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Journal articles on the topic 'CSN'

Author: Grafiati
Published: 4 June 2021
Last updated: 18 February 2022

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1

КОВАЛЮК, Н. В., В. Ф. САЦУК, Е. А. КУЛЕШОВА, Л. И. ЯКУШЕВА, and Ю. Ю. ШАХНАЗАРОВА. "THE INFLUENCE OF CSN 2 AND CSN 3 GENOTYPES ON THE MILK PRODUCTIVITY OF AYRSHIRE COWS." Molochnoe i miasnoe skotovodstvo, no. 2 (May 15, 2021): 25–28. http://dx.doi.org/10.33943/mms.2021.96.45.006.

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Настоящее исследование завершает цикл работ, связанных с генотипированием российских субпопуляций крупного рогатого скота по локусам CSN2 и CSN3. Проведено генотипирование коров и телок айрширской породы из трех хозяйств Краснодарского края (n=1107). Установлена частота встречаемости носителей CSN2- и CSN3-генотипов, оценена степень их влияния на молочную продуктивность. В различных группах животных частота встречаемости «предпочтительных» в хозяйственном отношении CSN2-генотипа А2А2 составляет от 0,23 до 0,37 и CSN3-генотипа ВВ — от 0,03 до 0,06. Генотипы А2А2 и ВВ не оказывают негативного влияния на молочную продуктивность их носителей. Целесообразно для отечественных племенных предприятий, реализующих спермопродукцию айрширских быков, увеличить долю производителей с генотипами А2А2 (локус CSN2), АВ и ВВ (локус CSN3 This study completes a series of studies related to the genotyping of Russian bovine subpopulations at the CSN2 and CSN3 loci. Genotyping of cows and heifers Ayrshire breed from three farms in the Krasnodar region (n=1107) and the incidence of carriers CSN2 and CSN3 genotypes, assess their degree of influence on milk production in animals Ayrshire breed .It was found that in different groups of animals, the frequency of occurrence of the "preferred" in economic terms CSN2 genotype A2A2 ranges from 0.23 to 0.37 and CSN3 genotype BB - from 0.03 to 0.06.Genotypes A2A2 and BB (loci CSN2 and CSN3) do not have a negative impact on the milk productivity of their carriers. We consider it expedient for domestic breeding enterprises that sell sperm products of Ayrshire bulls to increase the share of producers with genotypes A2A2 (CSN2 locus), AB and BB (CSN3 locus).
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2

Tremblay, Louis-Marie. "La concurrence syndicale : CSN-FTQ." Commentaires 19, no. 3 (January 20, 2014): 381–83. http://dx.doi.org/10.7202/1021276ar.

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Sommaire L'auteur analyse les implications de la querelle présente entre la CSN et la FTQ. Il compare un mouvement syndical construit sur la possession d'un pouvoir monopolistique à un autre où existent parallèlement des organismes concurrents.
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MEZULIÁNÍK, Miloslav, Josef PROKEŠ, and Vratislav PSOTA. "New CSN 56 6610 - Malt." Kvasny Prumysl 56, no. 6 (June 1, 2010): 276–77. http://dx.doi.org/10.18832/kp2010034.

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4

Gazdová, Veronika, Petr Humpolíček, Vanda Déduchová, Jitka Filkuková, and Josef Dvořák. "Effect of C-CSN and B-CSN genotypes on milk production traits in Czech Flekvieh and Holstein breed." Acta Universitatis Agriculturae et Silviculturae Mendelianae Brunensis 55, no. 1 (2007): 55–58. http://dx.doi.org/10.11118/actaun200755010055.

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The effect of the χ-casein (C-CSN) and β –casein (B-CSN) loci on the milk production traits (milk yield, fat, protein and lactose content) was estimated for 807 and 488 Czech Fleckvieh and 402 and 244 Holstein cows, respectively. Genotypes of C-CNS and B-CNS were determined by the use of PCR–RFLP method. The genotypes were detected by use of electrophoresis on agarose gel. The associations of studied polymorphisms with milk production traits were estimated using the mixed linear model procedure REML in SAS for Windows 9.1.3. Results indicated that protein content is significantly affected (P ≤ 0.01) by C-CSN genotype (genotype BB > AB > AA). Fat and lactose content were not affected by C-CSN locus. The B-CNS locus had no significant effect on any milk production traits.
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5

Milic, Tian, and Bernhagen. "Role of the COP9 Signalosome (CSN) in Cardiovascular Diseases." Biomolecules 9, no. 6 (June 5, 2019): 217. http://dx.doi.org/10.3390/biom9060217.

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The constitutive photomorphogenesis 9 (COP9) signalosome (CSN) is an evolutionarily conserved multi-protein complex, consisting of eight subunits termed CSN1-CSN8. The main biochemical function of the CSN is the control of protein degradation via the ubiquitin-proteasome-system through regulation of cullin-RING E3-ligase (CRL) activity by deNEDDylation of cullins, but the CSN also serves as a docking platform for signaling proteins. The catalytic deNEDDylase (isopeptidase) activity of the complex is executed by CSN5, but only efficiently occurs in the three-dimensional architectural context of the complex. Due to its positioning in a central cellular pathway connected to cell responses such as cell-cycle, proliferation, and signaling, the CSN has been implicated in several human diseases, with most evidence available for a role in cancer. However, emerging evidence also suggests that the CSN is involved in inflammation and cardiovascular diseases. This is both due to its role in controlling CRLs, regulating components of key inflammatory pathways such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and complex-independent interactions of subunits such as CSN5 with inflammatory proteins. In this case, we summarize and discuss studies suggesting that the CSN may have a key role in cardiovascular diseases such as atherosclerosis and heart failure. We discuss the implicated molecular mechanisms ranging from inflammatory NF-κB signaling to proteotoxicity and necrosis, covering disease-relevant cell types such as myeloid and endothelial cells or cardiomyocytes. While the CSN is considered to be disease-exacerbating in most cancer entities, the cardiovascular studies suggest potent protective activities in the vasculature and heart. The underlying mechanisms and potential therapeutic avenues will be critically discussed.
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6

Joe, Woojin, Jonghyun Lee, and Karpjoo Jeong. "CSN: The Conceptually Manageable Sensor Network." International Journal of Distributed Sensor Networks 11, no. 3 (January 2015): 720861. http://dx.doi.org/10.1155/2015/720861.

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7

Dubiel, Wolfgang. "Resolving the CSN and CAND1 Paradoxes." Molecular Cell 35, no. 5 (September 2009): 547–49. http://dx.doi.org/10.1016/j.molcel.2009.08.011.

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8

Miller, Rachel K., Hiroshi Qadota, Thomas J. Stark, Kristina B. Mercer, Tesheka S. Wortham, Akwasi Anyanful, and Guy M. Benian. "CSN-5, a Component of the COP9 Signalosome Complex, Regulates the Levels of UNC-96 and UNC-98, Two Components of M-lines in Caenorhabditis elegans Muscle." Molecular Biology of the Cell 20, no. 15 (August 2009): 3608–16. http://dx.doi.org/10.1091/mbc.e09-03-0208.

