Relevant bibliographies by topics / Interleukine-2, gene

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Interleukine-2, gene'

Author: Grafiati
Published: 4 June 2021
Last updated: 3 February 2022

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Journal articles on the topic "Interleukine-2, gene"

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Amini, Hamideh, Seyed Davood Hoseini, Jamileh Nowroozi, and Delavar Shahbazzadeh. "Cloning and Sequencing of Iranian Chicken Interleukine-2 Gene." Jundishapur Journal of Microbiology 5, no. 3 (2012): 502–6. http://dx.doi.org/10.5812/jjm.3636.

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Hejazi, M. S., E. Alipour, and M. H. Pournaghi-Azar. "Immobilization and voltammetric detection of human interleukine-2 gene on the pencil graphite electrode." Talanta 71, no. 4 (2007): 1734–40. http://dx.doi.org/10.1016/j.talanta.2006.08.010.

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Pournaghi-Azar, M. H., M. S. Hejazi, and E. Alipour. "Developing an electrochemical deoxyribonucleic acid (DNA) biosensor on the basis of human interleukine-2 gene using an electroactive label." Analytica Chimica Acta 570, no. 2 (2006): 144–50. http://dx.doi.org/10.1016/j.aca.2006.04.067.

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Pournaghi-Azar, Mohammad Hossein, Mohammad Saeid Hejazi, and Esmaeel Alipour. "Detection of Human Interleukine-2 Gene Using a Label-Free Electrochemical DNA Hybridization Biosensor on the Basis of a Non-Inosine Substituted Probe." Electroanalysis 19, no. 4 (2007): 466–72. http://dx.doi.org/10.1002/elan.200603746.

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Valibeik, Ali, Negar Naderi, Abdolhakim Amini, et al. "Effect of camphor on biochemical factors and gene expression of antioxidant enzymes, inflammatory and apoptotic factors against gentamicin-induced nephrotoxicity in rats." Journal of Renal Injury Prevention 10, no. 3 (2020): e21-e21. http://dx.doi.org/10.34172/jrip.2021.21.

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Introduction: Camphor is a natural antioxidant with anti-inflammatory and tissue repair properties. Nephrotoxicity is the most important side effect of gentamicin (GEM) administration. Therefore, investigating the effect of natural antioxidants can resolve this complication. Objectives: We aimed to assay the effect of camphor on biochemical factors and gene expression of antioxidant enzymes (catalase [CAT], glutathione peroxidase [GPX]) and inflammatory markers (tumor necrosis factor-alpha [TNF-α], nuclear factor kappa-B [NF-κB], interleukine-6 [IL-6]), and apoptotic indices (BCL2-associated X protein [Bax], B-cell lymphoma 2 [Bcl-2], caspase-3)], against GEM-induced nephrotoxicity in rats. Materials and Methods: Thirty adult male Wistar rats were allocated to five groups. Positive control and treatment groups were given GEM to induce nephrotoxicity. Animal treatment groups were treated with camphor in olive oil for 12 days. Renal biopsies, serum, extraction of renal tissue and urine of rats were taken after the twelfth day. Biopsies were examined for structural changes using a light microscope, moreover, apoptosis, desired biochemical and inflammatory factors, were investigated by suitable methods. Results: Camphor had no effect on biochemical factors, including malondialdehyde (MDA), glutathione (GSH), nitric oxide (NO), urea, creatinine and urine protein. However, it reduced the gene expression of TNF-α, NF-κB, IL-6, Bax, and caspase-3 and increased the gene expression of GPX and CAT and Bcl-2. Moreover, camphor improved kidney histopathological changes in the camphor groups in comparison with the GEM group. Conclusion: Camphor can be useful in the attenuation of GEM-induced nephrotoxicity based on expression levels of examined enzymes and factors and improving kidney histopathological changes.
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Espinoza-Culupú, Abraham, Ricardo Vázquez-Ramírez, Mariella Farfán-López, et al. "Acylpolyamine Mygalin as a TLR4 Antagonist Based on Molecular Docking and In Vitro Analyses." Biomolecules 10, no. 12 (2020): 1624. http://dx.doi.org/10.3390/biom10121624.

