx.doi.org/10.1201/9780203505281-10.

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Lambert, Charles. "Attenuating Cancer Cachexia-Prolonging Life." In Frailty and Sarcopenia - Recent Evidence and New Perspectives. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.101250.

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Death by cancer cachexia is dependent on the time allotted to cancer to cause muscle and fat wasting. If clinicians, nurses, researchers can prolong the life of a cancer patient other therapeutic interventions such as radiation and chemotherapy may be given the time to work and rid the cancer patient of tumors and save lives. Three areas by which cancer induces cachexia is through impaired insulin-like growth factor signaling, elevations in the proinflammatory cytokines TNF-α and IL-6 and subsequent reductions in muscle protein synthesis and increases in muscle protein degradation. Therefore, it is important to augment the IGF-1 signaling, block TNF-α and IL-6 in cancer cachexia and in other ways augment muscle protein synthesis or decrease muscle protein degradation. Ghrelin like growth hormone secretagogues, monoclonal antibodies to TNF-α and IL-6, testosterone, and anabolic steroids, the beta 2 agonist albuterol, resistance exercise, and creatine monohydrate (with resistance exercise) are beneficial in increasing muscle protein synthesis and/or reducing muscle protein breakdown. With these muscle augmenting agents/interventions, the duration that a cancer patient lives is prolonged so that radiation and chemotherapy as well as emerging technologies can rid the cancer patient of cancer and save lives.
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Arora, Disha, Sanjay Sharma, and Sumeet Gupta. "Natural Products Targeting Various Mediators in Rheumatoid Arthritis." In Natural Products for the Management of Arthritic Disorders, 135–63. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815050776122010009.

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Rheumatoid arthritis (RA) is a chronic autoimmune disease that leads to an inflammatory reaction, primarily affecting synovial joints and progressive cartilage and bone destruction resulting in gradual joint immobility. Possibly, a diversity of pharmacological intercessions are employed for treating arthritis. But modern treatment is linked with serious adverse outcomes and high expenses. Therefore, alternative therapies have been under examination. Scientific facts on RA have revealed that conventional therapy offers a favourable impact by various actions (cellular) like repression of oxidative stress, down-regulation of pro-inflammatory cytokines, such as IL-6, NF-ƙB, and TNF-α, and inhibiting cartilage degradation. A wide range of active phytoconstituents from the medicinal plants, such as terpenes, anthraquinones, glycosylflavons, flavonols, dihydroflavonols, lignans, coumarins, phytoestrogens, sesquiterpene lactones, thymoquinone, and alkaloids reduced the arthritic manifestations through selecting the pro-inflammatory indicators, which play a role in the pathogeny of the disease (RA). With numerous developments in the last few years regarding functional studies or characterization of plant materials, the phase is put down for extensive scientific trials or using the plants or their products to manage rheumatoid arthritis. The chapter discusses the plants used conventionally with phytoconstituents having anti-inflammatory action. This, in turn, leads to the innovation of new benefits from natural products in the future.
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Conference papers on the topic "Cytokinin degradation"

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Wolfe, Valerie M., Seonghun Park, Marjana Tomic, Peter A. Torzilli, and C. T. Christopher Chen. "Load Down-Regulates TNF-Alpha Induced Cartilage Degradation in Part Through NF-KB and P38 Pathways." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176541.

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Pro-inflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF), can induce cartilage degradation after acute injury or in inflammatory diseases [1,2,3,7]. The degradative events are coordinated through the elevation and activation of two classes of enzymes, namely matrix metalloproteinases (MMPs) and aggrecanases (ADAMTS-4 and −5) [1,6]. Prior studies suggested that pro-inflammatory responses induced by IL-1β can be inhibited by tensile load [2] and more recently by cyclic compression [8]. It is, however, not clear whether load affects other cytokines, such as TNF-α. TNF-α is known to bind its receptor (TNFR1) to cause a cascade that ends with degradation of an inhibitor, IκBα, and release of the transcription factor NF-κB [3]. The actions of TNF-α are also known to be affected by at least three NF-κB independent pathways including the p38, ERK, and JNK pathways [4]. The objective of this study was to determine whether cyclic compression could affect TNF-α induced cartilage degradation and to determine the roles of p38, ERK, and JNK pathways in TNF-induced cartilage degradation. We hypothesized that cyclic loading would inhibit the degradative effects caused by TNF-α.
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Chen, C. T., S. Park, M. Bhargava, and P. A. Torzilli. "Inhibitory Effect of Mechanical Load on IL-1 Induced Cartilage Degradation Is Mediated by Interferon-Gamma and IL-1 Receptor 1." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193230.