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In Caenorhabditis elegans two M-line proteins, UNC-98 and UNC-96, are involved in myofibril assembly and/or maintenance, especially myosin thick filaments. We found that CSN-5, a component of the COP9 signalosome complex, binds to UNC-98 and -96 using the yeast two-hybrid method. These interactions were confirmed by biochemical methods. The CSN-5 protein contains a Mov34 domain. Although one other COP9 signalosome component, CSN-6, also has a Mov34 domain, CSN-6 did not interact with UNC-98 or -96. Anti-CSN-5 antibody colocalized with paramyosin at A-bands in wild type and colocalized with abnormal accumulations of paramyosin found in unc-98, -96, and -15 (encodes paramyosin) mutants. Double knockdown of csn-5 and -6 could slightly suppress the unc-96 mutant phenotype. In the double knockdown of csn-5 and -6, the levels of UNC-98 protein were increased and the levels of UNC-96 protein levels were slightly reduced, suggesting that CSN-5 promotes the degradation of UNC-98 and that CSN-5 stabilizes UNC-96. In unc-15 and unc-96 mutants, CSN-5 protein was reduced, implying the existence of feed back regulation from myofibril proteins to CSN-5 protein levels. Taken together, we found that CSN-5 functions in muscle cells to regulate UNC-98 and -96, two M-line proteins.
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9

Fagundes, Mariana Costa, Pauli Adriano de Almada Garcia, Gustavo Da Silva Motta, and Daniel Reis Armond-de-Melo. "PERFIL TECNOLÓGICO DA CSN : UM ESTUDO PATENTOMÉTRICO." Review of Administration and Innovation - RAI 11, no. 1 (April 13, 2014): 276. http://dx.doi.org/10.5773/rai.v11i1.1307.

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10

Lortie, Guy. "L’évolution de l’action politique de la CSN." Relations industrielles 22, no. 4 (April 12, 2005): 532–57. http://dx.doi.org/10.7202/027837ar.

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Les syndicats ouvriers ne peuvent pas rester étrangers à l'action politique. Celle-ci peut cependant prendre plusieurs formes. Dans cette étude l'auteur montre l'évolution de la CSN (autrefois CTCC) face à l'action politique.
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11

Nesrallah, Gihad, Loreen Gilmour, Adeera Levin, Reem Mustafa, Steven Soroka, and Deborah Zimmerman. "The CSN COVID-19 Rapid Response Program." Canadian Journal of Kidney Health and Disease 7 (January 2020): 205435812094911. http://dx.doi.org/10.1177/2054358120949110.

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The coronavirus disease (COVID-19) pandemic has created unprecedented challenges in caring for individuals living with kidney disease. In response to a growing call for up-to-date information and evidence-informed advice, the Canadian Society of Nephrology has established a COVID-19 Rapid Response Team that will leverage existing evidence and national expertise to inform kidney care practices in the COVID-19 era. Given limited published evidence and compressed timelines, formal clinical practice guidelines are not feasible, and we have adopted rapid review methods to instead provide interim guidance across identified priority areas. In this article, we describe the methodological approach that was applied in developing a first iteration of guidance documents addressing clinical and operational aspects of care for patients treated with in-center hemodialysis, home dialysis, those with advanced chronic kidney disease, those with glomerulonephritis, and those with acute kidney injury. We further describe strategies for maintaining ongoing engagement with the renal community to elicit emerging needs and perspectives as the situation unfolds.
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12

Lammers, U., A. Mañanes, G. Borstel, and J. A. Alonso. "Electronic structure of CsN and CsNO clusters." Solid State Communications 71, no. 7 (August 1989): 591–94. http://dx.doi.org/10.1016/0038-1098(89)90542-5.

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13

Szweda, Roy. "Centres of excellence: IPRM, CSN & LDSD." III-Vs Review 7, no. 2 (April 1994): 2. http://dx.doi.org/10.1016/0961-1290(94)90031-0.

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14

Gonzalez, Alvaro, Fernando D. Gonzalez-Nilo, and Raul Cachau. "Collaboratory for Structural Nanobiology (CSN), Nanoparticles Database." Biophysical Journal 96, no. 3 (February 2009): 48a. http://dx.doi.org/10.1016/j.bpj.2008.12.146.

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15

Pearce, Claire, Rachel E. Hayden, Christopher M. Bunce, and Farhat L. Khanim. "Analysis of the role of COP9 Signalosome (CSN) subunits in K562; the first link between CSN and autophagy." BMC Cell Biology 10, no. 1 (2009): 31. http://dx.doi.org/10.1186/1471-2121-10-31.

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16

Gutierrez, Craig, Ilan E. Chemmama, Haibin Mao, Clinton Yu, Ignacia Echeverria, Sarah A. Block, Scott D. Rychnovsky, Ning Zheng, Andrej Sali, and Lan Huang. "Structural dynamics of the human COP9 signalosome revealed by cross-linking mass spectrometry and integrative modeling." Proceedings of the National Academy of Sciences 117, no. 8 (February 7, 2020): 4088–98. http://dx.doi.org/10.1073/pnas.1915542117.

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The COP9 signalosome (CSN) is an evolutionarily conserved eight-subunit (CSN1–8) protein complex that controls protein ubiquitination by deneddylating Cullin-RING E3 ligases (CRLs). The activation and function of CSN hinges on its structural dynamics, which has been challenging to decipher by conventional tools. Here, we have developed a multichemistry cross-linking mass spectrometry approach enabled by three mass spectometry-cleavable cross-linkers to generate highly reliable cross-link data. We applied this approach with integrative structure modeling to determine the interaction and structural dynamics of CSN with the recently discovered ninth subunit, CSN9, in solution. Our results determined the localization of CSN9 binding sites and revealed CSN9-dependent structural changes of CSN. Together with biochemical analysis, we propose a structural model in which CSN9 binding triggers CSN to adopt a configuration that facilitates CSN–CRL interactions, thereby augmenting CSN deneddylase activity. Our integrative structure analysis workflow can be generalized to define in-solution architectures of dynamic protein complexes that remain inaccessible to other approaches.
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17

Lim, Jae-Sung, Mi Sun Oh, Ju-Hun Lee, San Jung, Chulho Kim, Min Uk Jang, Sang-Hwa Lee, et al. "Prediction of post-stroke dementia using NINDS-CSN 5-minute neuropsychology protocol in acute stroke." International Psychogeriatrics 29, no. 5 (January 25, 2017): 777–84. http://dx.doi.org/10.1017/s1041610216002520.