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Toll-like receptors (TLRs) are transmembrane proteins that are key regulators of innate and adaptive immune responses, particularly TLR4, and they have been identified as potential drug targets for the treatment of disease. Several low-molecular-weight compounds are being considered as new drug targets for various applications, including as immune modulators. Mygalin, a 417 Da synthetic bis-acylpolyamine, is an analog of spermidine that has microbicidal activity. In this study, we investigated the effect of mygalin on the innate immune response based on a virtual screening (VS) and molecular docking analysis. Bone marrow-derived macrophages and the cell lines J774A.1 and RAW 264.7 stimulated with lipopolysaccharide (LPS) were used to confirm the data obtained in silico. Virtual screening and molecular docking suggested that mygalin binds to TLR4 via the protein myeloid differentiation factor 2 (MD-2) and LPS. Macrophages stimulated by mygalin plus LPS showed suppressed gene expression of tumor necrosis factor (TNF-α), interleukine 6 (IL-6), cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), as well as inhibition of signaling protein p65 of the nuclear factor κB (NF-κB), resulting in decreased production of nitric oxide (NO) and TNF-α. These results indicate that mygalin has anti-inflammatory potential, being an attractive option to be explored. In addition, we reinforce the importance of virtual screening analysis to assist in the discovery of new drugs.
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Qiu, Huiying, Yongquan Xue, Jinlan Pan, Yafang Wu, and Yong Wang. "The Establishment and Characterization of a Human Acute Myelocytic Leukemia Cell Line, SH-2 Carrying t(16;17))(q24;q12) Translocation." Blood 110, no. 11 (2007): 4128. http://dx.doi.org/10.1182/blood.v110.11.4128.4128.

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Abstract We report the establishment of a novel cell line from a patient with acute myelocytic leukemia. The initial growth of this cell line was dependent on the presence of the stromal cell and cytokine interleukine 3. Subsequently, a stroma and cytokine-independent cell line was established, named SH-2. The cell line has proliferated continuously in vitro for more than 24 months. The SH-2 cell line showed identical chromosomal alterations to that of the initial bone marrow aspiration specimen, demonstrated a t(16;17))(q24;q12) translocation accompanied by deletions of y and 17 and triple 19.Chromosome painting FISH and Multi-FISH conformed the karyotype.SH-2 cells expressed myeloid antigens CD13, CD33 and MPO, SH-2 co-expressed NK markers CD16 and CD56. The loss of one p53 allele were proven by chromosome painting, FISH. A point mutation of CAG to CAT at codon 576 of extron 5 in another p53 allele was found by direct sequencing of DNA. Neither Epstein-Barr virus nor mycoplasma was not detected in SH-2 cells. DNA fingerprinting confirmed the authenticity of the cell line. Cytokines of GM-CSF,IL-3,IL-6,SCF,IL-4 and IL-5 can improve the proliferation of SH-2. SH-2 has colony formality and tumorigenic capacity in nude mice. The breakpoints of chromosomes 16 and 17 were localized RP11-356C4(16q24.3)and between BAC clone RP1-161P9 and RP11-47L3 corresponding to 17q12. The establishment of an myelocytic leukemia cell line with t(16;17)(q24;q12) could be valuable for the study of leukemogenesis and for the research of cloning the new gene involved in the t(16;17)(q24;q12) translocation.
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Rios Ibarra, Clara Patricia, Barbara Verduzco Garza, Rocio Ortiz Lopez, et al. "Transcriptional gene expression profile in hepatocarcinoma cells induced by acetylsalicylic acid (ASA) in hepatitis C virus (HCV)-subgenomic replicon system." Journal of Clinical Oncology 31, no. 15_suppl (2013): e22016-e22016. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e22016.

