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Academic literature on the topic 'Gene nod'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Gene nod"

Zuanazzi, José Angelo Silveira, Pierre Henri Clergeot, Jean-Charles Quirion, Henri-Philippe Husson, Adam Kondorosi, and Pascal Ratet. "Production of Sinorhizobium meliloti nod Gene Activator and Repressor Flavonoids from Medicago sativa Roots." Molecular Plant-Microbe Interactions® 11, no. 8 (August 1998): 784–94. http://dx.doi.org/10.1094/mpmi.1998.11.8.784.

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During symbiosis between leguminous plants and rhizobia, flavonoids exuded by the plants act as chemoattractants and nodulation (nod) gene regulators in the other partner. To better understand the role of these compounds during the early steps of the alfalfa-Sinorhizobium meliloti symbiosis and the regulation of their production we have isolated nod gene inducers from alfalfa roots. All the compounds that we identified in this study as nod gene inducers in the root are flavonoids, indicating that other compounds with nod gene activator capacity may have little contribution, if any, to nod gene activation. Most of the intermediates of the flavonoid pathway were found in Medicago sativa roots and nodules, but only end products of the flavonoid pathway were identified in the root exudate. We have also studied flavonoid production in different parts of the root and found that it is developmentally regulated during root growth. Finally, we have shown that coumestrol and medicarpin, present in the exudates and previously described as phytoalexins, possess nod gene repressing activity, indicating that the in vivo nod gene inducing activity of the root exudate results from positive as well as negative controls of nod gene expression by the flavonoids.

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Southwick, Audrey M., Lai-Xi Wang, Sharon R. Long, and Yuan C. Lee. "Activity of Sinorhizobium meliloti NodAB and NodH Enzymes on Thiochitooligosaccharides." Journal of Bacteriology 184, no. 14 (July 15, 2002): 4039–43. http://dx.doi.org/10.1128/jb.184.14.4039-4043.2002.

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ABSTRACT Rhizobium bacteria synthesize signal molecules called Nod factors that elicit responses in the legume root during nodulation. Nod factors, modified N-acylated β-(1,4)-N-acetylglucosamine, are synthesized by the nodulation (nod) gene products. We tested the ability of three Sinorhizobium meliloti nod gene products to modify Nod factor analogs with thio linkages instead of O-glycosidic bonds in the oligosaccharide backbone.

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Peck, Melicent C., Robert F. Fisher, and Sharon R. Long. "Diverse Flavonoids Stimulate NodD1 Binding to nod Gene Promoters in Sinorhizobium meliloti." Journal of Bacteriology 188, no. 15 (August 1, 2006): 5417–27. http://dx.doi.org/10.1128/jb.00376-06.

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ABSTRACT NodD1 is a member of the NodD family of LysR-type transcriptional regulators that mediates the expression of nodulation (nod) genes in the soil bacterium Sinorhizobium meliloti. Each species of rhizobia establishes a symbiosis with a limited set of leguminous plants. This host specificity results in part from a NodD-dependent upregulation of nod genes in response to a cocktail of flavonoids in the host plant's root exudates. To demonstrate that NodD is a key determinant of host specificity, we expressed nodD genes from different species of rhizobia in a strain of S. meliloti lacking endogenous NodD activity. We observed that nod gene expression was initiated in response to distinct sets of flavonoid inducers depending on the source of NodD. To better understand the effects of flavonoids on NodD, we assayed the DNA binding activity of S. meliloti NodD1 treated with the flavonoid inducer luteolin. In the presence of luteolin, NodD1 exhibited increased binding to nod gene promoters compared to binding in the absence of luteolin. Surprisingly, although they do not stimulate nod gene expression in S. meliloti, the flavonoids naringenin, eriodictyol, and daidzein also stimulated an increase in the DNA binding affinity of NodD1 to nod gene promoters. In vivo competition assays demonstrate that noninducing flavonoids act as competitive inhibitors of luteolin, suggesting that both inducing and noninducing flavonoids are able to directly bind to NodD1 and mediate conformational changes at nod gene promoters but that only luteolin is capable of promoting the downstream changes necessary for nod gene induction.

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Renier, Adeline, Fabienne Maillet, Joel Fardoux, Véréna Poinsot, Eric Giraud, and Nico Nouwen. "Photosynthetic Bradyrhizobium Sp. Strain ORS285 Synthesizes 2-O-Methylfucosylated Lipochitooligosaccharides for nod Gene–Dependent Interaction with Aeschynomene Plants." Molecular Plant-Microbe Interactions® 24, no. 12 (December 2011): 1440–47. http://dx.doi.org/10.1094/mpmi-05-11-0104.

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Bradyrhizobium sp. strain ORS285 is a photosynthetic bacterium that forms nitrogen-fixing nodules on the roots and stems of tropical aquatic legumes of the Aeschynomene genus. The symbiotic interaction of Bradyrhizobium sp. strain ORS285 with certain Aeschynomene spp. depends on the presence of nodulation (nod) genes whereas the interaction with other species is nod gene independent. To study the nod gene-dependent molecular dialogue between Bradyrhizobium sp. strain ORS285 and Aeschynomene spp., we used a nodB-lacZ reporter strain to monitor the nod gene expression with various flavonoids. The flavanones liquiritigenin and naringenin were found to be the strongest inducers of nod gene expression. Chemical analysis of the culture supernatant of cells grown in the presence of naringenin showed that the major Nod factor produced by Bradyrhizobium sp. strain ORS285 is a modified chitin pentasaccharide molecule with a terminal N-C18:1-glucosamine and with a 2-O-methyl fucose linked to C-6 of the reducing glucosamine. In this respect, the Bradyrhizobium sp. strain ORS285 Nod factor is the same as the major Nod factor produced by the nonphotosynthetic Bradyrhizobium japonicum USDA110 that nodulates the roots of soybean. This suggests a classic nod gene-dependent molecular dialogue between Bradyrhizobium sp. strain ORS285 and certain Aeschynomene spp. This is supported by the fact that B. japonicum USDA110 is able to form N2-fixing nodules on both the roots and stems of Aeschynomene afraspera.

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O'Neill, Luke. "Crohn's disease gene is given the NOD." Trends in Immunology 22, no. 8 (August 2001): 418–19. http://dx.doi.org/10.1016/s1471-4906(01)02002-6.

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Hogg, Bridget, Andrea E. Davies, Karen E. Wilson, Ton Bisseling, and J. Allan Downie. "Competitive Nodulation Blocking of cv. Afghanistan Pea Is Related to High Levels of Nodulation Factors Made by Some Strains of Rhizobium leguminosarum bv. viciae." Molecular Plant-Microbe Interactions® 15, no. 1 (January 2002): 60–68. http://dx.doi.org/10.1094/mpmi.2002.15.1.60.

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Cultivar Afghanistan peas are resistant to nodulation by many strains of Rhizobium leguminosarum bv. viciae but are nodulated by strain TOM, which carries the host specificity gene nodX. Some strains that lack nodX can inhibit nodulation of cv. Afghanistan by strain TOM. We present evidence that this “competitive nodulation-blocking” (Cnb) phenotype may result from high levels of Nod factors inhibiting nodulation of cv. Afghanistan peas. The TOM nod gene region (including nodX) is cloned on pIJ1095, and strains (including TOM itself) carrying pIJ1095 nodulate cv. Afghanistan peas very poorly but can nodulate other varieties normally. The presence of pIJ1095, which causes increased levels of Nod factor production, correlates with Cnb. Nodulation of cv. Afghanistan by TOM is also inhibited by a cloned nodD gene that increases nod gene expression and Nod factor production. Nodulation of cv. Afghanistan can be stimulated if nodD on pIJ1095 is mutated, thus severely reducing the level of Nod factor produced. Repression of nod gene expression by nolR eliminates the Cnb phenotype and can stimulate nodulation of cv. Afghanistan. Addition of Nod factors to cv. Afghanistan roots strongly inhibits nodulation. The Cnb+ strains and added Nod factors inhibit infection thread initiation by strain TOM. The sym2A allele determines resistance of cv. Afghanistan to nodulation by strains of R. leguminosarum bv. viciae lacking nodX. We tested whether sym2A is involved in Cnb by using a pea line carrying the sym2A region introgressed from cv. Afghanistan; nodulation in the introgressed line was inhibited by Cnb+ strains. Therefore, the sym2A region has an effect on Cnb, although another locus (or loci) may contribute to the stronger Cnb seen in cv. Afghanistan.