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ABSTRACTBackground:The National Institute of Neurological Disease and Stroke-Canadian Stroke Network (NINDS-CSN) 5-minute neuropsychology protocol consists of only verbal tasks, and is proposed as a brief screening method for vascular cognitive impairment. We evaluated its feasibility within two weeks after stroke and ability to predict the development of post-stroke dementia (PSD) at 3 months after stroke.Method:We prospectively enrolled subjects with ischemic stroke within seven days of symptom onset who were consecutively admitted to 12 university hospitals. Neuropsychological assessments using the NINDS-CSN 5-minute and 60-minute neuropsychology protocols were administered within two weeks and at 3 months after stroke onset, respectively. PSD was diagnosed with reference to the American Heart Association/American Stroke Association statement, requiring deficits in at least two cognitive domains.Results:Of 620 patients, 512 (82.6%) were feasible for the NINDS-CSN 5-minute protocol within two weeks after stroke. The incidence of PSD was 16.2% in 308 subjects who had completed follow-up at 3 months after stroke onset. The total score of the NINDS-CSN 5-minute protocol differed significantly between those with and without PSD (4.0 ± 2.7, 7.4 ± 2.7, respectively; p < 0.01). A cut-off value of 6/7 showed reasonable discriminative power (sensitivity 0.82, specificity 0.67, AUC 0.74). The NINDS-CSN 5-minute protocol score was a significant predictor for PSD (adjusted odds ratio 6.32, 95% CI 2.65–15.05).Discussion:The NINDS-CSN 5-minute protocol is feasible to evaluate cognitive functions in patients with acute ischemic stroke. It might be a useful screening method for early identification of high-risk groups for PSD.
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Gautam, Devika, Ashutosh Vats, Mahima Verma, Pramod Kumar Rout, Amar Singh Meena, Murtaza Ali, Sameni Deepika, and Sachinandan De. "Genetic variation in CSN 3 exon 4 region of Indian goats and a new nomenclature of CSN 3 variants." Animal Genetics 50, no. 2 (February 6, 2019): 191–92. http://dx.doi.org/10.1111/age.12767.

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19

Vigneron, O., Y. Duchossoy, and P. Moissonnier. "The use of the cutaneous saphenous nerve as a source of nerve graft material in the dog (the use of the CSN as a graft)." Veterinary and Comparative Orthopaedics and Traumatology 14, no. 02 (2001): 84–89. http://dx.doi.org/10.1055/s-0038-1632680.

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This paper analyses the feasibility of using the cutaneous saphenous nerve (CSN) as a source of peripheral nerve graft (PNG). In 34 fresh dog cadavers, the PNG length (PNGL) was measured, pattern of collateralization was studied, fascicles diameter and number were assessed at multiple levels along the length of the CSN (levels of section A, B, C and D) and surgical approach was described. The PNGL was correlated to femoral length. The pattern of CSN collateralization was consistent for all but 2 of the dogs. The average cross section diameter and fascicle number of the CSN was 2.0 to 0.1 mm (1 to 7 fascicles). CSN provides a large-sized, easily accessible nerve graft that could be used to bridge nerve gaps in the dog.
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20

Araújo, Fábio Salgado. "A Companhia Siderúrgica Nacional (CSN) e a Políticas Sociais de Lazer para os Trabalhadores." LICERE - Revista do Programa de Pós-graduação Interdisciplinar em Estudos do Lazer 18, no. 3 (October 21, 2015): 1–35. http://dx.doi.org/10.35699/1981-3171.2015.1125.

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O presente artigo busca compreender as políticas sociais de lazer instituídas pela Companhia Siderúrgica Nacional (CSN) discutindo a influência da empresa sobre o tempo livre de seus trabalhadores. A CSN representava na década de 1940 a construção de um projeto de caráter nacional-desenvolvimentista que procurava criar uma nova concepção de relação entre o Estado e a classe trabalhadora, inclusive no tempo do não trabalho, com a promoção de atividades de lazer. O lazer oferecido e fomentado pela CSN tinha como característica atender, preservar, recuperar e aumentar a capacidade de produzir do trabalhador apresentando características do momento industrial-fordista no Brasil com destaque para as atividades sócio-culturais e esportivos que acontecia principalmente nos clubes sociorrecreativos vinculados a empresa.
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21

Denti, Simona, Maria Elena Fernandez-Sanchez, Lars Rogge, and Elisabetta Bianchi. "The COP9 Signalosome Regulates Skp2 Levels and Proliferation of Human Cells." Journal of Biological Chemistry 281, no. 43 (August 30, 2006): 32188–96. http://dx.doi.org/10.1074/jbc.m604746200.

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The COP9 signalosome (CSN) is a conserved, multisubunit complex first identified as a developmental regulator in plants. Gene inactivation of single CSN subunits results in early embryonic lethality in mice, indicating that the CSN is essential for mammalian development. The pleiotropic function of the CSN may be related to its ability to remove the ubiquitin-like peptide Nedd8 from cullin-RING ubiquitin ligases, such as the SCF complex, and therefore regulate their activity. However, the mechanism of CSN regulatory action on cullins has been debated, since, paradoxically, the CSN has an inhibitory role in vitro, while genetic evidence supports a positive regulatory role in vivo. We have targeted expression of CSN subunits 4 and 5 in human cells by lentivirus-mediated small hairpin RNA delivery. Down-regulation of either subunit resulted in disruption of the CSN complex and in Cullin1 hyperneddylation. Functional consequences of CSN down-regulation were decreased protein levels of Skp2, the substrate recognition subunit of SCFSkp2, and stabilization of a Skp2 target, the cyclin-dependent kinase inhibitor p27Kip1. CSN down-regulation caused an impairment in cell proliferation, which could be partially reversed by suppression of p27Kip1. Moreover, restoring Skp2 levels in CSN-deficient cells recovered cell cycle progression, indicating that loss of Skp2 in these cells plays an important role in their proliferation defect. Our data indicate that the CSN is necessary to ensure the assembly of a functional SCFSkp2 complex and therefore contributes to cell cycle regulation of human cells.
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22

Krekeler, Daniel, and Heribert Cypionka. "The preferred electron acceptor of Desulfovibrio desulfuricans CSN." FEMS Microbiology Ecology 17, no. 4 (August 1995): 271–77. http://dx.doi.org/10.1111/j.1574-6941.1995.tb00151.x.

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23

Schweitzer, Katrin, Przemyslaw M. Bozko, Wolfgang Dubiel, and Michael Naumann. "CSN controls NF-κB by deubiquitinylation of IκBα." EMBO Journal 26, no. 6 (February 22, 2007): 1532–41. http://dx.doi.org/10.1038/sj.emboj.7601600.

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24

Chartier, Roger. "Chronologie de l'évolution confessionnelle de la CTCC (CSN)." Informations 16, no. 1 (February 3, 2014): 102–12. http://dx.doi.org/10.7202/1021892ar.

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Sommaire Cette chronologie, qu'a préparée Roger Chartier, doit beaucoup au Procès-verbal de la 39e session du Congrès de la CTCC (Montréal, 25 septembre — 1er octobre 1960), et notamment au Rapport de l'Exécutif de la CTCC sur la confessionnalité rédigé par le secrétaire général, M. Jean Marchand.
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25

Marazziti, D., A. Rotondo, L. Palego, L. Pancioli-Guadagnucci, C. Mazzanti, C. Martini, A. Lucacchini, and G. B. Cassano. "Dysfunctions of peripheral CSN markers in anxiety disorders." European Neuropsychopharmacology 2, no. 3 (September 1992): 315–16. http://dx.doi.org/10.1016/0924-977x(92)90156-3.

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Ahmed, Zubair, Ellen L. Suggate, Ann Logan, and Martin Berry. "Retinal Ganglion Cell Survival and Axon Regeneration after Optic Nerve Transection is Driven by Cellular Intravitreal Sciatic Nerve Grafts." Cells 9, no. 6 (May 27, 2020): 1335. http://dx.doi.org/10.3390/cells9061335.