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e22016 Background: It has been demonstrated that ASA treatment could down-regulate in vitro HCV expression in hepatocarcinoma cells (~50%, p 0.05). However, the signaling pathway induced during ASA antiviral effect has not been elucidated. We analyzed the transcriptional expression profile of Huh-7-HCV-subgenomic replicon cells in presence or absence of ASA in order to identify the signaling pathway and the molecular mechanisms involved in the antiviral effect induced by ASA on HCV expression. Methods: Huh-7-HCV-replicon cells (hepatocarcinoma) were exposed to 4 mM ASA from 24 to 72 hours. Total RNA was isolated, quantified and validated by capillary electrophoresis. After that, we performed a retrotranscription in vitro. Synthesized transcripts were marked with biotin, purified, fragmentized and hybridized in HG-U133 Plus 2 Gene Expression. Hybridization signals were captured with Gen Chip 3000 7G Scanner and analyzed by Expression Console and Dchit Software. Results: After normalization, we obtained hierarchical maps with differentially-expressed genes. Among genetic targets over-expressed, the following stood out CCAAT-enhancer-binding proteins (C/EBP), interleukine-8 (IL-8), cytochrome P450 (CyP450) and methallothioneins (MT) genes were found. Among down-regulated genes we identified ribonucleotide reductase (RR) and superoxide dismutase (SOD) genes. Some of these genes have been previously associated with oxidative stress regulation. All results were validated by real time PCR. Conclusions: We observed that ASA modulates the expression of genes associated with antioxidant role as SOD and methallothioneins. Antioxidant agents can inhibit virus proliferation. HCV decreased antioxidant defense, which promotes the development of hepatic complications caused by HCV infection, including liver cancer. Therefore, ASA could be inducing an antioxidant environment regulating HCV replication. This study provides a tool for identifying novel host factors in hepatocarcinoma cells involved in the antiviral effect regulated by ASA against HCV and improves our understanding of the regulatory mechanism of HCV replication.
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Xue, F., H. Li, J. Zhang, J. Lu, Y. Xia, and Q. Xia. "miR-31 regulates interleukin 2 and kinase suppressor of ras 2 during T cell activation." Genes & Immunity 14, no. 2 (2013): 127–31. http://dx.doi.org/10.1038/gene.2012.58.

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Fleury, Vanessa, Alkisti Zekeridou, Vladimir Lazarevic, et al. "Oral Dysbiosis and Inflammation in Parkinson’s Disease." Journal of Parkinson's Disease 11, no. 2 (2021): 619–31. http://dx.doi.org/10.3233/jpd-202459.

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Background: Oral microbiota has largely escaped attention in Parkinson’s disease (PD), despite its pivotal role in maintaining oral and systemic health. Objective: The aim of our study was to examine the composition of the oral microbiota and the degree of oral inflammation in PD. Methods: Twenty PD patients were compared to 20 healthy controls. Neurological, periodontal and dental examinations were performed as well as dental scaling and gingival crevicular fluid sampling for cytokines measurement (interleukine (IL)-1β, IL-6, IL-1 receptor antagonist (RA), interferon-γ and tumor necrosis factor (TNF)-α). Two months later, oral microbiota was sampled from saliva and subgingival dental plaque. A 16S rRNA gene amplicon sequencing was used to assess bacterial communities. Results: PD patients were in the early and mid-stage phases of their disease (Hoehn & Yahr 2–2.5). Dental and periodontal parameters did not differ between groups. The levels of IL-1β and IL-1RA were significantly increased in patients compared to controls with a trend for an increased level of TNF-α in patients. Both saliva and subgingival dental plaque microbiota differed between patients and controls. Streptococcus mutans, Kingella oralis, Actinomyces AFQC_s, Veillonella AFUJ_s, Scardovia, Lactobacillaceae, Negativicutes and Firmicutes were more abundant in patients, whereas Treponema KE332528_s, Lachnospiraceae AM420052_s, and phylum SR1 were less abundant. Conclusion: Our findings show that the oral microbiome is altered in early and mid-stage PD. Although PD patients had good dental and periodontal status, local inflammation was already present in the oral cavity. The relationship between oral dysbiosis, inflammation and the pathogenesis of PD requires further study.
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Dissertations / Theses on the topic "Interleukine-2, gene"

