Bibliographies thématiques / Sephin1

Littérature scientifique sur le sujet « Sephin1 »

Auteur : Grafiati
Publié le 11 mars 2023

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Articles de revues sur le sujet "Sephin1"

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Ruiz, Asier, Jone Zuazo, Carolina Ortiz-Sanz, Celia Luchena, Carlos Matute et Elena Alberdi. « Sephin1 Protects Neurons against Excitotoxicity Independently of the Integrated Stress Response ». International Journal of Molecular Sciences 21, no 17 (24 août 2020) : 6088. http://dx.doi.org/10.3390/ijms21176088.

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Sephin1 is a derivative of guanabenz that inhibits the dephosphorylation of the eukaryotic initiation factor 2 alpha (eIF2α) and therefore may enhance the integrated stress response (ISR), an adaptive mechanism against different cellular stresses, such as accumulation of misfolded proteins. Unlike guanabenz, Sephin1 provides neuroprotection without adverse effects on the α2-adrenergic system and therefore it is considered a promising pharmacological therapeutic tool. Here, we have studied the effects of Sephin1 on N-methyl-D-aspartic acid (NMDA) receptor signaling which may modulate the ISR and contribute to excitotoxic neuronal loss in several neurodegenerative conditions. Time-course analysis of peIF2α levels after NMDA receptor overactivation showed a delayed dephosphorylation that occurred in the absence of activating transcription factor 4 (ATF4) and therefore independently of the ISR, in contrast to that observed during endoplasmic reticulum (ER) stress induced by tunicamycin and thapsigargin. Similar to guanabenz, Sephin1 completely blocked NMDA-induced neuronal death and was ineffective against AMPA-induced excitotoxicity, whereas it did not protect from experimental ER stress. Interestingly, both guanabenz and Sephin1 partially but significantly reduced NMDA-induced cytosolic Ca2+ increase, leading to a complete inhibition of subsequent calpain activation. We conclude that Sephin1 and guanabenz share common strong anti-excitotoxic properties with therapeutic potential unrelated to the ISR.
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Crespillo-Casado, Ana, Zander Claes, Meng S. Choy, Wolfgang Peti, Mathieu Bollen et David Ron. « A Sephin1-insensitive tripartite holophosphatase dephosphorylates translation initiation factor 2α ». Journal of Biological Chemistry 293, no 20 (4 avril 2018) : 7766–76. http://dx.doi.org/10.1074/jbc.ra118.002325.

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Thapa, Simrika, Dalia H. Abdelaziz, Basant A. Abdulrahman et Hermann M. Schatzl. « Sephin1 Reduces Prion Infection in Prion-Infected Cells and Animal Model ». Molecular Neurobiology 57, no 5 (24 janvier 2020) : 2206–19. http://dx.doi.org/10.1007/s12035-020-01880-y.

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Chen, Yanan, Joseph R. Podojil, Rejani B. Kunjamma, Joshua Jones, Molly Weiner, Wensheng Lin, Stephen D. Miller et Brian Popko. « Sephin1, which prolongs the integrated stress response, is a promising therapeutic for multiple sclerosis ». Brain 142, no 2 (17 janvier 2019) : 344–61. http://dx.doi.org/10.1093/brain/awy322.

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Callejo, Gerard, Luke A. Pattison, Jack C. Greenhalgh, Sampurna Chakrabarti, Evangelia Andreopoulou, James R. F. Hockley, Ewan St John Smith et Taufiq Rahman. « In silico screening of GMQ-like compounds reveals guanabenz and sephin1 as new allosteric modulators of acid-sensing ion channel 3 ». Biochemical Pharmacology 174 (avril 2020) : 113834. http://dx.doi.org/10.1016/j.bcp.2020.113834.

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Maltsev, Alexander V., Anna B. Nikiforova, Natalia V. Bal et Pavel M. Balaban. « Amyloid Aβ25-35 Aggregates Say ‘NO’ to Long-Term Potentiation in the Hippocampus through Activation of Stress-Induced Phosphatase 1 and Mitochondrial Na+/Ca2+ Exchanger ». International Journal of Molecular Sciences 23, no 19 (6 octobre 2022) : 11848. http://dx.doi.org/10.3390/ijms231911848.