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Arai, Satoko, Christina Minjares, Seiho Nagafuchi, and Toru Miyazaki. "Improved Experimental Procedures for Achieving Efficient Germ Line Transmission of Nonobese Diabetic (NOD)-Derived Embryonic Stem Cells." Experimental Diabesity Research 5, no. 3 (2004): 219–26. http://dx.doi.org/10.1080/15438600490486877.

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The manipulation of a specific gene in NOD mice, the best animal model for insulin-dependent diabetes mellitus (IDDM), must allow for the precise characterization of the functional involvement of its encoded molecule in the pathogenesis of the disease. Although this has been attempted by the cross-breeding of NOD mice with many gene knockout mice originally created on the 129 or C57BL/6 strain background, the interpretation of the resulting phenotype(s) has often been confusing due to the possibility of a known or unknown disease susceptibility locus (e.g.,Iddlocus) cosegregating with the targeted gene from the diabetes-resistant strain. Therefore, it is important to generate mutant mice on a pure NOD background by using NOD-derived embryonic stem (ES) cells. By using the NOD ES cell line established by Nagafuchi and colleagues in 1999 (FEBSLett., 455, 101–104), the authors reexamined various conditions in the context of cell culture, DNA transfection, and blastocyst injection, and achieved a markedly improved transmission efficiency of these NOD ES cells into the mouse germ line. These modifications will enable gene targeting on a “pure” NOD background with high efficiency, and contribute to clarifying the physiological roles of a variety of genes in the disease course of IDDM.

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Dugas, V., A. Liston, E. E. Hillhouse, R. Collin, G. Chabot-Roy, A.-N. Pelletier, C. Beauchamp, K. Hardy, and S. Lesage. "Idd13 is involved in determining immunoregulatory DN T-cell number in NOD mice." Genes & Immunity 15, no. 2 (January 16, 2014): 82–87. http://dx.doi.org/10.1038/gene.2013.65.

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&NA;. "GAD65 gene therapy exhibits promise in NOD mice." Inpharma Weekly &NA;, no. 1345 (July 2002): 8. http://dx.doi.org/10.2165/00128413-200213450-00015.

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Banfalvi, Zsofia, Anthony Nieuwkoop, Maria Schell, Linda Besl, and Gary Stacey. "Regulation of nod gene expression in Bradyrhizobium japonicum." Molecular and General Genetics MGG 214, no. 3 (November 1988): 420–24. http://dx.doi.org/10.1007/bf00330475.

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Dissertations / Theses on the topic "Gene nod"

Mavridou, Annoula. "Genetic loci of Rhizobium leguminosarum affecting nod gene expression." Thesis, University of East Anglia, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316102.

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Grob, Philipp. "Identification of two homologous two-component regulatory systems, NodV/NodW and NWsA/NwsB, in Bradyrhizobium japonicum and analysis of their role in nodulation and nod gene regulation /." [S.l.] : [s.n.], 1993. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10399.

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Eliziário, Fernando Celso Eufigénio. "Análise e sobre-expressão de genes de simbiose de rizóbios de grão-de-bico." Master's thesis, Universidade de Évora, 2016. http://hdl.handle.net/10174/18214.

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Dos genes envolvidos na simbiose entre rizóbios e plantas leguminosas, destaca-se o gene nodD, que codifica o activador da transcrição dos genes de nodulação. No entanto, este gene está pouco estudado em Mesorhizobium. Esta tese compreende o estudo detalhado do gene nodD em espécies de Mesorhizobium noduladoras de grão-de-bico, nomeadamente a investigação da sua diversidade, e a análise do efeito da sua sobre-expressão na eficiência simbiótica. Investigou-se ainda se a sua presença seria capaz de mudar a gama de hospedeiros de um rizóbio. Obteve-se um grande aumento da eficiência simbiótica nas estirpes V-15b e ST-2, transformadas com a cópia extra de nodD. Este trabalho constitui a primeira tentativa de melhorar a eficiência simbiótica de mesorizóbios através da sua transformação com um gene simbiótico, mostrando que esta é uma estratégia promissora para a obtenção de rizóbios inoculantes mais eficientes; Abstract: Among the genes involved in the rhizobia-legume symbiosis, the gene nodD has an important role, since it encodes the major transcriptional activator of nodulation genes. However, this gene is not fully study in Mesorhizobium. This thesis describes the study of the nodD gene from Mesorhizbium species that nodulate chickpea, namely the investigation of its diversity and the analysis of the effect of its overexpression in the symbiotic efficiency. In addition, it was investigated if nodD presence would be able to change the host range in rhizobia. A high improvement in the symbiotic efficiency of the strains V-15b and ST-2 was obtained after transformation with a nodD extra copy. This report describes the first attempt to enhance the symbiotic efficiency through the transformation of mesorhizobia with a symbiosis gene, showing that this approach could be a promising strategy to obtain efficient rhizobia inoculants.

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Salie, S. "The symbiotic interaction of Bradyrhizobium japonicum with bambara groundnut and cowpea and the effects of NOD gene-inducers, daidzein and genistein." Bachelor's thesis, University of Cape Town, 1998. http://hdl.handle.net/11427/26054.

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The aim of this project was to investigate whether nodulation, and nitrogen concentration of legumes can be increased by providing additional nod geneinducer compounds. Both daidzein and genistein are nod gene-inducers for rhizobia nodulating cowpea, bambara groundnut, soybean and the common bean.

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Mallol, Domínguez Cristina. "Estudi del paper de la sobreexpressió pancreàtica d’IGF-1 en ratolins NOD per contrarestar la diabetis tipus 1." Doctoral thesis, Universitat Autònoma de Barcelona, 2014. http://hdl.handle.net/10803/285361.