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Matrix remodeling in articular cartilage is regulated by the elevation and activation of aggrecanases (ADAMTS-4 and ADAMTS-5) and matrix metalloproteinases (MMPs) [2–4, 7–9, 10]. Several recent studies from our and other groups have shown that mechanical loading can counteract interleukin 1 (IL-1) induced pro-inflammatory and catabolic events by down-regulating aggrecanases, MMPs, and pro-inflammatory genes [1, 3, 5, 6], but the molecular mechanism is not clear. Many previous studies have shown that the regulation of pro-inflammatory effect of IL-1 come from several aspects: anti-inflammatory cytokines (TGF-β, IL-10, IL-6 and interferon γ), IL-1 receptor related proteins (IL-1R1, IL-1R2, and IL-1Ra) as well as a family of intracellular inhibitory protein called Suppressor Of Cytokine Signaling (SOCS.) SOCS1 and SOCS3 are especially important, since they can inhibit both MAPK and NF-κB pathways induced by IL-1 [12]. The objective of this study was to determine whether mechanical load affected anti-inflammatory mediators along with anti-catabolic events.
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Yeger-McKeever, Meira, Alice H. Huang, Ashley F. Stein, and Robert L. Mauck. "Engineered MSC-Laden Cartilage Constructs are Sensitive to Inflammatory Cytokine-Mediated Degradation." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176186.

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Degeneration of cartilage resulting from trauma or disease processes is an increasingly prevalent problem in the aging population. Intrinsic repair of cartilage is limited and few methodologies exist, short of prosthetic replacement, for restoring damaged articular surfaces. These realities engender a need for new strategies for extrinsic repair. One strategy, tissue engineering, generates replacement cartilage composed of scaffolds and differentiated chondrocytes [1]. In addition to chondrocytes, recent work has demonstrated that mesenchymal stem cells (MSCs) isolated from bone marrow may be induced to take on a chondrocyte-like phenotype [2]. Tissue engineered constructs of either cell type can yield near-native properties (though those derived from MSCs are typically lower) [3]. While such constructs may be surgically implanted to replace areas denuded of cartilage, one factor to consider is that these defect sites exist in an already inflamed joint [4]. In addition, surgical interventions trigger further inflammatory responses, greatest in the area of intervention [5]. Recent literature has shown that pro-inflammatory cytokines, such as interleukin-1beta (IL-1β), instigate catabolic destruction not only of cartilage explants, but also of chondrocyte-based engineered cartilage constructs [6–9]. Still other studies have shown that un-differentiated MSCs themselves may exert an anti-inflammatory effect on their local environment [10–12]. Thus the current study examined the effect of varying doses of IL-1β exposure on both chondrocyte- and MSC-based engineered cartilage constructs to determine the relative sensitivity of neo-cartilage derived from each cell type to cytokine induced degradation.
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Kashyap, Meghana, Kristen T. Carter, Brent C. Sauer, and Christopher T. Chen. "NF-κB Mediates Cartilage Degradation Induced by Trauma Injury and Interleukin-1." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14513.

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Chondrocyte death, induced by impact injury (necrosis) and/or apoptotic inducers such as cytokines, and high level of nitric oxide, is important for the development of post-traumatic arthritis (PTA) [1–3]. The upregulation of pro-inflammatory cytokines, such as interleukin −1 (IL-1) and Tumor necrosis factor (TNF) α, is known to mediate cartilage degradation in inflammatory diseases and after trauma injury [1,2, 6–9]. IL-1 induces the degradation of proteoglycan (PG) in cartilage through NF-κB and Mitogen-activated protein kinases (MAPK: p38, ERK and JNK) pathways [1,2,6]. IL-1 is highly upregulated in synovial joint after impact injury, but the role of IL-1 induced chondrocyte death and matrix/PG degradation in injured cartilage is not completely clear.
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Tan, Andrea R., Eric G. Lima, Kacey G. Marra, and Clark T. Hung. "Genipin Protects Engineered Cartilage Against IL-1alpha Induced Degradation." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193070.