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Neurotrophic factors (NTF) secreted by Schwann cells in a sciatic nerve (SN) graft promote retinal ganglion cell (RGC) axon regeneration after either transplantation into the vitreous body of the eye or anastomosis to the distal stump of a transected optic nerve. In this study, we investigated the neuroprotective and growth stimulatory properties of SN grafts in which Schwann cells had been killed (acellular SN grafts, ASN) or remained intact (cellular SN grafts, CSN). We report that both intravitreal (ivit) implanted and optic nerve anastomosed CSN promote RGC survival and when simultaneously placed in both sites, they exert additive RGC neuroprotection. CSN and ASN were rich in myelin-associated glycoprotein (MAG) and axon growth-inhibitory ligand common to both the central nervous system (CNS) and peripheral nervous system (PNS) myelin. The penetration of the few RGC axons regenerating into an ASN at an optic nerve transection (ONT) site is limited into the proximal perilesion area, but is increased >2-fold after ivit CSN implantation and increased 5-fold into a CSN optic nerve graft after ivit CSN implantation, potentiated by growth disinhibition through the regulated intramembranous proteolysis (RIP) of p75NTR (the signalling trans-membrane moiety of the nogo-66 trimeric receptor that binds MAG and associated suppression of RhoGTP). Mϋller cells/astrocytes become reactive after all treatments and maximally after simultaneous ivit and optic nerve CSN/ASN grafting. We conclude that simultaneous ivit CSN plus optic nerve CSN support promotes significant RGC survival and axon regeneration into CSN optic nerve grafts, despite being rich in axon growth inhibitory molecules. RGC axon regeneration is probably facilitated through RIP of p75NTR, which blinds axons to myelin-derived axon growth-inhibitory ligands present in optic nerve grafts.
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Subramanian, K., G. Harivignesh, and A. Jeevitha. "The in vitro release features of 5-Fluorouracil from tablets with chitosan, soy protein extract and chitosan-soyprotein extract blend as carriers and their thermal degradation characteristics." Research Journal of Chemistry and Environment 25, no. 7 (June 25, 2021): 104–13. http://dx.doi.org/10.25303/257rjce10421.

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Natural polymers are finding widespread applications in drug delivery, scaffold fabrication, bio plastic production, food packaging, wound dressing etc. due to their availability, biodegradability, biocompatibility, renewable nature, ease of modification to achieve the desirable properties etc. In the present study, the commercially available soy protein extract (SPE), chitosan(CSN) and their physical blend(CSN-SPE) have been chosen as drug carrier matrices to campare their in vitro drug release features in simulated intestinal fluid for controlled release applications taking 5-fluorouracil (5-FU) as a typical drug. The percentages of 5-FU released from the SPE, CSN and CSN-SPE tablets as a function of time were quantified by reverse phase High Performance Liquid Chromatography using KH2PO4 solution (pH 6.8) as the mobile phase and C-18 column as the stationery phase. The observed drug release features were found to be different for these polymer carriers. The percentages of drug released during the initial periods upto 60 min were less in the CSN-SPE tablet than those observed for CSN and SPE tablets. This implied that the drug release rate can be modified by the proper choice of natural polymers in the blends as carriers. The thermal degradation characteristics of CSN, SPE and CSN-SPE blend and their 5-FU tablets were also analysed by simultaneous Thermogravimetry (TG) and Differential Thermal Analysis (DTA). Comparative analysis of the TG and DTA traces of these polymers and their 5-FU tablets implied that there may be a drug-matrix interaction. This along with different degrees of swellability and degradability of these polymers might account for the differences in the drug release features. The structures of CSN, SPE and CSN-SPE blend were characterized by FT-IR spectroscopy.
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Carvalho, Rita de Cássia Santos, José Luiz Trinta, and Fátima Cristina Trindade Bacellar. "CSN e Responsabilidade Sócio-Ambiental: Conscientização, Estratégia ou Necessidade? CSN and Corporate Social and Environmental Responsibility: Awareness, Strategy or Necessity?" Cadernos UniFOA 4, no. 10 (March 27, 2017): 41. http://dx.doi.org/10.47385/cadunifoa.v4i10.978.

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O presente caso para ensino aborda temas relacionados à Responsabilidade Sócio-Ambiental em ações praticadas pela Companhia Siderúrgica Nacional (CSN). Para tal, primeiramente é relatado o histórico da empresa, começando por sua fundação como uma empresa estatal que, após passar por um processo de privatização, tornou-se uma empresa internacionalizada e de capital aberto. Em seguida, dentro desse contexto, busca-se caracterizar a responsabilidade sócio-ambiental como elemento do planejamento estratégico da empresa, bem como de sua internacionalização e da diversificação do campo de negócios. O objetivo é discutir, no caso da empresa, como tais ações podem contribuir para a sustentabilidade, trazer vantagens competitivas e auxiliar na ampliação de seus negócios, principalmente, no exterior. Também estão incluídas neste trabalho questões para discussão em sala de aula, assim como, notas de ensino que, além de relacionar a literatura pertinente ao tema, são finalizadas com depoimentos de especialistas em Meio Ambiente sobre a importância dos programas de responsabilidade social empresarial. Espera-se que este caso proporcione uma estimulante discussão junto a alunos de graduação e de pós-graduação, em especial de programas lato sensu, sobre um tema tão importante e atual.
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Md Shahrodin, Nur Shazrynda, Abdul Razak Rahmat, and Agus Arsad. "Synthesis and Characterization of Cassava Starch Nanocrystals by Hydrolysis Method." Advanced Materials Research 1113 (July 2015): 446–52. http://dx.doi.org/10.4028/www.scientific.net/amr.1113.446.

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Cassava starch nanocrystals (CSN) has not been reported in open literature, although other starches such as rice, corn, potato and bean were widely used as the main material. Thus, the objective of this research was to investigate the possibility of synthesizing high yield of CSN at different concentration of sulphuric acid (H2SO4). The physical and chemical properties of synthesize CSN was also investigated. Synthesized CSN was prepared by hydrolysing native cassava starch (NCS) with several concentration of H2SO4 (2.8 M, 3.0 M, 3.2 M and 3.4 M). The acid hydrolysis process took five days with continuous stirring speed of 300 to 400 rpm, with constant temperature of 37 °C. The hydrolysed solution of CSN underwent centrifuging process with distilled water until neutral to make sure that no acid residues remain in the CSN solution. The CSN precipitate was dried in an oven over night at 60 °C. The highest yield (1.1 %) produced was from 3.4 M CSN. Morphology test by Transmission Electron Microscopy indicated that the samples have been destructed and degraded to be nanocrystals with a size range of 5 - 20 nm. X-ray Diffraction (XRD) and 13C Nuclear Magnetic Resonance (NMR) were used to indicate the type of crystallinity for both NCS and CSN.
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Harshuk-Shabso, Dana, Noam Castel, Ran Israeli, Sheri Harari, and Elah Pick. "Saccharomyces cerevisiae as a Toolkit for COP9 Signalosome Research." Biomolecules 11, no. 4 (March 25, 2021): 497. http://dx.doi.org/10.3390/biom11040497.