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La diabetis tipus 1 (T1D) és una malaltia autoimmune causada per la destrucció de les cèl·lules β productores d’insulina. La incidència de la T1D està augmentant arreu del món i cada vegada es diagnostica a edats més joves. Aquesta malaltia esdevé clínicament aparent després d’un període preclínic de longitud variable, durant el qual la destrucció autoimmune redueix la massa de cèl·lula β en l’illot pancreàtic de tal manera que els nivells de glucosa en sang no es poden continuar mantenint en un rang fisiològic. Donat que els pacients de T1D requereixen teràpia amb insulina al llarg de tota la seva vida i presenten un elevat risc de complicacions secundàries, noves teràpies preventives o curatives són necessàries. Entre elles, la teràpia gènica ofereix una nova eina de tractament amb grans possibilitats. Entre els possibles gens candidats al tractament de la diabetis, el factor de creixement a la insulina tipus 1 (IGF-1) destaca per les seves propietats immunomoduladores i el seu control sobre la proliferació i supervivència de la massa de cèl·lula β. El nostre laboratori havia descrit prèviament que la sobreexpressió d’IGF-1 a les cèl·lules β d’animals transgènics contrarresta la citotoxicitat i la insulitis induïda pel tractament amb estreptozotocina (STZ) i potencia la regeneració de l’illot. A més, també ha demostrat que l’expressió pancreàtica d’IGF-1 prevé la destrucció de l’illot i la mort de la cèl·lula β en un ratolí transgènic que sobreexpressa interferó-β (IFN-β) a la cèl·lula β, un model d’infiltració limfocítica del pàncrees endocrí. La primera part d’aquest treball es va centrar en l’estudi del paper d’IGF-1 en la preservació de la massa de cèl·lula β en un model espontani de diabetis autoimmune: el ratolí NOD (Non Obese Diabetic). Amb l’objectiu d’estudiar el mecanisme mitjançant el qual la sobreexpressió d’IGF-1 en les cèl·lules β pot prevenir la destrucció autoimmune del pàncrees endocrí, es van generar ratolins NOD transgènics que sobreexpresaven IGF-1 sota el control del promotor RIP-1 (Rat Insulin Promoter) (NOD-IGF1). Els resultats obtinguts van mostrar que els ratolins transgènics NOD-IGF1 eren resistents al desenvolupament de diabetis. Davant una prevalença del 70% en els ratolins NOD, només un 3% dels ratolins NOD-IGF1 desenvolupaven diabetis a les 30 setmanes d’edat. Aquesta prevenció era mediada per un efecte local d’IGF-1 al pàncrees donat que els nivells circulants del factor no estaven augmentats. La reducció en la incidència de diabetis observada en els animals NOD-IGF1 tenia lloc en paral·lel amb una menor infiltració limfocítica dels illots, menor expressió de citoquines inflamatòries i reducció del nombre de cèl·lules β apoptòtiques, suggerint un bloqueig de l’atac autoimmune contra el pàncrees. Aquest bloqueig podria estar mediat per una reducció de les molècules presentadores d’antígens en els illots i un augment de les cèl·lules T reguladores en el pàncrees. Els ratolins NOD-IGF1 preservaven la massa de cèl·lula β amb el temps, presentaven una insulinèmia normal i mostraven un perfil de tolerància a la glucosa normal després de ser administrats amb una càrrega de glucosa intraperitoneal. Tots aquests resultats indicaven que la producció local d’IGF-1 podia protegir les cèl·lules β de la destrucció induïda pel sistema immune i contrarestava la diabetis en una varietat de models de la malaltia que inclou el ratolí amb desenvolupament espontani de diabetis NOD. Per tant, la transferència del gen IGF-1 a pàncrees podria ser una aproximació segura per al tractament de la diabetis tipus 1. A més, estudis realitzats en el nostre laboratori han demostrat que l’administració intraductal de vectors virals adenoassociats de serotip 8 (AAV8) és capaç de transduir de manera eficient i a llarg termini tant el pàncrees exocrí com les cèl·lules β dels illots. Per tant, l’objectiu de la segona part d’aquest treball va ser combinar l’ús dels vectors AAV8 amb els efectes protectors de l’IGF-1 per a desenvolupar una estratègia de teràpia gènica dirigida al pàncrees per a contrarestar la diabetis autoimmune en el ratolí NOD. Amb aquesta finalitat es va generar un vector AAV8 que expressava IGF-1 sota el control del promotor ubic CAG. Per tal de restringir l’expressió d’IGF-1 al pàncrees es van incorporar al constructe les seqüències diana del microRNA 122a (expressat al fetge) i del miroRNA 1 (expressat al cor)a l’extrem 3’-UTR del constructe. Es va observar que l’administració intraductal d’aquest vector era capaç de prevenir la hiperglucèmia en el ratolí NOD. Així, la majoria dels animals administrats amb el vector AAV8 que codificava per IGF-1 van mostrar valors normals de glucèmia al llarg de les 28 setmanes de seguiment i la incidència de diabetis es va veure significativament reduïda. En conjunt, aquest estudi posa de manifest el paper clau d’IGF-1 en la protecció de la massa de cèl·lula β enfront la destrucció autoimmune, i indica que la transferència gènica d’IGF-1 a pàncrees mitjançant vectors AAV podria representar una nova aproximació de teràpia gènica per la diabetis tipus 1.
Type 1 diabetes (T1D) is an autoimmune disease caused by the destruction of insulin-producing β cells. The incidence of T1D is increasing worldwide and is being diagnosed at increasingly younger ages. T1D becomes clinically apparent after a preclinical period of varying length, during which autoimmune destruction reduces the mass of β cells in the pancreatic islets such that blood glucose levels can no longer be maintained in a normal physiologic range. T1D patients require life-long insulin treatment and have a high risk of suffering from medical complications. Therefore, preventative or curative therapies are urgently needed. Among them, gene therapy offers a new tool with great potential treatment opportunities for T1D. Among the possible candidate genes for the treatment of diabetes, the insulin growth factor type 1 (IGF-1) is known for its immunomodulatory properties and its control over the proliferation and survival of β cell mass. Our laboratory has previously reported that the overexpression of IGF-1 in β cells of transgenic animals counteracts cytotoxicity and insulitis induced by streptozotocin (STZ) treatment and promotes islet regeneration. We also described that pancreatic expression of IGF-1 prevents islet destruction and β cell death in a transgenic mouse overexpressing IFNβ (Interferon β) in β cells, a model of lymphocytic infiltration in endocrine pancreas. The first part of this thesis is focused on the study of the role of IGF-1 in the preservation of β cell mass in a spontaneous model of autoimmune diabetes: NOD mouse (Non obese Diabetic). With the aim of studying the mechanism by which the overexpression of IGF-1 in β cells can prevent the autoimmune destruction of the endocrine pancreas, we generated NOD transgenic mice that overexpress IGF-1 under the control of RIP-1 promoter (Rat Insulin Promoter-1) (NOD-IGF1). Our results showed that IGF1-NOD mice were resistant to develop diabetes. As the prevalence of diabetes was of 70% in NOD mice, only 3% of the IGF1-NOD mice developed diabetes at 30 weeks of age. This prevention was mediated by the local effect of IGF-1 in pancreas given that the circulating levels of the factor were not increased. The reduction in the incidence of diabetes observed in NOD-IGF1 animals was in parallel with lower islet lymphocytic infiltration, reduced inflammatory cytokine expression and reduced number of apoptotic β cells, suggesting a blockage of the autoimmune attack against the pancreas. This arrest could be mediated by a reduction of antigen-presenting molecules in islets and an increase in regulatory T cells in the pancreas. IGF1-NOD mice preserved β cell mass with time, showed normal insulinemia and a normal glucose tolerance profile after an intraperitoneal glucose load administration. These results indicate that the local production of IGF-1 protected β cells from the destruction induced by the immune system and counteracted diabetes in a variety of models of the disease, including the spontaneously diabetic NOD mouse. Therefore, IGF-1 gene transfer to the pancreas could be a safe approach for the treatment of type 1 diabetes. Furthermore, studies in our laboratory have shown that intraductal administration of adeno-asociated viral vectors with serotype 8 (AAV8) can efficiently transduce long term both the exocrine pancreas and the islet β cells. Thus, the aim of the second part of this study was to combine the use of AAV8 vectors with the protective effects of IGF-1 to develop a gene therapy approach directed to the pancreas in order to counteract autoimmune diabetes in NOD mouse. For this purpose, we generated an AAV8 vector expressing IGF-1 under the control of the ubiquitous CAG promoter. In order to restrict IGF-1 expression in the pancreas, the target sequences of microRNA 122a (expressed in the liver) and micrRNA 1 (expressed in the heart) were incorporated to the 3’-UTR of the construct. It was observed that the intraductal administration of this vector was able to prevent diabetic hyperglycaemia in NOD mouse. Thus, most animals administered with the AAV8 vector encoding the IGF-1 gene showed normal blood glucose values during 28 weeks and a significant reduction in the incidence of diabetes. In conclusion, this study demonstrates the key role of IGF-1 protecting β cell mass against the autoimmune destruction, and indicates that gene transfer of IGF-1 in the pancreas by AAV vectors could represent a new gene therapy approach for the treatment of type 1 diabetes.