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Chérel, Michel. "Construction d'un recepteur soluble de haute affinite pour l'interleukine 2 : clonage de l'adn complementaire et du gene du recepteur a l'interleukine 11 humaine." Nantes, 1995. http://www.theses.fr/1995NANT10VS.

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ZELUS, DOMINIQUE. "Evolution des systemes de communication intercellulaire : l'interleukine-2 et le recepteur nucleaire usp (doctorat : parasitologie)." Lille 2, 1999. http://www.theses.fr/1999LIL2T008.

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Paradon, Michel. "Regulation transcriptionnelle du gene de la phospholipase a 2 secretee de type iia par les cytokines pro-inflammatoires interleukine 6 et interleukine 1." Paris 6, 1999. http://www.theses.fr/1999PA066383.

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La phospholipase a 2 secretee de type iia (pla 2s-iia) est l'une des enzymes les plus importantes dans la synthese des mediateurs lipidiques. A partir d'un phospholipide, elle libere un lysophospholipide et un acide gras. Lorsque celui-ci est l'acide arachidonique, il peut etre a l'origine des mediateurs tels que les prostaglandines ou les leucotrienes. Les phospholipase a2 representent un groupe d'enzymes heterogene tant en structure, qu'en conditions d'actions et en localisation. La pla 2s-iia n'agit pas seule. Son action serait coordonnee avec les autres phospholipases a 2 et les cyclooxygenases dans la synthese des mediateurs lipidiques. Son expression est modifiee par les cytokines pro-inflammatoires, les facteurs de croissance et les glucocorticoides. La regulation de son expression est principalement transcriptionnelle. Les cytokines interleukine-6 et interleukine-1 augmentent sa transcription dans les cellules d'hepatome humain hepg2 et de chondrocytes articulaires de lapin, respectivement. L'etude de sa regulation transcriptionnelle a montre que les facteurs c/ebp et sont responsables de l'augmentation de la transcription de la pla 2s-iia par les cytokines pro-inflammatoires interleukine-6 dans les cellules d'hepatome humain hepg2 et interleukine-1 dans les chondrocytes articulaires de lapin.
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DUFFOUR, MARIE-THERESE. "Immunotherapie antitumorale par transfert du gene de l'il-2 ou de l'antigene de tumeur p815a a l'aide d'adenovirus recombinants (doctorat : immunologie)." Paris 5, 1997. http://www.theses.fr/1997PA05N135.

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Beraud, Christophe. "Mecanismes d'activation de la transcription par le transactivateur tax1 du virus htlv-1 : cas des promoteurs du virus htlv-1 et du gene codant pour la sous-unite alpha du recepteur de l'interleukine-2." Lyon 1, 1991. http://www.theses.fr/1991LYO1BH52.

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Herblot, Sabine. "Etude des mécanismes moléculaires impliqués dans la différenciation et l'activation des cellules du système immunitaire : différenciation des macrophages, activation des lymphocytes T par l'IL-2." Bordeaux 2, 1997. http://www.theses.fr/1997BOR28518.

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Bukhari, Zahida. "Controle genetique de la production d'interleukine-2 chez la souris." Paris 7, 1987. http://www.theses.fr/1987PA077022.

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Hebenstreit, Daniel. "Signal transduction and gene activation by STAT6 gene regulation processes involved in type 2 immune polarisation." Saarbrücken VDM Verlag Dr. Müller, 2005. http://d-nb.info/988797763/04.