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The COP9 signalosome (CSN) is a highly conserved eukaryotic multi-subunit enzyme, regulating cullin RING ligase activities and accordingly, substrate ubiquitination and degradation. We showed that the CSN complex of Saccharomyces cerevisiae that is deviated in subunit composition and in sequence homology harbors a highly conserved cullin deneddylase enzymatic core complex. We took advantage of the non-essentiality of the S. cerevisiae CSN-NEDD8/Rub1 axis, together with the enzyme-substrate cross-species activity, to develop a sensitive fluorescence readout assay, suitable for biochemical assessment of cullin deneddylation by CSNs from various origins. We also demonstrated that the yeast catalytic subunit, CSN5/Jab1, is targeted by an inhibitor that was selected for the human orthologue. Treatment of yeast by the inhibitor led to the accumulation of neddylated cullins and the formation of reactive oxygen species. Overall, our data revealed S. cerevisiae as a general platform that can be used for studies of CSN deneddylation and for testing the efficacy of selected CSN inhibitors.
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Lin, Hong, Xiaozhe Zhang, Li Liu, Qiuyu Fu, Chuanlong Zang, Yan Ding, Yang Su, et al. "Basis for metabolite-dependent Cullin-RING ligase deneddylation by the COP9 signalosome." Proceedings of the National Academy of Sciences 117, no. 8 (February 11, 2020): 4117–24. http://dx.doi.org/10.1073/pnas.1911998117.

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The Cullin-RING ligases (CRLs) are the largest family of ubiquitin E3s activated by neddylation and regulated by the deneddylase COP9 signalosome (CSN). The inositol polyphosphate metabolites promote the formation of CRL–CSN complexes, but with unclear mechanism of action. Here, we provide structural and genetic evidence supporting inositol hexakisphosphate (IP6) as a general CSN cofactor recruiting CRLs. We determined the crystal structure of IP6 in complex with CSN subunit 2 (CSN2), based on which we identified the IP6-corresponding electron density in the cryoelectron microscopy map of a CRL4A–CSN complex. IP6 binds to a cognate pocket formed by conserved lysine residues from CSN2 and Rbx1/Roc1, thereby strengthening CRL–CSN interactions to dislodge the E2 CDC34/UBE2R from CRL and to promote CRL deneddylation. IP6 binding-deficient Csn2K70E/K70E knockin mice are embryonic lethal. The same mutation disabled Schizosaccharomyces pombe Csn2 from rescuing UV-hypersensitivity of csn2-null yeast. These data suggest that CRL transition from the E2-bound active state to the CSN-bound sequestered state is critically assisted by an interfacial IP6 small molecule, whose metabolism may be coupled to CRL–CSN complex dynamics.
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Choo, Yin Yin, Boon Kim Boh, Jessica Jie Wei Lou, Jolane Eng, Yee Chin Leck, Benjamin Anders, Peter G. Smith, and Thilo Hagen. "Characterization of the role of COP9 signalosome in regulating cullin E3 ubiquitin ligase activity." Molecular Biology of the Cell 22, no. 24 (December 15, 2011): 4706–15. http://dx.doi.org/10.1091/mbc.e11-03-0251.

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Cullin RING ligases (CRLs) are the largest family of cellular E3 ubiquitin ligases and mediate polyubiquitination of a number of cellular substrates. CRLs are activated via the covalent modification of the cullin protein with the ubiquitin-like protein Nedd8. This results in a conformational change in the cullin carboxy terminus that facilitates the ubiquitin transfer onto the substrate. COP9 signalosome (CSN)-mediated cullin deneddylation is essential for CRL activity in vivo. However, the mechanism through which CSN promotes CRL activity in vivo is currently unclear. In this paper, we provide evidence that cullin deneddylation is not intrinsically coupled to substrate polyubiquitination as part of the CRL activation cycle. Furthermore, inhibiting substrate-receptor autoubiquitination is unlikely to account for the major mechanism through which CSN regulates CRL activity. CSN also did not affect recruitment of the substrate-receptor SPOP to Cul3, suggesting it may not function to facilitate the exchange of Cul3 substrate receptors. Our results indicate that CSN binds preferentially to CRLs in the neddylation-induced, active conformation. Binding of the CSN complex to active CRLs may recruit CSN-associated proteins important for CRL regulation. The deneddylating activity of CSN would subsequently promote its own dissociation to allow progression through the CRL activation cycle.
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Zhang, Xiaozhe, and Feng Rao. "Are Inositol Polyphosphates the Missing Link in Dynamic Cullin RING Ligase Regulation by the COP9 Signalosome?" Biomolecules 9, no. 8 (August 7, 2019): 349. http://dx.doi.org/10.3390/biom9080349.

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The E3 ligase activity of Cullin RING Ligases (CRLs) is controlled by cycles of neddylation/deneddylation and intimately regulated by the deneddylase COP9 Signalosome (CSN), one of the proteasome lid-CSN-initiation factor 3 (PCI) domain-containing “Zomes” complex. Besides catalyzing the removal of stimulatory Cullin neddylation, CSN also provides a docking platform for other proteins that might play a role in regulating CRLs, notably protein kinases and deubiquitinases. During the CRL activity cycle, CRL–CSN complexes are dynamically assembled and disassembled. Mechanisms underlying complex dynamics remain incompletely understood. Recently, the inositol polyphosphate metabolites (IP6, IP7) and their metabolic enzymes (IP5K, IP6K) have been discovered to participate in CRL–CSN complex formation as well as stimulus-dependent dissociation. Here we discuss these mechanistic insights in light of recent advances in elucidating structural basis of CRL–CSN complexes.
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Bunker, Richard D. "Tackling the crystallographic structure determination of the COP9 signalosome." Acta Crystallographica Section D Structural Biology 72, no. 3 (March 1, 2016): 326–35. http://dx.doi.org/10.1107/s2059798316001169.

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The COP9 signalosome (CSN) is an essential multi-protein complex in eukaryotes. CSN is a master regulator of intracellular protein degradation, controlling the vast family of cullin–RING ubiquitin (E3) ligases (CRLs). Important in many cellular processes, CSN has prominent roles in DNA repair, cell-cycle control and differentiation. The recent crystal structure of human CSN provides insight into its exquisite regulation and functionality [Lingarajuet al.(2014),Nature (London),512, 161–165]. Structure determination was complicated by low-resolution diffraction from crystals affected by twinning and rotational pseudo-symmetry. Crystal instability and non-isomorphism strongly influenced by flash-cooling, radiation damage and difficulty in obtaining heavy-atom derivatives, were overcome. Many different subunits of the same fold class were distinguished at low resolution aided by combinatorial selenomethionine labelling. As an example of how challenging projects can be approached, the structure determination of CSN is described as it unfolded using cluster-compound MIRAS phasing, MR-SAD with electron-density models and cross-crystal averaging exploiting non-isomorphism among unit-cell variants of the same crystal form.
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Xiang, Guangbiao, Yanwen Wu, Yushuang Li, Chen Cheng, Jiancai Leng, and Hong Ma. "Structural and Optoelectronic Properties of Two-Dimensional Ruddlesden–Popper Hybrid Perovskite CsSnBr3." Nanomaterials 11, no. 8 (August 20, 2021): 2119. http://dx.doi.org/10.3390/nano11082119.