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Fornari, Thaís Arouca. "Análise da expressão gênica promíscua no timo de camundongos NOD (non obese diabetic) durante a emergência do Diabetes melitus tipo 1." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/17/17135/tde-13042009-150027/.

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A tolerância imunológica é a propriedade essencial do sistema imune que controla as reações patológicas contra antígenos do próprio. O timo é visto como o principal órgão envolvido com a indução de tolerância aos antígenos próprios que são expressos pelas células tímicas (tolerância central), enquanto que a indução de tolerância aos antígenos relacionados a outros tecidos (TRAs) tem sido atribuída aos mecanismos de tolerância extratímica (tolerância periférica). Entretanto, a evidência da expressão de TRAs de órgãos e tecidos parenquimais no timo pelas células medulares epiteliais (mTECs) de camundongos e de humanos a qual foi referida como expressão gênica promíscua (PGE) reforçou a concepção de tolerância central de TRAs. O controle molecular dessa expressão tem sido atribuído ao gene Aire (Auto immune regulator) que é um regulador de transcrição. No presente estudo, procurou-se retratar a expressão gênica promíscua no timo de camundongos NOD (Non Obese Diabetic) por meio da análise da expressão gênica em grande escala, ou seja, descrevendo seu transcriptoma usando a tecnologia de cDNA microarrays. Para a análise dos dados utilizamos programas de bioinformática dedicados a microarrays bem como dados de bancos para a caracterização da PGE e susceptibilidade genética ao diabetes melitus do tipo 1 (DM-1). Três conjuntos de resultados puderam ser evidenciados. No primeiro conjunto observou-se a ocorrência da PGE de antígenos tecidos/órgãos parenquimatosos (TRAs) em timos recém removidos e em in vitro em cultura ATOC de camundogos NOD pré-autoimunes e autoimunes (diabéticos). O segundo conjunto de resultados consistiu na análise do efeito da inativação do transcrito de gene Aire na expressão gênica do timo de camundongos NOD in vitro em cultura ATOC. Finalmente, no último conjunto de dados, demonstrou-se que certos genes de TRAs com expressão promíscua, se encontram em regiões cromossômicas de susceptibilidade ao DM - 1 (idds). Como três deles (Il-4, Cd4 e Cdk4) são diretamente relacionados com a patogenia do DM-1 em camundongos foi possível estabelecer um paralelo entre PGE e susceptibilidade genética.
Immunologic tolerance is an essential property of the immune system, which controls immune reactions directed against the body self components. The thymus is seen as the main organ involved with the tolerance induction to self antigens, which are expressed by the thymic cells (central tolerance), while the tolerance induction to the diverse other peripheral tissues and organs is attributed to extra thymic mechanisms (peripheral tolerance). Nevertheless, the evidence for the expression of peripheral tissue related antigens (TRAs) in the thymus by the medullary thymic epithelial cells (mTECs) of mice and humans, which have been termed to as promiscuous gene expression (PGE), has contributed to the concept of central tolerance to TRAs. The molecular control of such gene expression has been attributed to the Aire (autoimmune regulator) gene, which plays a role as a transcriptional regulator. In the present study, we searched to picture PGE in the thymus of NOD (non obese diabetic) mice by means of high throughput gene expression, analyzing the transcriptome by the cDNA microarray method. To analyzing data we used bioinformatics programs dedicated to microarrays and specialized data banks to characterize PGE and genetic susceptibility to type 1 diabetes mellitus (DM-1). Studying pre and autoimmune NOD mice, we evidentiate three sets of results. In the first set, it was observed the occurrence of PGE of parenchymal tissue/organs antigens (TRAs) in fresh thymuses and in thymuses cultured in vitro in adult thymus organ cultures (ATOC). The second set of results consisted in the analysis of the effect of in vitro (ATOC) Aire gene silencing on PGE. Finally, in the third data set, we demonstrated that certain promiscuously expressed genes are positioned in DM-1 genetic susceptibility chromosomal regions (idds). As three of such genes (IL4, Cd4 and Cdk4) are directly associated to the DM-1 pathogenesis in mice, it was possible to establishing a parallel between PGE in the thymus and genetic susceptibility to this autoimmune disease.

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Andersson, Åsa. "B cell repertoire development in normal physiology and autoimmune disease." Doctoral thesis, Umeå universitet, Institutionen för molekylärbiologi (Medicinska fakulteten), 1993. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-101767.

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The B cell repertoire in the neonatal immune system (IS) is characterised by reactivity towards self-components, including other immunoglobulin (Ig) V-regions. These properties have been suggested to be a requirement for the development of a normal immune system. DNA sequencing of two interacting Ig idiotypes, derived from neonatal, preimmune mice, demonstrated that such idiotypic connectivity is germ- line encoded and devoid of VDJ junctional diversity. The serum levels of the same Ig idiotypes were studied in normal mice and demonstrated that the expression in serum fluctuated over time in a pattern compatible with a complex dynamic system. In contrast, similar analyses in autoimmune mice or humans demonstrated fluctuations in Ig titers that differed significantly from the healthy individuals. These findings suggested that pathological autoimmunity may be associated with fundamental alterations in the dynamics of natural antibody (ab) expression. This was further investigated in the nonobese diabetic (NOD) mouse, an animal model for human Type I diabetes. Suppression of the early B cell development in the NOD mouse prevented the development of diabetes, suggesting a role for B cells/Igs in the development of diabetes in these mice. Furthermore, neonatal injections of polyclonal Ig preparations or single, monoclonal natural abs inhibited disease induction. The prevention of diabetes development by one such natural ab was demonstrated to be dependent on both the dose injected and the timing of administration. Studies of the B cell repertoire development in NOD mice, compared to normal mice, by DNA-sequence analyses of IgVH rearrangements utilising genes from the most D-proximal Vh family, Vh7183, supported the idea of an aberrant B cell repertoire in this mouse model. Thus, the adult NOD mouse retained a neonatal pattern of Vh7183 rearrangements. This pattern could, however, be "normalised" by neonatal injection of a natural antibody, previously demonstrated to prevent the development of T cell dependent autoimmunity in the NOD mouse.

Diss. (sammanfattning) Umeå : Umeå universitet, 1993, härtill 6 uppsatser

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Bersoult, Anne. "Rôle du récepteur kinase DMI2 dans la perception et la transduction du signal symbiotique Facteur Nod de Sinorhizobium meliloti chez la légumineuse Medicago truncatula." Toulouse 3, 2006. http://www.theses.fr/2006TOU30018.

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Le gène DMI2 joue un rôle central dans l'établissement des symbioses Endomycorhizienne à Arbuscule et Légumineuse-Rhizobium. Il est impliqué dans les étapes précoces de la perception/transduction du signal Nod Factor. DMI2 code un Receptor-Like-Kinase à trois domaines LRR et un domaine NSL dans la partie extracellulaire. Son expression est spécifique des racines et induite dans les primordia nodulaires et la zone de préinfection du nodule suggèrant un rôle dans la préparation des cellules à l'infection. DMI2 est situé dans la membrane plasmique et semble former des homodimères et interagir avec d'autres proteines des étapes précoces de la voie de transduction du signal, DMI1 and LYK3. L'interaction avec NFP reste incertaine. L'analyse fonctionnelle des RLKs NFP, LYK3 et DMI2 montre l'autophosphorylation des kinases LYK3 et DMI2, contrairement à NFP. La transphosphorylation de NFP par DMI2 et/ou LYK3 n'a pas été obtenue. Nous proposons un modèle de transduction des signaux symbiotiques
The DMI2 gene plays a central role for the establishment of the Arbuscular Mycorrhizal and the Legume-Rhizobium symbioses. It is involved in the early steps of perception and transduction of the rhizobial Nod Factor signal. DMI2 encodes a Receptor-Like-Kinase with three LRR and one NSL domain in the extracellular part. DMI2 expression is specific of roots and is induced in nodule primordial and nodule preinfection zone which suggests a role in preparation of the cell to the infection. DMI2 is localised in the plasma membrane and seems to form homodimers and interact with other proteins of the early steps of the signalling pathway, DMI1 and LYK3. Interaction with NFP remains hypothetical. A functional analysis of the NFP, LYK3 and DMI2 RLKs shows autophosphorylation of the LYK3 and DMI2 kinases, contrary to NFP. No evidence of transphosphorylation of NFP by DMI2 and/or LYK3 were obtained. We propose a model of the symbiotic signal transduction

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Duarte, Nádia. "Molecular and cellular mechanisms contributing to the pathogenesis of autoimmune diabetes." Doctoral thesis, Umeå universitet, Medicinsk biovetenskap, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-601.