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Lauder, Angus James. "Regulation of the c myb gene by interleukin 2." Thesis, Institute of Cancer Research (University Of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271255.

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Wattanakaroon, Wanida. "Development of an interleukin 2 receptor targeted gene therapy vehicle." Texas A&M University, 2005. http://hdl.handle.net/1969.1/3724.

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The effectiveness of most chemotherapeutic regimens is limited by the toxicity of the therapy to normal healthy cells. Therapies to selectively modulate abnormal T cells bearing the interleukin 2 receptor (IL-2R) have been developed to treat diseases associated with aberrant immune response. This study describes the development and optimization of a targeted gene or oligonucleotide therapy vehicle to IL-2R bearing T cells for selective elimination of these cells. In this work, a monoclonal antibody to the IL-2R was used to target the oligonucleotide delivery vehicle which consisted of a polyamidoamine dendrimer. Optimization of the delivery vehicle involves understanding the factors that govern its association with oligonucleotide, the pathway of IL-2R endocytic trafficking, and the stability of the oligonucleotide in the biological milieu. Oligonucleotide stability in a cellular environment was examined intra- and extracellularly. Results showed that the rate of intracellular degradation of oligonucleotides was much greater than extracellular degradation. Binding of oligonucleotides to dendrimers was demonstrated as a function of dendrimer generation. The total binding capacities for dendrimers differed depending upon dendrimer size and surface group, whereas equilibrium binding affinity was comparable for all dendrimers tested. Binding of oligonucleotide delivery vehicle to the cell surface and subsequent internalization was inversely related to dendrimer size, and in all cases, significantly less than binding and internalization of the natural ligand for the IL-2R. Based on experimental results, a kinetic model of the delivery vehicle was derived which includedthe dependence of binding and internalization on dendrimer size and surface charge and intracellular degradation of oligonucleotide. Based on model predictions, we show that larger dendrimers carry more oligonucleotide than the smaller dendrimer vehicles, and delivery is more effective with larger vehicles. This work establishes our ability to predict the effects of different delivery vehicle properties on oligonucleotide delivery and aids in the development of design criteria for new vehicles for delivery of antisense, siRNA, or genes to IL-2R bearing cells.
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Book chapters on the topic "Interleukine-2, gene"

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Podoltseva, E., and E. Morozova. "Production of Interleukin-2 and Natural Killer (NK) Activity in Patients with Multiple Myeloma." In Gene Technology. Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61122-3_34.

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Riegel, Jeffrey S., Blaise Corthesy, Michael Flanagan, and Gerald R. Crabtree. "Regulation of the Interleukin-2 Gene (Part 2 of 2)." In Chemical Immunology and Allergy. KARGER, 1992. http://dx.doi.org/10.1159/000319093.

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Tamai, Tadakazu, Nobuyuki Sato, Syoji Kimura, Sanetaka Shirahata, and Hiroki Murakami. "Cloning and Expression of Flatfish Interleukin 2 Gene." In Animal Cell Technology: Basic & Applied Aspects. Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2844-5_68.

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Riegel, Jeffrey S., Blaise Corthesy, Michael Flanagan, and Gerald R. Crabtree. "Regulation of the Interleukin-2 Gene (Part 1 of 2)." In Chemical Immunology and Allergy. KARGER, 1992. http://dx.doi.org/10.1159/000319092.

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Hasegawa, Katsushige, Mitsuo Maruyama, Takashi Fujita, et al. "Structure and Regulation of the Genes Encoding Interleukin-2 and its Receptor." In Regulation of Immune Gene Expression. Humana Press, 1986. http://dx.doi.org/10.1007/978-1-4612-5014-2_8.

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Waldmann, Thomas A., Carolyn Goldman, and Mitsuro Tsudo. "The Multichain Interleukin-2 Receptor: From the Gene to the Bedside." In Clinical Chemistry. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0753-2_68.