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Ultrathin inorganic halogenated perovskites have attracted attention owing to their excellent photoelectric properties. In this work, we designed two types of Ruddlesden–Popper hybrid perovskites, Csn+1SnnBr3n+1 and CsnSnn+1Br3n+2, and studied their band structures and band gaps as a function of the number of layers (n = 1–5). The calculation results show that Csn+1SnnBr3n+1 has a direct bandgap while the bandgap of CsnSnn+1Br3n+2 can be altered from indirect to direct, induced by the 5p-Sn state. As the layers increased from 1 to 5, the bandgap energies of Csn+1SnnBr3n+1 and CsnSnn+1Br3n+2 decreased from 1.209 to 0.797 eV and 1.310 to 1.013 eV, respectively. In addition, the optical absorption of Csn+1SnnBr3n+1 and CsnSnn+1Br3n+2 was blue-shifted as the structure changed from bulk to nanolayer. Compared with that of Csn+1SnnBr3n+1, the optical absorption of CsnSnn+1Br3n+2 was sensitive to the layers along the z direction, which exhibited anisotropy induced by the SnBr2-terminated surface.
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36

Mifflin, S. W., and R. B. Felder. "An intracellular study of time-dependent cardiovascular afferent interactions in nucleus tractus solitarius." Journal of Neurophysiology 59, no. 6 (June 1, 1988): 1798–813. http://dx.doi.org/10.1152/jn.1988.59.6.1798.

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1. We used a model of bilateral carotid sinus nerve (CSN) stimulation to investigate cardiovascular afferent interactions in nucleus tractus solitarius (NTS) in anesthetized cats. In some instances, interactions with afferent inputs from vagus or renal nerves were also examined. 2. Intracellular recordings were made from 88 NTS neurons activated by electrical stimulation of one or both CSNs. Excitatory (EPSPs), inhibitory (IPSPs), and combined excitatory and inhibitory (EPSP/IPSP) postsynaptic membrane potential responses to ipsilateral CSN stimulation were observed. The input from opposite CSN (30 of 34 neurons tested) or from other ipsilateral afferent sources (vagus nerve, 10 tested; renal nerve, 9 tested) was qualitatively the same as that from ipsilateral CSN. 3. Conditioning tests demonstrated that the response (EPSP, IPSP, or EPSP/IPSP) evoked by a test stimulus to one CSN was reduced in amplitude and/or duration by a prior stimulus (1-5 pulses) to the same (82 of 85 neurons) or to the opposite (30 of 37 neurons) CSN at conditioning intervals ranging from 50 to 550 ms. For cells in which CSN stimulation evoked an EPSP, this inhibitory interaction occurred with no change in resting membrane potential and no change in input resistance. For cells in which CSN stimulation evoked an IPSP, the inhibitory interaction persisted beyond the duration of the CSN evoked IPSP. 4. We infrequently (3 cells) observed an excitatory interaction, in which the conditioning stimulus resulted in rhythmic depolarization of the neuron and a facilitated action potential response to an appropriately timed test stimulus. 5. During continuous CSN stimulation, postsynaptic potentials (PSPs) evoked by ipsilateral CSN were abolished in the steady state at stimulus frequencies of 5-20 Hz (n = 14). In cells that received a convergent input from contralateral CSN, the PSP evoked by contralateral CSN was usually (6 of 8 tested) abolished at lower stimulus frequencies (median difference = 5.0 Hz). 6. We conclude that individual NTS neurons frequently have the same PSP response to peripheral afferent inputs of different origins. Time-dependent interactions among cardiovascular afferent inputs that evoke PSPs of like kind may determine the nature of the integrated signal conveyed from NTS to subsequent cardiovascular related central nuclei. Both inhibitory and, less frequently, excitatory time-dependent interactions between cardiovascular afferent inputs occur. The absence of membrane potential changes associated with the inhibitory interaction suggests it may be mediated by disfacilitation.
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Silva, S. N., E. C. Romão, G. S. Barbosa, W. B. da Costa, F. Vernilli, J. M. G. Lopes, and B. V. de Almeida. "Revamping of CSN BF2 hot blast stove no. 1." Ironmaking & Steelmaking 39, no. 8 (November 2012): 622–30. http://dx.doi.org/10.1179/1743281212y.0000000021.

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Pick, Elah, Kay Hofmann, and Michael H. Glickman. "PCI Complexes: Beyond the Proteasome, CSN, and eIF3 Troika." Molecular Cell 35, no. 3 (August 2009): 260–64. http://dx.doi.org/10.1016/j.molcel.2009.07.009.

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Wu, June-Tai, Ya-Ru Chan, and Cheng-Ting Chien. "Protection of cullin–RING E3 ligases by CSN–UBP12." Trends in Cell Biology 16, no. 7 (July 2006): 362–69. http://dx.doi.org/10.1016/j.tcb.2006.05.001.

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Luke-Glaser, Sarah, Marcia Roy, Brett Larsen, Thierry Le Bihan, Pavel Metalnikov, Mike Tyers, Matthias Peter, and Lionel Pintard. "CIF-1, a Shared Subunit of the COP9/Signalosome and Eukaryotic Initiation Factor 3 Complexes, Regulates MEL-26 Levels in the Caenorhabditis elegans Embryo." Molecular and Cellular Biology 27, no. 12 (April 2, 2007): 4526–40. http://dx.doi.org/10.1128/mcb.01724-06.

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ABSTRACT The COP9/signalosome (CSN) is an evolutionarily conserved macromolecular complex that regulates the cullin-RING ligase (CRL) class of E3 ubiquitin ligases, primarily by removing the ubiquitin-like protein Nedd8 from the cullin subunit. In the Caenorhabditis elegans embryo, the CSN controls the degradation of the microtubule-severing protein MEI-1 through CUL-3 deneddylation. However, the molecular mechanisms of CSN function and its subunit composition remain to be elucidated. Here, using a proteomic approach, we have characterized the CSN and CUL-3 complexes from C. elegans embryos. We show that the CSN physically interacts with the CUL-3-based CRL and regulates its activity by counteracting the autocatalytic instability of the substrate-specific adaptor MEL-26. Importantly, we identified the uncharacterized protein K08F11.3/CIF-1 (for CSN-eukaryotic initiation factor 3 [eIF3]) as a stoichiometric and functionally important subunit of the CSN complex. CIF-1 appears to be the only ortholog of Csn7 encoded by the C. elegans genome, but it also exhibits extensive sequence similarity to eIF3m family members, which are required for the initiation of protein translation. Indeed, CIF-1 binds eIF-3.F and inactivation of cif-1 impairs translation in vivo. Taken together, our results indicate that CIF-1 is a shared subunit of the CSN and eIF3 complexes and may therefore link protein translation and degradation.
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Bech-Otschir, Dawadschargal, Michael Seeger, and Wolfgang Dubiel. "The COP9 signalosome: at the interface between signal transduction and ubiquitin-dependent proteolysis." Journal of Cell Science 115, no. 3 (February 1, 2002): 467–73. http://dx.doi.org/10.1242/jcs.115.3.467.