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Type 1 diabetes is an autoimmune disorder determined both by genetic and environmental factors. The Non-obese diabetic (NOD) mouse is one of the best animal models of this disease. It spontaneously develops diabetes through a process resembling the human pathogenesis. The strong association of NOD Type 1 diabetes to the MHC region and the existence of other diabetes susceptibility loci are also in parallel with the human disease. The identity of the genetic factors and biological function mediated by these loci remain, however, largely unknown. Like in other autoimmune diseases, defects in tolerance mechanisms are thought to be at the origin of type 1 diabetes. Accordingly, defects in both central and peripheral tolerance mechanisms have been reported in the NOD mouse model. Using a subphenotype approach that aimed to dissect the disease into more simple phenotypes, we have addressed this issue. In paper I, we analyzed resistance to dexamethasone-induced apoptosis in NOD immature thymocytes previously mapped to the Idd6 locus. Using a set of congenic mice carrying B6-derived Idd6 regions on a NOD background and vice-versa we could restrict the Idd6 locus to an 8cM region on the telomeric end of chromosome 6 and the control of apoptosis resistance to a 3cM region within this area. In paper II, further analysis of diabetes incidence in these congenic mice separated the genes controlling these two traits, excluding the region controlling the resistance to apoptosis as directly mediating susceptibility to diabetes. These results also allowed us to further restrict the Idd6 locus to a 3Mb region. Expression analysis of genes in this chromosomal region highlighted the Lrmp/Jaw1 gene as a prime candidate for Idd6. Lrmp encodes an endoplasmatic reticulum resident protein. Papers III and IV relate to peripheral tolerance mechanisms. Several T cell populations with regulatory functions have been implicated in type 1 diabetes. In paper III, we analyzed NOD transgenic mice carrying a diverse CD1d-restricted TCR αVa3.2b9), named 24abNOD mice. The number of nonclassical NKT cells was found to be increased in these mice and almost complete protection from diabetes was observed. These results indicate a role for nonclassical NKT cells in the regulation of autoimmune diabetes. In paper IV, we studied the effects of introducing the diverse CD1d-restricted TCR (Va3.2b9) in immunodeficient NOD Rag-/- mice (24abNODRag-/- mice). This resulted in a surprising phenotype with inflammation of the ears and augmented presence of mast cells as well as spleenomegaly and hepatomegaly associated with extended fibrosis and increased numbers of mast cells and eosinophils in the tissues. These observations supported the notion that NKT cells constitute an “intermediary” cell type, not only able to elicit the innate immune system to mount an inflammatory response, but also able to interact with the adaptive immune system affecting the action of effector T cells in an autoimmune situation. In this context the 24abNODRag-/- mice provide an appropriate animal model for studying the interaction of NKT cells with both innate and adaptive components of the immune systemα.

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Lala, Sanjay Govind. "NOD2 gene expression in Paneth cells and monocytes." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1444913/.

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Introduction: Mutations in the NOD2 gene are associated with the development of Crohn's disease, an inflammatory disorder of the gastrointestinal tract. The NOD2 protein induces cellular activation in response to the bacterial antigen muramyl dipeptide (MDP). The NOD2 gene is mainly expressed by circulating blood monocytes although NOD2-associated Crohn's disease involves mainly the terminal ileum. Paneth cells, which are most numerous in the terminal ileum, are specialised intestinal epithelial cells that secrete antimicrobial peptides in response to bacterial products and are critically important in enteric antibacterial defence. I hypothesised that Paneth cells express the NOD2 gene: this thesis describes the expression and quantification of the NOD2 gene in Paneth cells in inflammatory diseases such as Crohn's disease and necrotizing enterocolitis. I also identified factors that regulate NOD2 gene expression in intestinal epithelial cells and peripheral blood mononuclear cells (PBMC).;Methods: In situ hybridisation and immunohistochemistry were used to localize NOD2 mRNA and protein expression in intestinal tissue. Laser capture microdissection (LCM), and calcium chelation followed by mechanical disruption were used to isolate intestinal crypt and villus epithelial cells. Real-time RT-PCR was used to determine NOD2 gene expression in intestinal epithelial cells and PBMC.;Results: NOD2 mRNA and protein expression was readily detected in Paneth cells in normal and Crohn's disease affected terminal ileum NOD2 was also expressed by monocytes, but not by mature macrophages in the lamina propria or within granulomas. NOD2 mRNA levels were enriched in isolated crypt compared to villous epithelial cells, and NOD2 expression was mainly detected in LCM-acquired Paneth cells but not villous epithelial cells. In vitro, tumour necrosis factor alpha (TNFalpha) up-regulates NOD2 gene expression in intestinal epithelial cells. There is a possibility that Paneth cell antimicrobials are reduced in patients with NOD2-related Crohn's disease.;Conclusions: Paneth cells express NOD2 and could therefore play an important and hitherto unrecognized role in the development of NOD2-associated Crohn's disease.

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Books on the topic "Gene nod"

Mavridou, Annoula. Genetic loci of Rhizobium leguminosarum affecting nod gene expression. Norwich: University of East Anglia, 1992.

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Burn, Joanne Elizabeth. Analysis of the regulatory nodulation gene nodD of Rhizobium leguminosarum. Norwich: Universityof East Anglia, 1989.

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Dawkins, Richard. The Selfish Gene. Oxford: Oxford University Press, 1999.

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Dawkins, Richard. The Selfish Gene. Oxford: Oxford University Press, 1989.

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Dawkins, Richard. The selfish gene. 3rd ed. Oxford: Oxford University Press, 2006.

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Barrett, Lucy W. Untranslated gene regions and other non-coding elements: Regulation of eukaryotic gene expression. Basel: Springer, 2013.

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Brusselmans, Herman. Nog steeds geen paniek: Doorgrondelijke waarheden van Herman Brusselmans. 2nd ed. Amsterdam: Prometheus, 2007.

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Song, Chi-hwan. Tʻoehaengsŏng noe chirhwan chʻiryo rŭl wihan sepʻo punhwa chʻoejŏkhwa yŏnʼgu =: Optimization of cell differentiation for the treatments of neuro-degenerative diseases. [Seoul]: Sikpʻum Ŭiyakpʻum Anjŏnchʻŏng, 2007.

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Erdmann, V. A., and Jan Barciszewski. Non coding RNAs in plants. Heidelberg: Springer, 2011.

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Non coding RNAs in plants. Heidelberg: Springer, 2011.

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Book chapters on the topic "Gene nod"

Wijffelman, Carel, Herman Spaink, Helmi Schlaman, Bas Zaat, Kees Recourt, Ruud de Maagd, Rob Okker, and Ben Lugtenberg. "Regulation of Nod Gene Expression: The Role of Nod D Protein." In NATO ASI Series, 137–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74158-6_15.