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Li, Gang, and Li-Chang Chen. "Regulation of methionine-enkephalin on expression of interleukin-2 receptor α chain gene." In Peptides. Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-010-9069-8_61.

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Foa, Robert, Alessandro Cignetti, Anna Gillio Tos, Anna Carbone, Paola Francia do Celle, and Anna Guarini. "Is There a Role for Interleukin-2 Gene Transfer in the Management of Acute Leukemia?" In Acute Leukemias V. Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-78907-6_47.

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Schackert, G., A. Buttler, A. Mehrabi, H. K. Schackert, C. Herfarth, and S. Kunze. "Monocyte- and Lymphocyte-Mediated Cytotoxicity After Gene Transfer and Expression of Human Interleukin-2 in a Human Glioblastoma Cell Line." In Cerebellar Infarct. Midline Tumors. Minimally Invasive Endoscopic Neurosurgery (MIEN). Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78801-7_31.

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Favrot, Marie C., Yacine Merrouche, Jean-Yves Blay, et al. "Adoptive Immunotherapy with Interleukin-2 and LAK Cells or Gene Modified TIL in Patients with Renal Cell Carcinoma: Clinical and Laboratory Data." In Biology of Renal Cell Carcinoma. Springer New York, 1995. http://dx.doi.org/10.1007/978-1-4612-2536-2_22.

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Conference papers on the topic "Interleukine-2, gene"

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DiTullio, A. E., S. Park, P. A. Torzilli, and C. T. Chen. "Cyclic Compression of Chondrocytes Counteracts Pro-Inflammatory Tissue Remodeling Induced by Interleukin-1." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193027.

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Chondrocytes in tissue engineered constructs face challenging environments when first transplanted into a synovial joint, including high levels of compression/shear and pro-inflammatory cytokines. The joint level of interleukin 1 (IL-1) after trauma injury and in a repaired joint is acutely elevated. Matrix remodeling in tissue engineered constructs can be easily affected by the elevation and activation of aggrecanases (ADAMTS-4 and ADAMTS-5) and matrix metalloproteinases (MMPs) [2–4, 7–9, 11]. Several recent studies suggest that tensile loading and unconfined compression of chondrocytes has some anti-inflammatory effects against interleukin 1 (IL-1) by the downregulation of COX-2 and iNOS genes [1, 5, 6]. However, the role of loading in tissue repair at physiological levels is not clear. The objective of this study was to determine the effect of cyclic confined compression on the gene expression of MMPs and tissue inhibitors of metalloproteinases (TIMPs) in agarose-embedded chondrocytes in the presence of interleukin 1 (IL-1).
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Daulay, Milahayati, and Mutiara Indah Sari. "Interleukin-4 Gene Polymorphisms in Type 2 Diabetes Mellitus in Medan, Indonesia." In International Conference of Science, Technology, Engineering, Environmental and Ramification Researches. SCITEPRESS - Science and Technology Publications, 2018. http://dx.doi.org/10.5220/0010078905750577.

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Li, Yang, Miaojing Li, Xinyu Cui, et al. "Research Progress on the Relationship between Interleukins Gene Polymorphism and Type 2 Diabetes." In International Conference on Biomedical and Biological Engineering. Atlantis Press, 2016. http://dx.doi.org/10.2991/bbe-16.2016.54.

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Killian, Megan L., Barbara Zielinska, and Tammy L. Haut Donahue. "Role of IL-1 on Aggrecanase and COX-2 Gene Expression of Meniscal Explants Following Dynamic Compression." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19110.