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Recently the COP9 signalosome (CSN) has become a focus of interest for many researchers, because of its function at the interface between signal transduction and ubiquitin-dependent proteolysis. It is required for the proper progression of the cell cycle in Schizosaccharomyces pombe and is essential for development in plants and Drosophila. However, its function in mammalian cells remains obscure. Although the CSN shares structural similarities with the 26S proteasome lid complex (LID), its functions seem to be different from that of the LID. A variety of CSN-specific protein-protein interactions have been described in mammalian cells. However,it is currently unclear how many reflect true functions of the complex. Two activities associated with the CSN have been identified so far: a protein kinase and a deneddylase. The CSN-associated kinase phosphorylates transcription factors, which determines their stability towards the ubiquitin system. The associated deneddylase regulates the activity of specific SCF E3 ubiquitin ligases. The CSN thus appears to be a platform connecting signalling with proteolysis.
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WANG, Yanlin, Wendy DEVEREUX, Tracy M. STEWART, and Robert A. CASERO. "Polyamine-modulated factor 1 binds to the human homologue of the 7a subunit of the Arabidopsis COP9 signalosome: implications in gene expression." Biochemical Journal 366, no. 1 (August 15, 2002): 79–86. http://dx.doi.org/10.1042/bj20020211.

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Polyamines have been identified to play a role in the transcription of various growth-related genes. The recently discovered polyamine responsive element and the associated trans-acting proteins involved in polyamine-regulated transcription have provided a model system for the study of the role of polyamines in transcription. Polyamine-modulated factor 1 (PMF-1) was identified as one of the transacting factors that binds to NF-E2 related factor-2 (Nrf-2) to regulate the transcription of spermidine/spermine N1-acetyltransferase (SSAT). The possibility that PMF-1 also binds to other proteins involved in transcriptional regulation cannot be ruled out. Using a yeast two-hybrid strategy, it was found that PMF-1 binds to a human homologue of the Arabidopsis COP9 signalosome subunit 7a (CSN 7) protein. In the present study, we describe human CSN 7, a 275-amino-acid- containing protein that may have a direct role in regulating gene expression. CSN 7 and PMF-1 bind to each other, as well as compete with each other for binding to Nrf-2. This competition for Nrf-2 binding and interaction with each other is implicated in the regulation of SSAT transcription. CSN 7 possesses a C-terminal coiled-coil domain similar to the domain that mediates the interaction between PMF-1 and Nrf-2, suggesting that coiled-coil domains also mediate the interaction between CSN 7 and PMF-1. Since CSN 7 does not contain a DNA-binding domain, its effects on transcription must occur in conjunction with binding to other proteins. The results presented here demonstrate that PMF-1 and Nrf-2 can act as protein partners of CSN 7.
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Li, Xue Yong, Jun Hui Fu, Guo Hong Gao, and Shi Yong Li. "The Safety Control of Computer Systems and Networks Based on Adaptive Approach." Advanced Materials Research 121-122 (June 2010): 699–704. http://dx.doi.org/10.4028/www.scientific.net/amr.121-122.699.

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The safety control tools in CSN perform supervision and analysis of the parameters of security systems, so these tools are an important part of the security system. The crucial problem is to develop effective methods and tools for the adaptive control of CSN safety. The suggested adaptive safety control module for CSN based on the safety monitoring tools provides the flexible, correct and effective reaction of security system to the intruder actions. This module allows dynamical evaluation of the information value of each CSN resource and setting the optimal parameters of security system. As a result, the suggested tools allow decrease of the possible damage to the CSN resource from successful intrusions, along with decreasing of security system implementation cost.
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Brown, Steven, Hilary Minor, Theresa O’Brien, Yousaf Hameed, Brandon Feenstra, Dustin Kuebler, Will Wetherell, et al. "Review of Sunset OC/EC Instrument Measurements During the EPA’s Sunset Carbon Evaluation Project." Atmosphere 10, no. 5 (May 22, 2019): 287. http://dx.doi.org/10.3390/atmos10050287.

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To evaluate the feasibility of the Sunset semicontinuous organic and elemental carbon (OC/EC) monitor, the U.S. Environmental Protection Agency (EPA) sponsored the deployment of this monitor at Chemical Speciation Network (CSN) sites with OC and EC measurements via quartz fiber filter collection in Chicago, Illinois; Houston, Texas; Las Vegas, Nevada; St. Louis, Missouri; Rubidoux, California; and Washington, D.C. Houston, St. Louis, and Washington also had collocated Aethalometer black carbon (BC) measurements. Sunset OC generally compared well with the CSN OC (r2 = 0.73 across five sites); the Sunset/CSN OC ratio was, on average, 1.06, with a range among sites of 0.96 to 1.12. Sunset thermal EC and CSN EC did not compare as well, with an overall r2 of 0.22, in part because 26% of the hourly Sunset EC measurements were below the detection limit. Sunset optical EC had a much better correlation to CSN EC (r2 = 0.67 across all sites), with an average Sunset/CSN ratio of 0.90 (range of 0.7 to 1.08). There was also a high correlation of Sunset optical EC with Aethalometer BC (r2 = 0.77 across all sites), though with a larger bias (average Sunset/Aethalometer ratio of 0.56). When the Sunset instrument was working well, OC and OptEC data were comparable to CSN OC and EC.
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Raij, T. T., T. Mäntylä, O. Mantere, T. Kieseppä, and J. Suvisaari. "Cortical salience network activation precedes the development of delusion severity." Psychological Medicine 46, no. 13 (July 18, 2016): 2741–48. http://dx.doi.org/10.1017/s0033291716001057.

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BackgroundDelusion is the most characteristic symptom of psychosis. While researchers suggested an association between changes of the cortical salience network (CSN) and delusion, whether these CSN findings are a cause or a consequence of delusion remains unknown.MethodTo assess the effect of CSN functioning to forthcoming changes in delusion scores, we measured brain activation with 3-T functional magnetic resonance imaging in two independent samples of first-episode psychosis patients (total of 27 patients and 23 healthy controls). During scanning, the patients evaluated statements about whether an individual's psychosis-related experiences should be described as a mental illness, and control statements that were also evaluated by healthy controls. Symptoms were assessed at the baseline and at 2 months follow-up with Brief Psychiatric Rating Scale.ResultsBoth tasks activated the CSN in comparison with rest. Activation of CSN (‘illness evaluation v. control task’ contrast) in patients positively correlated with worsening of or less improvement in delusions at the 2-month follow-up assessment. This finding was independent of delusion and clinical insight scores at the baseline evaluation.ConclusionsOur findings link symptom-evaluation-related CSN functioning to severity of delusion and, importantly, add a new layer of evidence for the contribution of CSN functioning to the longitudinal course of delusions.
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He, Q., and Y. Liu. "Degradation of the Neurospora circadian clock protein FREQUENCY through the ubiquitin–proteasome pathway." Biochemical Society Transactions 33, no. 5 (October 26, 2005): 953–56. http://dx.doi.org/10.1042/bst0330953.