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Bisseling, Ton, Henk Franssen, Renze Heidstra, Beatrix Horvath, Panagiotis Katinakis, Marja Moerman, Herman Spaink, Ton van Bussel, and Irma Vijn. "Rhizobium Nod Metabolites and Early Nodulin Gene Expression." In Advances in Molecular Genetics of Plant-Microbe Interactions, Vol. 2, 365–68. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-017-0651-3_39.

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Loh, J., J. P. Y. Yuen, M. G. Stacey, and G. Stacey. "Unique Aspects of Nod Gene Expression in Bradyrhizobium Japonicum." In Highlights of Nitrogen Fixation Research, 115–20. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4795-2_22.

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Grisebach, Hans, Lambert Edelmann, Daniela Fischer, Georg Kochs, and Roland Welle. "Biosynthesis of Phytoalexins and Nod-Gene Inducing Isoflavones in Soybean." In NATO ASI Series, 57–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74158-6_5.

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Hong, G. F., J. L. Burn, and A. W. B. Johnston. "Analysis of the Mechanism of nod Gene Regulation in Rhizobium leguminosarum." In Plant Molecular Biology, 523–30. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4615-7598-6_48.

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McCorry, T. P., R. Fellay, X. Perret, W. J. Broughton, A. J. Bjourson, and J. E. Cooper. "Non nod Gene Expression in Rhizobia During Exposure to Aromatic Compounds." In Biological Nitrogen Fixation for the 21st Century, 239. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5159-7_108.

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Sanjuan-Pinilla, J. M., J. Olivares, and J. Sanjuan. "The Rhizobium meliloti leuA Gene is Required for Flavonoid-Dependent Expression of Nod Genes." In Biological Nitrogen Fixation for the 21st Century, 237. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5159-7_106.

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Wijffelman, Carel, Bas Zaat, Herman Spaink, Ine Mulders, Ton van Brussel, Rob Okker, Elly Pees, Ruud de Maagd, and Ben Lugtenberg. "Induction of Rhizobium Nod Genes by Flavonoids: Differential Adaptation of Promoter, nodD Gene and Inducers for Various Cross-Inoculation Groups." In Recognition in Microbe-Plant Symbiotic and Pathogenic Interactions, 123–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71652-2_12.

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Ramakrishnan, Neela, and Alan G. Atherly. "NOD-Linked Host Specific Gene for Soybean (Peking) Nodulation in Rhizobium Fredii USDA193." In Molecular genetics of plant-microbe interactions, 211–13. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-4482-4_52.

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O’Callaghan, K. J., M. R. Davey, and E. C. Cocking. "Crack Entry Invasion of Sesbania rostrata by Azorhizobium caulinodans ORS571 is Nod Gene-Independent." In Biological Nitrogen Fixation for the 21st Century, 266. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5159-7_135.

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Conference papers on the topic "Gene nod"

Chubukova, O. V., Z. R. Vershinina, R. T. Matnyazov, and Al Kh Baymiev. "Using nod genes control system to create rhizospheric microorganisms with regulated gene expression." In 2nd International Scientific Conference "Plants and Microbes: the Future of Biotechnology". PLAMIC2020 Organizing committee, 2020. http://dx.doi.org/10.28983/plamic2020.054.

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Inducible vector containing the full-sized nodD gene and the promoter region of the nod-box under the control of which was cloned the gfp gene was constructed. Modified bacteria R. galegae in which the synthesis of GFP protein was activated by plant flavonoids were obtained.

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Guro, P., V. Safronova, A. Sazanova, I. Kuznetsova, A. Belimov, V. Yakubov, E. Chirak, A. Afonin, E. Andronov, and I. Tikhonovich. "Rhizobial microsymbionts of the narrowly endemic Oxytropis species growing in Kamchatka possess a set of genes that are associated with T3SS and T6SS secretion systems and can affect the development of symbiosis." In 2nd International Scientific Conference "Plants and Microbes: the Future of Biotechnology". PLAMIC2020 Organizing committee, 2020. http://dx.doi.org/10.28983/plamic2020.099.

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A collection of rhizobial strains isolated from root nodules of the narrowly endemic legume species Oxytropis erecta, O. anadyrensis, O. kamtschatica and O. pumilio growing on the Kamchatka Peninsula (Russian Federation) was obtained. Analysis of the 16S rRNA gene sequence showed a significant diversity of isolates belonging to the families Rhizobiaceae (Rhizobium), Phyllobacteriaceae (Mesorhizobium, Phyllobacterium) and Bradyrhizobiaceae (Bosea, Tardiphaga). Pairs of taxonomically different strains in various combinations were isolated from some nodules of Oxytropis plants. Plant nodulation assays showed that only strains belonging to the genus Mesorhizobium (M. jarvisii, M. loti and M. huakuii) could form nitrogen-fixing nodules. The nitrogen-fixing activity of the strains was more associated with the host plant than with the species of strains. The whole genome sequences analysis showed that the strains M. loti 582 and M. huakuii 583 possessed symbiotic genes necessary for the formation of effective symbiosis and grouped into Sym-clusters. In contrast, the strain T. robiniae 581 had only a reduced number of fix genes, while the strains Phyllobacterium sp. 628 and R. lusitanum 629 possesed only individual symbiotic genes, which obviously did not participate in the formation of nodules. It was also stated that the strains M. loti 582 and M. huakuii 583 had a significantly larger set of genes related to the secretion systems T3SS and T6SS that can affect the host specificity of strains, compared with 6 commercial strains used as reference. These two strains formed nodules of two types (typical elongated and atypical rounded) on Oxytropis plants. We suggest that a possible cause of the observed phenomenon is the availability of different nodulation strategies in these strains (dependent and independent of Nod-factors). Thus, as a result of studying the collection of strains isolated from the narrow endemic species of Kamchatka Oxytropis, interesting objects were selected to study the functions of the T3SS and T6SS genes, and their role in the development of rhizobia-legume symbiosis. The prospects of using strains with gene systems for both symbiotic and non-symbiotic nodulation to enhance the efficiency of plant-microbe interactions by expanding the host specificity and increasing the efficiency of nodulation are discussed.

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Chu, Reamin, Hang‐Rong Lei, Cheng‐Se Lin, Cheng‐Se Lin, Chien‐Yueh Lee, Lih‐Seng Yeh, and Shih‐Chieh Chang. "Abstract B58: Gene expression study on a highly aggressive canine transmissible venereal tumor of a NOD/SCID mice model." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Dec 6–9, 2009; Houston, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1940-6207.prev-09-b58.

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Pannekoek, H., M. Linders, J. Keijer, H. Veerman, H. Van Heerikhuizen, and D. J. Loskutoff. "THE STRUCTURE OF THE HUMAN ENDOTHELIAL PLASMINOGEN ACTIVATOR INHIBITOR (PAI-1) GENE: NON-RANDOM POSITIONING OF INTRONS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644767.