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The menisci within the knee likely respond to adverse loading conditions, leading to aggravated cartilage damage and fissuring [1]. Upregulation of catabolic molecules such as interleukin-1α (IL-1α), metalloproteinases (MMPs), aggrecanases (ADAMTS-4 and -5), and cyclooxygenase-2 (COX-2), as well as release of proteoglycans [2], have been shown in vitro for meniscal explants following dynamic loading [3]. A crucial event in matrix degradation is the loss of aggrecan, caused by the ADAMTS family [4]. In osteoarthritic cartilage, IL-1 has been shown to influence COX-2 activity, leading to increased synthesis of prostaglandin E2 and subsequent proteinase activity [5].
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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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Shen, Li, and Roberto Pili. "Abstract 5437: The histone deacetylase (HDAC) inhibitor SNDX-275 enhances the antitumor effect of interleukin 2 (IL-2) by suppressing regulatory T cell gene expression and function." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5437.

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Vaillancourt, Vanessa, Emmanuelle Bouzigon, Florent Monier, et al. "Association Study Between Interleukin 1 Receptor Type 2 (IL1R2) Pathway Genes And Asthma Related Phenotypes In Two Independent Familial Studies." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6172.

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Loskutoff, D. J., J. Mimuro, and C. Hekman. "PLASMINOGEN ACTIVATOR INHIBITOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644763.

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Plasminogen activation provides an important source of localized proteolytic activity not only during fibrinolysis, but also during ovulation, cell migration, epithelial cell differentiation, tumor invasion and a variety of other physiological processes. Precise regulation of plasminogen activator (PA) activity thus constitutes a critical feature of many biological processes. This control is achieved in large part through the action of specific PA inhibitors (PAIs). Although 4 distinct PAIs have been detected,1the endothelial cellTderived inhibitor (PAI-1) is the only one that efficiently inhibits both urokinase (Kd=2.3×10−13M; Kassoc =1.6×108 M−1s−1) and single-chaintissue-type PA (tPA; Kd=1.3×lO−15 M Kd=3.9×lO7M−1s−1). It also inhibits trypsin (Kassoc=6.8×106M−1 s−1 ) ancl Plasmin (Kassoc=7.6×l05 M−1 s5 Analysis of the effect of PAI-1 on the rate of plasminogen activation revealed a competitive type of inhibition when urokinase was employed but a linear mixed type of inhibition when single chain tPA was employed. These results suggest that the interaction of PAI-1 with tPA, in contrast to its interaction with urokinase, may involve 2 sites on the tPA molecule.PAI-1 has been purified from medium conditioned by cultured bovine aortic endothelial cells and partially characterized. It is a major biosynthetic product of these cells, accounting for as much as 12% of the total protein released by the cells in 24 h. It has an M of 50,000, an isoelectric point of 4.5-5.0, and is immunologically and biochemically related to the rapidly acting inhibitor present in human platelets and in the plasma of some patients at risk to develop thrombotic problems. Although it is relatively stable to conditions which inactivate most protease inhibitors (acid pH, SDS), it is extremely sensitive to oxidants. The molecular cloning of the PAI-1 gene revealed that the mature human protein is 379 amino acids long, contains an NH2-terminal valine, lacks cysteines and has a methionine at the Pi position of it's reactive center. The conversion of this methionine to methionine sulfoxide may be responsible for the rapid inactivation of PAI-1 by oxidants. Human PAI-1 has extensive (30%) homology with α1-antitrypsin and antithrombin III and is thus a member of the serine proteinase inhibitor (serpin) family; a group of related molecules that control the major protease cascades of the blood. The PAI-1 gene is approximately 12.2 kilobase pairs in length and is organized into nine exons and eight introns.The production of PAI-1 by endothelial cells is stimulated by endotoxin, interleukin-1, tumor necrosis factor, and transforming growth factor β(TGFβ). The cells are extremely sensitive to TGFβwith maximal effects (100-fold stimulation) observed with 1-2 ng/ml. These changes were relatively specific for PAI-1, and could be detected at both the protein and the RNA level. Interestingly, TGFgalso stimulated the amount of PAI-1 present in the extracellular matrix (ECM) of BAEs. PAI-1 was one of the primary ECM components of these cells, constituting 10-20% of the ECM proteins detected after SDS-PAGE.One of the most unusual properties of PAI-1 is that it exists in blood and in various cellular samples in both an active and an inactive (latent) form, the ratio depending on the source. The latent form can be converted into the active one by treatment with denaturants like SDS or guanidine-HCl. Although the majority of the cell-associated PAI-1 is active, it rapidly decays (t1/2=3 h) into the latent form once it is released from the cells. In contrast, the half-life of ECM associated PAI-1 was greater than 24 h. These data suggest that PAI-1 is produced by BAEs in an active form, and is then either released into the medium where it is rapidly inactivated, or released into the subendothelium where it binds to ECM. The specific binding of PAI-1 to ECM protects it from this inactivation.
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Dejana, E., F. Breviario, F. Bussolino, L. Mussoni, and A. Mantovani. "PLEIOTROPIC EFFECT OF INTERLEUKIN-1 ON ENDOTHELIAL CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643984.