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Phosphorylation of the Neurospora circadian clock protein FREQUENCY (FRQ) promotes its degradation through the ubiquitin–proteasome pathway. Ubiquitination of FRQ requires FWD-1 (F-box/WD-40 repeat-containing protein-1), which is the substrate-recruiting subunit of an SCF (SKP/Cullin/F-box)-type ubiquitin ligase. In the fwd-1 mutant strains, FRQ degradation is defective, resulting in the accumulation of hyperphosphorylated FRQ and the loss of the circadian rhythmicities. The CSN (COP9 signalosome) promotes the function of SCF complexes in vivo. But in vitro, deneddylation of cullins by CSN inhibits SCF activity. In Neurospora, the disruption of the csn-2 subunit impairs FRQ degradation and compromises the normal circadian functions. These defects are due to the dramatically reduced levels of FWD-1 in the csn-2 mutant, a result of its rapid degradation. Other components of the SCFFWD−1 complex, SKP-1 and CUL-1 are also unstable in the mutant. These results establish important roles for SCFFWD−1 and CSN in the circadian clock of Neurospora and suggest that they are conserved components of the eukaryotic circadian clocks. In addition, these findings resolve the CSN paradox and suggest that the major function of CSN is to maintain the stability of SCF ubiquitin ligases in vivo.
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Felder, R. B., and C. M. Heesch. "Interactions in nucleus tractus solitarius between right and left carotid sinus nerves." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 5 (November 1, 1987): H1127—H1135. http://dx.doi.org/10.1152/ajpheart.1987.253.5.h1127.

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Bilateral carotid sinus nerve stimulation was used as a model for studying cardiovascular afferent interactions in the nucleus tractus solitarius (NTS) region of dorso-medial medulla. Extracellular action potential recordings were made from 69 single units, 33 of which were excited independently by both right and left carotid sinus nerves (CSNs). Fifteen of these were located in NTS. Peak latencies to electrical stimulation of NTS neurons were 17.7 +/- 2.1 ms to ipsilateral CSN and 20.9 +/- 1.5 ms to contralateral CSN. Summation of afferent input was routinely demonstrated. In 10 units in NTS, a conditioning stimulus applied to one CSN caused prolonged inhibition of the response to a test stimulus to the same or the other CSN. The duration of inhibition was dependent on the intensity of the conditioning stimulus, not on prior excitation of the unit by the conditioning stimulus. In five additional excitability testing experiments, we found limited evidence to suggest that primary afferent depolarization of the central fibers of one CSN by stimulation of the contralateral CSN might be contributing to this inhibitory interaction. The data suggest that the outcome of integrative interactions between right and left CSN inputs to NTS neurons may depend largely on the temporal sequence of convergent afferent impulses.
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Oron, Efrat, Mattias Mannervik, Sigal Rencus, Orit Harari-Steinberg, Shira Neuman-Silberberg, Daniel Segal, and Daniel A. Chamovitz. "COP9 signalosome subunits 4 and 5 regulate multiple pleiotropic pathways inDrosophila melanogaster." Development 129, no. 19 (October 1, 2002): 4399–409. http://dx.doi.org/10.1242/dev.129.19.4399.

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The COP9 signalosome (CSN) is an essential eight-subunit repressor of light-regulated development in Arabidopsis. This complex has also been identified in animals, though its developmental role remains obscure. CSN subunits have been implicated in various cellular processes, suggesting a possible role for the CSN as an integrator of multiple signaling pathways. In order to elucidate the function of the CSN in animals, a Drosophila model system has previously been established. Gel-filtration analysis with antibodies against CSN subunits 4, 5 and 7 revealed that these proteins act as a complex in Drosophila that is similar in size to the plant and mammalian complexes. Null mutations in either one of two subunits, CSN4 or CSN5, are larval lethal. Successful embryogenesis appears to be a consequence of maternal contribution of the complex. Biochemical analysis indicates that the different subunits are found in both CSN-dependent and CSN-independent forms, and that these forms are differentially affected by the mutations. Phenotypic characterization of these two mutants indicates that they show both shared and unique phenotypes, which suggest specific roles for each subunit. Both mutants have defective oocyte and embryo patterning, and defects in response to DNA damage, while csn5 mutants develop melanotic tumors and csn4 mutants have phenotypes reminiscent of defects in ecdysone signaling.
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Fouad, AA, and WN Al-Melhim. "Vanillin mitigates the adverse impact of cisplatin and methotrexate on rat kidneys." Human & Experimental Toxicology 37, no. 9 (December 8, 2017): 937–43. http://dx.doi.org/10.1177/0960327117745694.

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The present study investigated the probable protective effect of vanillin (VLN) against kidney injury induced by cisplatin (CSN) and methotrexate (MTX) in rats. The rats received a single injection of either CSN (7.5 mg/kg, i.p.) or MTX (20 mg/kg, i.p.). VLN treatment (150 mg/kg/day, i.p.) was started 1 day before administration of the nephrotoxic agents and continued for 7 days. Both CSN and MTX significantly increased serum creatinine, cystatin C, and neutrophil gelatinase–associated lipocalin and kidney tissue renal malondialdehyde, inducible nitric oxide synthase, tumor necrosis factor-α, interleukin-18, nuclear factor-κB p65, cytosolic cytochrome C, and caspase-3 and significantly decreased renal total antioxidant capacity and Bcl-2/Bax ratio in rats. VLN significantly ameliorated the changes of biochemical parameters induced by CSN and MTX. VLN also significantly reduced CSN- and MTX-induced histopathological injury and the expression of Fas ligand in rat kidneys. In conclusion, VLN significantly protected against CSN- and MTX-induced kidney injury in rats by inhibiting oxidative/nitrosative stress, inflammation, and apoptosis.
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50

Taal, Maarten W., Glenn M. Chertow, Helmut G. Rennke, Anuradha Gurnani, Tang Jiang, Aliakbar Shahsafaei, Julia L. Troy, Barry M. Brenner, and Harald S. Mackenzie. "Mechanisms underlying renoprotection during renin-angiotensin system blockade." American Journal of Physiology-Renal Physiology 280, no. 2 (February 1, 2001): F343—F355. http://dx.doi.org/10.1152/ajprenal.2001.280.2.f343.

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Abstract:
Potential determinants of chronic renal disease (CRD) progression were studied in male Munich-Wistar rats subjected to 5/6 nephrectomy and treated with candesartan (Csn; n = 30) or enalapril (Ena; n = 27) from 5 wk postsurgery. Despite control of systolic blood pressure (SBP; 24 wk: Csn = 143 ± 9; Ena = 148 ± 8 mmHg), urinary protein excretion rates (UprV) increased over 24 wk (Csn = 92 ± 10; Ena = 99 ± 8mg/day). Glomerulosclerosis scores (GS) at 24 wk were similar for Csn (42 ± 7%) vs. Ena (42 ± 4%), values close to those of untreated controls at 12 wk (43 ± 4%). At 24 wk, SBP and UprV correlated strongly with GS, together accounting for 72% of the variance in GS. Renal cortex mRNA levels (determined by competitive RT-PCR) for transforming growth factor (TGF)-β1 and monocyte chemoattractant protein (MCP)-1 were elevated in Csn and Ena at 12 wk and remained higher at 24 wk vs. sham. Strong correlations were evident among TGF-β1, MCP-1, and interleukin-1β and renal injury at 24 wk. Cns and Ena are thus equally effective renoprotective agents in this model. During renin-angiotensin system inhibition, renoprotection is dependent on control of both SBP and UprV. Incomplete suppression of renal cytokine gene expression may also contribute to CRD progression.
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