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The endothelium plays a crucial role in the regulation of the fibrinolytic process, since it synthesizes and secretes tissue-type plasminogen activator (t-PA) as well as the fast-acting plasminogen activator inhibitor (PAI-1). Molecular cloning of full-length PAI-1 cDNA, employing a human endothelial cDNA expression library, and a subsequent determination of the complete nucleotide sequence, allowed a prediction of the amino-acid sequence of the PAI-1 glycoprotein. It was observed that the amino-acid sequence is significantly homologous to those of members of the serine protease inhibitor ("Serpin") family, e.g. αl-antitrypsin and antithrombin III. Serpins are regulators of various processes, such as coagulation, inflammatory reactions, complement activation and share a common functional principle and a similar structure, indicative for a common primordial gene. The intron-exon arrangement of Serpin genes may provide a record for the structure of a primordial gene. A comparison of the location of introns among members of the Serpin family reveals that some introns are indeed present at identical or almost identical positions, however in many other cases there is no correspondence between the intron positions among different Serpin genes.Obviously, more data on the chromosomal gene structure of members of this family are required to formulate a scheme for the evolutionary creation of the Serpins. To that end, we have established the number and the precise location of the introns in the PAI-1 gene and have compared these data with those reported on other Serpin genes. For that purpose a human genomic cosmid DNA library of about 340.000 independent colonies was screened with radiolabelled full-length PAI-1 cDNA as probe. Two clones were found which contain the entire PAI-1 gene. Restriction site mapping, electron microscopic inspection of heteroduplexes and nucleotide sequence analysis demonstrate that the PAI-1 gene comprises about 12.2kilo basepairs and consists of nine exons and eight introns. Intron-exon boundaries are all in accord with the "GT-AG" rule, including a cryptic acceptor splice site found in intron 7. Furthermore, it is observed that intron 3 of the PAI-1 gene occupies an identical position as intron E of chicken ovalbumin and intron E of the ovalbumin-related gene Y. The location of the other seven introns is unrelated to the known location of introns in the genes encoding the Serpins, rat angiotensin, chicken ovalbumin (and gene Y), human antithrombin III and human al-antitrypsin. The 3' untranslated region of the PAI-1 gene is devoid of introns, indicating that the two mRNA species detected in cultured endothelial cells which share an identical 5' untranslated segment and codogenic region, but differ in the length of the 3' untranslated region, arise by alternative polyadenylation. An extrapolation of the position of the introns to the amino-acid sequence of PAI-1, and adaption of the view that the subdomain structure of the Serpins is analogous, shows that the introns of PAI-1 are non-randomly distributed. Except for intron 7, the position of the other seven introns corresponds with randon-coil regions of the protein or with the borders of β-sheets and a-helices. Extrapolation of the position of introns in the genes of other Serpins to their respective amino-acid sequences and subdomain structures also reveals a preference for random-coil regions and borders of subdomains. These observations are reminiscent of an evolutionary model, called "intron sliding", that accounts for variations in surface loops of the same protein in different species by aberrant splicing (Craik et al., Science 220 (1983) 1125). The preferential presence of introns in gene segments, encoding these variable regions, and absence in regions determining the general folding of these proteins would explain conservation of the structure during the evolution of those genes.

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Edenbrandt, C.-M., S. Gershagen, P. Femlund, R. Wydro, J. Stenflo, and Å. Lundwall. "GENE STRUCTURE OF VITAMIN K-DEPENDENT PROTEIN S; A REGION HOMOLOGOUS TO SEX HORMONE BINDING GLOBULIN (SHBG) REPLACES THE SERINE PROTEASE REGION OF FACTORS IX, X AND PROTEIN C." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644640.

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It has recently been shown that the similarity between coagulation factors IX, X and protein C in the protein sequence is also evident in the organization of their genes. To further elucidate the relation of protein S to the other vitamin K-dependent clotting factors, we are now characterizing the human protein S gene. The size of the gene was estimated to be more than 45 kb, by hybridization of a cDNA for human protein S with chromosomal DNA in a Southern blot.We have isolated three overlapping clones from a human genomic DNA library in bacteriophage λ Charon 4A, which cover approximately 40 kb of the gene. The clones have been mapped by single- and double restriction enzyme digestion. Genomic subclones in pUC 18 which hybridize with cDNA probes for protein S have been isolated and sequenced to establish the intron/exon structure of the gene. The 5’- part of the human protein S gene closely resembles the corresponding part of the genes for factors IX, X and protein C. However, the thrombin sensitive region (amino acids 46-75), which is unique for protein S among the vitamin K-dependent clotting factors, is coded for by a separate exon. The 3'- end of the protein S gene, coding for amino acids 247-635, is not homologous to the catalytic region of the vitamin K-dependent serine proteases but shows a significant homology to human sex hormone binding globulin (SHBG).

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Cool, D. E., and R. T. A. MacGillivray. "CHARACTERIZATION OF THe HUMAN FACTOR XII GENE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642800.

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Surface activation of the plasma systems involved with coagulation, fibrinolysis, renin formation and kinin generation involves factor XII (Hageman factor). This protein is a 76,000 dalton glycoprotein which circulates in plasma as an inactive form of a serine protease. A human liver cDNA coding for factor XII was used to screen a human genomic phage library. Two overlapping clones were isolated, XHXII27 and XHXII76, and contain the entire gene for human factor XII. The gene is 13.5 Kbp in length and consists of 14 exons and 13 introns. The transcriptional start site of the mRNA was determined using S1 mapping and primer extension analysis. The results indicate that the 5′ untranslated end of the mRNA has a leader sequence of 47 bp and is not interrupted by an intron in the gene. DNA sequence analysis of the region upstream of the transcriptional start site does not contain TATA or CAAT sequences, which are often found in other genes transcribed by RNA polymerase II. The positions of the introns in the coding sequence separate the protein into domains which are homologous to similar regions found in fibronectin and tissue-type plasminogen activator. Furthermore, wherever protein homologies are found, the positions of the introns in the triplet codon occur in the same reading frame as in the tissue-type plasminogen activator, urokinase plasminogen activator and factor XII genes. The intron/exon organization of the factor XII gene is different to the organization of other coagulation genes such as prothrombin, factor IX and factor X. Therefore, factor XII appears to have evolved as a member of the plasminogen activator family of genes rather than as a member of the clotting factor gene family.

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Ploos van Amstel, J. K., A. L. van der Zanden, P. H. Reitsma, and R. M. Bertina. "RESTRICTION ANALYSIS AND SOUTHERN BLOTTING OF TOTAL HUMAN DNA REVEALS THE EXISTENCE OF MORE THAN ONE GENE HOMOLOGOUS WITH PROTEIN S cDNA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644639.

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A deficiency in protein S, the cofactor of activated protein C, is associated with an increased risk for the development of venous thrombosis. It is inherited as an autosomal dominant disorder. To improve the detection of heterozygotes in affected families, we have started to search for restriction fragment length polymorphism (RFLP) in the protein S gene. This study revealed the existence of two genes containing sequences homologous to protein S cDNA.Three non-overlapping fragments of clone pSUL5, which codes for the carboxy-terminal part of protein S and contains the complete 3' untranslated region, were isolated and used as probes in search for RFLP of the protein S gene.Surprisingly the non-overlapping probes shared more than one hybridizing band. The hybridization took place under stringent assay conditions.This observation is contradictory to the intron-exon organization of a gene and suggests the existence of two genes, containing sequences homologous with pSUL5. Both genes could be assigned to chromosome 3 by mapping through somatic cell hybrids. Whether two functional protein S genes are present in the human genome remains to be established.

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Giannelli, B. F. "MOLECULAR GENETICS OF HAEMOPHILIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643981.