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The search for strategies for strengthening the synaptic efficiency in Aβ25-35-treated slices is a challenge for the compensation of amyloidosis-related pathologies. Here, we used the recording of field excitatory postsynaptic potentials (fEPSPs), nitric oxide (NO) imaging, measurements of serine/threonine protein phosphatase (STPP) activity, and the detection of the functional mitochondrial parameters in suspension of brain mitochondria to study the Aβ25-35-associated signaling in the hippocampus. Aβ25-35 aggregates shifted the kinase–phosphatase balance during the long-term potentiation (LTP) induction in the enhancement of STPP activity. The PP1/PP2A inhibitor, okadaic acid, but not the PP2B blocker, cyclosporin A, prevented Aβ25-35-dependent LTP suppression for both simultaneous and delayed enzyme blockade protocols. STPP activity in the Aβ25-35-treated slices was upregulated, which is reverted relative to the control values in the presence of PP1/PP2A but not in the presence of the PP2B blocker. A selective inhibitor of stress-induced PP1α, sephin1, but not of the PP2A blocker, cantharidin, is crucial for Aβ25-35-mediated LTP suppression prevention. A mitochondrial Na+/Ca2+ exchanger (mNCX) blocker, CGP37157, also attenuated the Aβ25-35-induced LTP decline. Aβ25-35 aggregates did not change the mitochondrial transmembrane potential or reactive oxygen species (ROS) production but affected the ion transport and Ca2+-dependent swelling of organelles. The staining of hippocampal slices with NO-sensitive fluorescence dye, DAF-FM, showed stimulation of the NO production in the Aβ25-35-pretreated slices at the dendrite-containing regions of CA1 and CA3, in the dentate gyrus (DG), and in the CA1/DG somata. NO scavenger, PTIO, or nNOS blockade by selective inhibitor 3Br-7NI partly restored the Aβ25-35-induced LTP decline. Thus, hippocampal NO production could be another marker for the impairment of synaptic plasticity in amyloidosis-related states, and kinase–phosphatase balance management could be a promising strategy for the compensation of Aβ25-35-driven deteriorations.
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BRAILOVSKY, HARRY, et ERNESTO BARRERA. « Illustrated key to the species in the genus Sephina (Hemiptera : Heteroptera : Coreidae : Coreinae : Spartocerini), with descriptions of three new species and new distributional records ». Zootaxa 5048, no 1 (5 octobre 2021) : 77–98. http://dx.doi.org/10.11646/zootaxa.5048.1.4.

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Three new species of Sephina Amyot and Serville 1843, are described: S. crassa from Ecuador, S. effrena from Colombia and S. ornata from Panama. A key to the 27 known species and photographs of the dorsal habitus are included. Also included are photographs of the male genital capsule of S. vinula Stål 1862, and parameres of S. indierae Wolcott 1924 and S. vinula. New distributional records for S. dorsalis (White 1842), S. esquivelae Brailovsky & Sánchez 1983, S. faceta Brailovsky 2001, S. formosa (Dallas 1852), S. geniculata Distant 1881, S. limbata Stål 1862, S. nigripes Schmidt 1907, S. pagella Brailovsky & Sánchez 1983, S. pubera (Erichson 1848), S. pustulata (Fabricius 1803), S. rogersi Distant 1881, S. subulata Brailovsky & Sánchez 1983, and S. vinula are included. Sephina excellens Schmidt, 1907 is synonymized under S. pubera (Erichson 1848). The synonymy of Sephina grayi Van Duzee, 1909 under S. gundlachi (Guérin-Méneville 1857) is here corroborated.
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Jung, Jisu, Yoomin Kim, Jiwoon Na, Lu Qiao, Jeyoung Bang, Dongin Kwon, Tack-Jin Yoo et al. « Constitutive Oxidative Stress by SEPHS1 Deficiency Induces Endothelial Cell Dysfunction ». International Journal of Molecular Sciences 22, no 21 (28 octobre 2021) : 11646. http://dx.doi.org/10.3390/ijms222111646.