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Tissue-engineering has great potential for treating cartilage pathologies such as osteoarthritis by replacing degraded tissue with newly developed engineered tissue. However proinflammatory cytokines such as interleukin-1α (IL-1α) are a confounding issue as they are often present in high concentrations as part of the chronic pathology or as a result of the surgical intervention itself(1). The catabolic effects of these mediators may be especially pronounced in engineered tissues whose cells are not yet fully embedded in the potentially chondroprotective enclosure of a cartilaginous extracellular matrix(2). One method to protecting initially fragile constructs from degradation may be through the use of non-toxic cross-linking agents. Genipin is a naturally occurring crosslinking agent that reacts with amino acids or amine groups and leads to the formation of stable crosslinked products that are identifiable by a dark blue pigment (Figure 1). Cartilage cross-linked with genipin has been shown to be more resistant to collagenase digestion(3) and to injection of chondroitinase-ABC(4). In this study, we examined whether engineered constructs pre-treated with genipin would better resist IL-1α induced catabolic degradation.
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Ling, Carrie H., Janice H. Lai, James F. Nishimuta, and Marc E. Levenston. "Dose-Dependent Effects of Interleukin-1Alpha on Functional Degradation of Lateral and Medial Menisci." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19523.

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Despite a growing recognition that meniscal degeneration often precedes cartilage degeneration in the development of knee osteoarthritis (OA), little is known about the role of meniscal degeneration in the onset and progression of knee OA. Even a mild degenerative lesion increases meniscal extrusion, implying changes in biomechanical function. Understanding the mechanisms of meniscal degeneration may enable the diagnosis and disease-modifying treatment of early knee OA, potentially preventing or slowing the progression of the disease. The roles of pro-inflammatory cytokines such as interleukin-1 (IL-1) in promoting cartilage matrix degradation and mediating inflammation in the progression of OA have been widely demonstrated [1,2]. Recent results from our group indicated that 20ng/ml hrIL-1α produced similar cell-mediated degradation and loss of mechanical properties in immature cartilage and meniscus, but progresses more rapidly in meniscus explants [3]. This study further explored the effects of IL-1α dosage and medial-lateral differences on the functional degradation of meniscal explants.
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Lima, Eric G., Liming Bian, Francis B. Gonzales, Gerard A. Ateshian, and Clark T. Hung. "Influence of Interleukin Treatment on Engineered and Native Articular Cartilage." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176220.

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Injury to the diarthrodial joint is often associated with elevated levels of cytokines and other inflammatory molecules. While the influence of interleukin on articular cartilage has been well-studied, its effects on engineered cartilage are not. The presence of inflammatory factors in the injured joint would be expected to affect the performance of implanted engineered cartilage repair tissue [1] and this effect may be especially pronounced in underdeveloped tissues [2]. The current study addresses this issue by examining the influence of interleukin (IL-1α and IL-1β) on engineered cartilage mechanical and biochemical properties at sequential stages of development. Furthermore, dexamethasone, an anti-inflammatory steroid that has been shown in some cases to suppress interleukin-induced degradation of native cartilage [3], was examined in the context of engineered constructs.
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Harel, M., T. Garraud, B. Le Goff, and F. Blanchard. "P060 Il-38 in arthritis maturation and degradation of this new IL-1 family anti-inflammatory cytokine." In 38th European Workshop for Rheumatology Research, 22–24 February 2018, Geneva, Switzerland. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2018.79.

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Angiolilli, C., P. Kabala, A. Grabiec, M. Rossato, W. Lai, P. Blackshear, K. Reedquist, D. Baeten, and T. Radstake. "SAT0023 Control of cytokine mrna degradation by the histone deacetylase inhibitor itf2357 in rheumatoid arthritis fibroblast-like synoviocytes." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.3547.

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Killian, Megan L., and Tammy L. Haut Donahue. "Effect of Pathological and Physiological Loads on Interleukin-1α Protein Production in Porcine Menisci." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192145.