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Haemophilia B, an X-linked recessive disease with an incidence of 1/30,000 newborn males, is due to defects in the gene for coagulation factor IX, which is on the long am of the X chromosome at band Xq27.1. This gene consists of approximately 34 Kb and contains 8 exons which specify a mRtfc of 2803 residues coding for a protein of 415 aa preceded by a prepro signal peptide of 46 aa. Coripanson of the functional domains of the factor IX protein with the exon structure of the gene supports the exon/protein domain hypothesis of gene evolution. The factor IX gene seems to be formed by a number of functionally and evolutionally independent modules. The signal peptide and the gla (γcarboxy-glutamic) region encoded in the first three exons are homologous to those of factor X, protein C and prothrombin. Thevfourth and fifth exons which code for the connecting peptide are homologous to one another and to the epidermal growth factor, a module that has been used in the construction of a great variety of proteins including different members of the coagulation and fibrinolytic pathways. The sixth exon encodes the activation peptide region, while the catalytic region of factor IX is coded by the seventh and eighth exon. This is at variance with other serine protease genes that have different exons for the segments containing the cardinal ami no-acids of the active centre (histidine, aspartic acid and serine).Natural selection acts against detrimental mutations of the factor IX gene and at each generation a proportion of haemophilia B genes is eliminated, as a significant number of patients does not reproduce. There appears to be no selective advantage to the heterozygote and therefore haemophilia B is maintained in the population by new mutations. Consequently, a significant proportion of patients should be born to non-carrier mothers, and unrelated patients should carry different gene defects, as recently verified by detailed analysis of individual haemophilia B genes.The defects of factor IX described so far comprise both point mutations and gene deletions. The latter affect either part or the whole of the gene and are often associated with the development of antibodies against therapeutically adninistered factor IX (the inhibitor complication). Since gene deletions may result in the complete absenceof factor IX synthesis or in the production of an extremely abnormal product, it has been suggested that mutationspreventing the synthesis of a factor IX gene product capable of inducing immune tolerance to normal factor IX is important in predisposing to the inhibitor complication.Among the point mutations described so far, those affecting the signal peptide are of particular interest. Substitutions of the arginine at positions -4 and -1 cause failure of propeptide cleavage. Thus they indicate that the propeptide consists of 18 aa an(lthat lts excision is necessary for factor IX function. It appears also that the propeptide contains a signal for γcarboxylation which has been conserved during the evolution of different γcarboxylated proteins.In spite of coagulant treatment, haemophilia B is a serious disease and one for which genetic counselling is required. Paramount for this is the detection of carriers and the diagnosis ofaffected male fetuses. DNA probes derived from the cloned factor IX gene have been used for this purpose. Carrier and first or second trimester prenatal diagnoses have been done using factors IX gene markers to follow the transmission of haemophilia B genes. Six sequence variations causing restriction fragment length polymorphisms (RFLP) in the factor IX gene have been detected and used as markers for such indirect diagnoses The efficiency of the above markers is reduced by linkage disequilibrium but, nevertheless, they offer definite carrier and nremtal diagnoses in 75-80% of the relatives of familial cases of haemophilia B.The indirect detection of gene defects is of modest help in the counselling of individuals from the families of isolated patients, but new methods for the direct detection of gene mutations promise better results in such families and also the attainment of % diagnostic success in relatives of familial cases.Finally the successful expression of recombinant factor IX genes in tissue culture and transgenic mammals raises hopes of therapeutic advances.

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Koloskova, E. M., V. A. Ezerskii, and T. P. Trubitsina. "Effect of microinjection of CRISPR / Cas9 components in plasmid form on the development of rabbit embryos during in vitro culture." In CURRENT STATE, PROBLEMS AND PROSPECTS OF THE DEVELOPMENT OF AGRARIAN SCIENCE. Federal State Budget Scientific Institution “Research Institute of Agriculture of Crimea”, 2020. http://dx.doi.org/10.33952/2542-0720-2020-5-9-10-131.

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The survival rate of rabbit embryos microinjected by the plasmid form of CRISPR/Cas9 components specific to the sour whey protein gene was evaluated. At high concentrations of plasmid components, embryo survival decreased slightly, possibly because the WAP gene does not belong to the housekeeping genes. After microinjection of a genetic construct with a sequence of green fluorescent protein under a cytomegalovirus promoter, the embryo survival significantly decreased. This is most likely due to the superexpression of GFP at the 2-16 cell stage of development.

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Polstein, Lauren R., and Charles A. Gersbach. "Photoregulated Gene Expression in Human Cells With Light-Inducible Engineered Transcription Factors." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80573.

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Systems for controlling gene expression in mammalian cells have a wide range of applications in medicine, biotechnology and basic science. An ideal gene regulatory system would allow for precise and specific control over the magnitude and kinetics of gene expression in space and time, while also exerting minimal influence on other genes and cellular components. Several gene regulatory systems have been developed in which orthogonal transcription machinery from prokaryotes or insects has been imported into mammalian cells and used to control the expression of a specific gene. Despite the transformative impact of these systems in biomedical and biological research, several limitations of these technologies restrict the scope of possible applications. For example, gene expression in these systems is controlled by a freely diffusible small molecule, such as an antibiotic or steroid. Consequently, it is not possible to achieve spatial control over gene expression within cell culture, tissues, or whole organisms. This is in contrast to natural mechanisms of biological regulation in which spatial control is critical, such as developmental patterning and tissue morphogenesis. Second, dynamic gene regulation requires the removal of these small molecules, which may be slow, laborious, and/or impractical for a particular application. To overcome these limitations, we have engineered an optogenetic system in which the magnitude of gene expression in human cells can be finely tuned by photoregulated synthetic transcription factors.

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Reports on the topic "Gene nod"

Pardridge, William M. Non-Invasive Gene Therapy of Experimental Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada407779.

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Pardridge, William M. Non-Invasive Gene Therapy of Experimental Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, September 2006. http://dx.doi.org/10.21236/ada462348.

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Pardridge, William M. Non-Invasive Gene Therapy of Experimental Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada419493.

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Brufsky, Adam M. Determination of a Unique Pattern of Gene Expression in Node Positive Breast Cancer Using Serial Analysis of Gene Expression (SAGE). Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada417855.

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Spinassé Dettogni, Raquel, Elaine Stur, Lauziene Andrade Soares, Diego do Prado Ventorim, Raquel Silva Reis, Fernanda Mariano Garcia, and Iúri Drumond Louro. Variação Patogênica no Gene RAD51C no Carcinoma Renal de Células Claras. Buenos Aires: siicsalud.com, April 2019. http://dx.doi.org/10.21840/siic/159359.

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Arnett, Clint, Justin Lange, Ashley Boyd, Martin Page, and Donald Cropek. Expression and secretion of active Moringa oleifera coagulant protein in Bacillus subtilis. Engineer Research and Development Center (U.S.), August 2021. http://dx.doi.org/10.21079/11681/41546.

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Cationic polypeptide proteins found in the seeds of the tropical plant Moringa oleifera have coagulation efficiencies similar to aluminum and ferric sulfates without their recalcitrant nature. Although these proteins possess great potential to augment or replace traditional coagulants in water treatment, harvesting active protein from seeds is laborious and not cost-effective. Here, we describe an alternative method to express and secrete active M. oleifera coagulant protein (MO) in Bacillus subtilis. A plasmid library containing the MO gene and 173 different types of secretory signal peptides was created and cloned into B. subtilis strain RIK1285. Fourteen of 440 clones screened were capable of secreting MO with yields ranging from 55 to 122 mg/L of growth medium. The coagulant activity of the highest MO secreting clone was evaluated when grown on Luria broth, and cell-free medium from the culture was shown to reduce turbidity in a buffered kaolin suspension by approximately 90% compared with controls without the MO gene. The clone was also capable of secreting active MO when grown on a defined synthetic wastewater supplemented with 0.5% tryptone. Cell-free medium from the strain harboring the MO gene demonstrated more than a 2-fold reduction in turbidity compared with controls. Additionally, no significant amount of MO was observed without the addition of the synthetic wastewater, suggesting that it served as a source of nutrients for the effective expression and translocation of MO into the medium.

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Immaneni, Anand, and Peter O'Connell. Can Gene Expression Pattern Analysis Predict Recurrence in Node-Negative Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada417924.

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O'Connell, Peter. Can Gene Expression Pattern Analysis Predict Recurrence in Node-Negative Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2002. http://dx.doi.org/10.21236/ada427708.

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Dillman III, James F., and Christopher S. Phillips. Comparison of Non-Human Primate and Human Whole Blood Tissue Gene Expression Profiles. Fort Belvoir, VA: Defense Technical Information Center, March 2005. http://dx.doi.org/10.21236/ada443193.

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