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The primary function of selenophosphate synthetase (SEPHS) is to catalyze the synthesis of selenophosphate that serves as a selenium donor during selenocysteine synthesis. In eukaryotes, there are two isoforms of SEPHS (SEPHS1 and SEPHS2). Between these two isoforms, only SEPHS2 is known to contain selenophosphate synthesis activity. To examine the function of SEPHS1 in endothelial cells, we introduced targeted null mutations to the gene for SEPHS1, Sephs1, in cultured mouse 2H11 endothelial cells. SEPHS1 deficiency in 2H11 cells resulted in the accumulation of superoxide and lipid peroxide, and reduction in nitric oxide. Superoxide accumulation in Sephs1-knockout 2H11 cells is due to the induction of xanthine oxidase and NADPH oxidase activity, and due to the decrease in superoxide dismutase 1 (SOD1) and 3 (SOD3). Superoxide accumulation in 2H11 cells also led to the inhibition of cell proliferation and angiogenic tube formation. Sephs1-knockout cells were arrested at G2/M phase and showed increased gamma H2AX foci. Angiogenic dysfunction in Sephs1-knockout cells is mediated by a reduction in nitric oxide and an increase in ROS. This study shows for the first time that superoxide was accumulated by SEPHS1 deficiency, leading to cell dysfunction through DNA damage and inhibition of cell proliferation.
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Bang, Jeyoung, Minguk Han, Tack-Jin Yoo, Lu Qiao, Jisu Jung, Jiwoon Na, Bradley A. Carlson et al. « Identification of Signaling Pathways for Early Embryonic Lethality and Developmental Retardation in Sephs1−/− Mice ». International Journal of Molecular Sciences 22, no 21 (28 octobre 2021) : 11647. http://dx.doi.org/10.3390/ijms222111647.

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Selenophosphate synthetase 1 (SEPHS1) plays an essential role in cell growth and survival. However, the underlying molecular mechanisms remain unclear. In the present study, the pathways regulated by SEPHS1 during gastrulation were determined by bioinformatical analyses and experimental verification using systemic knockout mice targeting Sephs1. We found that the coagulation system and retinoic acid signaling were most highly affected by SEPHS1 deficiency throughout gastrulation. Gene expression patterns of altered embryo morphogenesis and inhibition of Wnt signaling were predicted with high probability at E6.5. These predictions were verified by structural abnormalities in the dermal layer of Sephs1−/− embryos. At E7.5, organogenesis and activation of prolactin signaling were predicted to be affected by Sephs1 knockout. Delay of head fold formation was observed in the Sephs1−/− embryos. At E8.5, gene expression associated with organ development and insulin-like growth hormone signaling that regulates organ growth during development was altered. Consistent with these observations, various morphological abnormalities of organs and axial rotation failure were observed. We also found that the gene sets related to redox homeostasis and apoptosis were gradually enriched in a time-dependent manner until E8.5. However, DNA damage and apoptosis markers were detected only when the Sephs1−/− embryos aged to E9.5. Our results suggest that SEPHS1 deficiency causes a gradual increase of oxidative stress which changes signaling pathways during gastrulation, and afterwards leads to apoptosis.
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Varol, Marie-Christine Bornes. « Haïm Vidal Sephiha (1923 – 2019) ». Tsafon, no 79 (1 juillet 2020) : 181–83. http://dx.doi.org/10.4000/tsafon.2993.

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Thèses sur le sujet "Sephin1"

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Frapporti, Giulia. « Lysosome orchestrates autophagy and integrated stress response : new insights from Sephin1 ». Doctoral thesis, Università degli studi di Trento, 2023. https://hdl.handle.net/11572/363904.