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Abstract:
Inflammatory processes are often associated with pathological alteration of the vessel wall and sometimes with local or disseminated thrombotic phenomena. Interleukin-1 (IL-1), a monokine produced by activated cells of the monocyte/macrophage lineage and responsible of most of the changes associated with the inflammatory acute phase response, appears to dramatically' modify several endothelial cell (EC) functions. Some groups including ours (for review 1) have shown that IL-1 stimulates prostacyclin (PGI2), platelet activating factor (PAF), plasminogen activator inhibitor (PAi), thromboplastin (PCA) synthesis by cultured human EC in vitro. In addition IL-1 can act directly on EC to increase neuthophil and other leukocyte adhesion on their surface (2). All these effects, in contrast to previously described inducers, require a long time of interaction (30 min to 4 hours) of IL-1 with EC to be apparent and then last for several hours (4 to 12 hours). The IL-1 effects are concentration dependent (minimal active concentration being about 1 unit/ml) and require protein and RNA synthesis. To better define the structural requirement for IL-1 induced modification of EC functions we compared the activity of different IL-1 molecular species. Our approach is based on the observation that IL-1 is indeed a family of polypeptides biochemically different(3). At least two dissimilar gene products have been cloned with very limited homology (denominated α and β). These molecules, though biochemically different, share common activities and possibly the same receptor in different cell types. On EC we investigated whether the αand β IL-1 forms have similar biological activities (4). All the IL-1 preparations used were active on thymocyte costimulatory assay and comparison was made on the basis of the concentrations of these agents equally active on this assay.Human recombinant IL- αandβ (hr IL-1 α and hr IL-1 β) were both active in stimulating PGI2, PCA, PAi production and in increasing neutrophil adhesion to EC. In contrast PAF synthesis was Stimulated by hr IL-1 α but not by hr IL-1 β. Murine recombinant IL-1 (mr IL-1 α highly homologous with hr IL-1 < α, at concentrations able to maximally activate thymocytes was inactive on PGI2, PCA and in increasing neutrophil adhesion to EC. In contrast, mr IL-1 α was equally effective on PAF production as hr IL-1 α. A short peptide fragment of hr IL-1β (fragment 167-171) was synthesized on the basis of its predicted exposure on the surface of the molecule (5). This peptide is also located in a region (150-186) of high homology between hr IL-1α and β sequences. While the peptide showed high thymocyte activation capacity it was inactive on EC activities. Overall these results indicate that the α and β forms of human IL-1 elicit largely but not completely overlapping patterns of response in EC. In addition they suggest that the structural requirement for activation by IL-1 is not identical for thymocytes and EC. These results might provide some clues to novel strategies for modulation of IL-1 vascular and immunological activities.1. Mantovani A. and E. Dejana (1987) Biochem. Pharm. 36:301.2. Bevilacqua M. et al. (1985) J. Clin. Invest. 76:20033. Dinarello C.A. (1985) J. Clin. Immunol. 5:287.4. Dejana E. et al. (1987) Blood 69:695.5. Antoni G. et al. (1987) J. Immunol, (in press).
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