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The meniscus performs several functions for the maintenance of knee joint health, such as load transmission and joint stability. Meniscal lesions have been suggested as a precursor to the onset of osteoarthritis (OA)[1]. Such lesions often lead to surgical removal of the torn portion of the meniscus, increasing cartilage to cartilage contact area. Partial meniscectomies have been shown using finite element analysis and histology to lead to altered and increased mechanical loading on the remaining meniscus and underlying articular cartilage[2,3]. Consequently, pathological compressive strains of more than 15% have been shown to increase proteoglycan breakdown and meniscal matrix degradation[4]. Preliminary investigations in our laboratory have demonstrated an increase in interleukin-1α (IL-1α) gene expression of meniscal explants subjected to pathological levels of dynamic compressive strain [6,7]. This inflammatory cytokine has been attributed to apoptosis and matrix degradation[5]. However, gene expression measurements merely suggest possible matrix remodeling mechanisms and do not necessarily result in protein syntheses from which matrix changes occur. Therefore, the purpose of this study was to quantify protein synthesis of IL-1α in porcine meniscal implants after compressive strain exercises. It was hypothesized that, similar to mRNA expression, protein synthesis for pathologically loaded (0 or 20% dynamic strain) samples would be greater than samples loaded to physiological levels (10% strain).
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Reports on the topic "Cytokinin degradation"

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Friedman, Haya, Chris Watkins, Susan Lurie, and Susheng Gan. Dark-induced Reactive Oxygen Species Accumulation and Inhibition by Gibberellins: Towards Inhibition of Postharvest Senescence. United States Department of Agriculture, December 2009. http://dx.doi.org/10.32747/2009.7613883.bard.

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Dark-induced senescence could pose a major problem in export of various crops including cuttings. The assumption of this work was that ROS which is increased at a specific organelle can serve as a signal for activation of cell senescence program. Hormones which reduce senescence in several crops like gibberellic acid (GA) and possibly cytokinin (CK) may reduce senescence by inhibiting this signal. In this study we worked on Pelargonium cuttings as well as Arabidopsis rosette. In Pelargonium the increase in ROS occurred concomitantly with increase in two SAGs, and the increase persisted in isolated chloroplasts. In Arabidopsis we used two recentlydeveloped technologies to examine these hypotheses; one is a transcriptome approach which, on one hand, enabled to monitor expression of genes within the antioxidants network, and on the other hand, determine organelle-specific ROS-related transcriptome footprint. This last approach was further developed to an assay (so called ROSmeter) for determination of the ROS-footprint resulting from defined ROS stresses. The second approach involved the monitoring of changes in the redox poise in different organelles by measuring fluorescence ratio of redox-sensitive GFP (roGFP) directed to plastids, mitochondria, peroxisome and cytoplasm. By using the roGFP we determined that the mitochondria environment is oxidized as early as the first day under darkness, and this is followed by oxidation of the peroxisome on the second day and the cytoplast on the third day. The plastids became less oxidized at the first day of darkness and this was followed by a gradual increase in oxidation. The results with the ROS-related transcriptome footprint showed early changes in ROS-related transcriptome footprint emanating from mitochondria and peroxisomes. Taken together these results suggest that the first ROS-related change occurred in mitochondria and peroxisomes. The analysis of antioxidative gene’s network did not yield any clear results about the changes occurring in antioxidative status during extended darkness. Nevertheless, there is a reduction in expression of many of the plastids antioxidative related genes. This may explain a later increase in the oxidation poise of the plastids, occurring concomitantly with increase in cell death. Gibberellic acid (GA) prevented senescence in Pelargonium leaves; however, in Arabidopsis it did not prevent chlorophyll degradation, but prevented upregulation of SAGs (Apendix Fig. 1). Gibberellic acid prevented in Pelargonium the increase in ROS in chloroplast, and we suggested that this prevents the destruction of the chloroplasts and hence, the tissue remains green. In Arabidopsis, reduction in endogenous GA and BA are probably not causing dark-induced senescence, nevertheless, these materials have some effect at preventing senescence. Neither GA nor CK had any effect on transcriptome footprint related to ROS in the various organelles, however while GA reduced expression of few general ROS-related genes, BA mainly prevented the decrease in chloroplasts genes. Taken together, GA and BA act by different pathways to inhibit senescence and GA might act via ROS reduction. Therefore, application of both hormones may act synergistically to prevent darkinduced senescence of various crops.
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