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The maintenance of protein homeostasis is vital for all cells, but it is of utmost importance in post-mitotic cells, such as neurons that cannot dilute aggregates by cell division. Dysregulation of the proteostasis network can lead to neurodegenerative disorders such as Parkinson’s disease (PD), Alzheimer’s disease, Huntington’s disease, Amyotrophic Lateral Sclerosis (ALS), and prion diseases. The small molecule Sephin1 is a promising lead against proteostasis disruption, but its mechanism of action is uncertain. We assessed the therapeutic efficacy of Sephin1 in an established PD mouse model. Our laboratory has recently characterized a mouse expressing via bacterial artificial chromosome (BAC) the human LRRK2 G2019S protein, a variant linked to PD. Our data show that Sephin1 treatment rescues the motor deficit observed in BAC human-G2019S mice. Our experimental evidence shows that Sephin1 binds the monomeric globular actin (G-actin) in cell-free assays. By combining PAL chemistry to MS/MS analysis we identified the putative Sephin1 binding site on actin. In vitro, Sephin1 drives actin misfolding, and eventually, its precipitation. Upon Sephin1 treatment in HeLa cells, we visualized actin clusters localized to the lysosomes. This event at the lysosome impairs the normal autophagic flux. At the same time, Sephin1 induces the inactivation of the mammalian target of rapamycin (mTORC1), thus allowing the nuclear translocation of the transcription Factor EB (TFEB) and the expression of TFEB-direct target genes, on the longer term. In parallel, Sephin1 elicits the phosphorylation of the α subunit of the Eukaryotic Initiation Factor 2 (eIF2) and the ER-stress independent expression of the C/EBP homologous protein (CHOP). CHOP is a transcription factor that contributes to the integrated stress response as well as to autophagy. As such, Sephin1 triggers the activation of two main players in the autophagic response, TFEB and CHOP. Accordingly, we reported that, after the initial impairment, Sephin1 stimulates autophagy. Taken together, our results reveal a novel Sephin1 molecular mechanism in which lysosomal stress may regulate autophagy via mTORC1-TFEB complemented with the eIF2α signalling pathway. Although several questions remain to be answered, Sephin1, which successfully completed the phase I clinical trial for ALS and Charcot–Marie–Tooth disease, represents a promising therapeutic strategy that targets autophagy to regulate the homeostatic balance of proteins in neurodegenerative diseases.
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Di, Lalla Matthew. « Validation of synthetic lethal hits of microtubule targeting agents ». Thesis, 2020. http://hdl.handle.net/1866/25171.

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Les microtubules, composants clés du cytosquelette des cellules eucaryotes, sont des polymères de tubuline très dynamiques et impliqués dans une grande variété de processus cellulaires. Leur rôle essentiel dans le cycle cellulaire a fait d’eux une cible validée en thérapie anticancéreuse. Malgré l’efficacité clinique des agents ciblant les microtubules (ACM), les effets secondaires compliquent l’utilisation. Nous avons cherché à identifier des vulnérabilités génétiques qui peuvent être exploitées pour diminuer la dose requise tout en maintenant l'efficacité, et donc réduire les effets secondaires. En collaboration avec le laboratoire Tyers à l’IRIC, nous avons réalisé un criblage génétique basé sur la létalité synthétique avec des agents antiprolifératifs, dont les ACMs. Nous avons sélectionné les gènes dont l’extinction sensibilisait les cellules aux ACMs. J’ai confirmé que l’invalidation de chacun des gènes GNA13, SEPHS1, DLGAP5 et des gènes QRICH1, DLGAP5 sensibilisaient les cellules NALM6 au docétaxel et la vincristine respectivement. En revanche, aucune invalidation de ces gènes n'a augmenté la sensibilité au docétaxel dans les cellules U2OS. En plus de son effet avec le docétaxel, le gène GNA13 s’est distingué être une cible particulièrement intéressante. En effet, la perte complète de GNA13 augmente considérablement la fréquence et la gravité d’erreurs de ségrégation des chromosomes dans les cellules U2OS. Cette augmentation n’a pas été rectifiée à la suite d’un traitement avec la molécule UMK57, connue pour réduire le taux d’erreurs de ségrégation des chromosomes. De manière intéressante, la perte complète de GNA13 augmente également la fréquence des erreurs de ségrégation des chromosomes dans les cellules RPE1, cellules non-cancéreuses et stables au niveau chromosomique. Cela suggère que la perte complète de GNA13 ne nécessite pas de transformation ni d'instabilité chromosomique, comme conditions préalables pour exacerber l'instabilité chromosomique. L’ensemble de ces résultats ouvre une nouvelle voie de stratégies thérapeutiques anticancéreuses, à savoir, le traitement des cancers présentant une mutation des gènes QRICH1, DLGAP5, GNA13, et SEPHS1 avec de faibles doses d’ACMs. En particulier, GNA13 est fréquemment muté dans certains lymphomes. De plus, les résultats obtenus démontrent que la perte complète de GNA13 aggrave l’instabilité chromosomique et par conséquent, pourrait être impliquée dans la cancérogenèse.
Microtubules, key components of the eukaryotic cytoskeleton, are highly dynamic polymers of tubulin implicated in a wide variety of cellular processes. Their essential roles in the cell cycle have made them a valid target in cancer therapy. Despite the clinical efficacy of microtubule targeting agents (MTA), their use is hampered by side effects. We sought to identify genetic vulnerabilities that can be exploited to decrease the required dose while maintaining efficacy, and therefore reduce side effects. In collaboration with the Tyers laboratory at IRIC, we carried out a genetic screen based on synthetic lethality with antiproliferative agents, including MTAs. We have selected genes whose knockout sensitized cells to MTAs. I have confirmed that the knockout of GNA13, SEPHS1, DLGAP5, and QRICH1, DLGAP5, sensitize NALM6 cells to docetaxel and vincristine respectively. However, no knockout of these genes increased the sensitivity to docetaxel in U2OS cells. In addition to its effect with docetaxel, GNA13 stood out as being a particularly exciting target. GNA13 knockout increased the frequency and severity of chromosome segregation errors in U2OS cells. This increase was not corrected following treatment with UMK57, a molecule known to reduce the rate of chromosome segregation errors. Interestingly, the GNA13 knockout also increased the frequency of chromosome segregation errors in non-cancerous and chromosomally stable RPE1 cells. This suggests that GNA13 does not require transformation nor chromosomal instability as prerequisites for exacerbating chromosomal instability. Overall, these results open up a new avenue of anticancer therapeutic strategies, namely, the treatment of cancers presenting mutations in QRICH1, DLGAP5, GNA13, and SEPHS1 with lower doses of MTAs. In particular, GNA13 is frequently mutated in certain lymphomas. In addition, the results obtained demonstrate that GNA13 knockout exacerbates chromosomal instability and, therefore, could be involved in carcinogenesis.
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Oudouhou, Flore. « Analyse biochimique et inhibition de complexes macromoléculaires dans des cellules humaines et bactériennes ». Thèse, 2018. http://hdl.handle.net/1866/21802.

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Livres sur le sujet "Sephin1"

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Lorato lwa sephiri : Tswana drama. Midrand : Educum Publishers, 1994.

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Blade, Adam. Sephir, the storm monster. Sydney : Orchard Books, 2009.

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Hamilton, Joe L. Kia Sephia & Spectra automotive repair manual. Sparkford, Nr Yeovil, Somerset : Haynes Pub. Group, 2010.

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Hamilton, Joe L. Kia Sephia & Spectra automotive repair manual. Somerset, England : Haynes Pub. Group, 2005.

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Hamilton, Joe L. Chilton's Kia Sephia & Spectra 1994-04 repair manual. Newbury Park, Calif : Haynes North America, 2005.

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Hamilton, Joe L. Chilton's Kia Sephia & Spectra 1994-04 repair manual. Newbury Park, Calif : Haynes North America, 2005.

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Makean, John. Sephira. Lulu.com, 2006.

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Vari, Autori Autori, Danilo Simoni, Nathan Blade et Silvia Licetti. Sephir. Independently Published, 2017.

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Sephiri (Children's Stories). Juta Gariep, 2004.

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al, et, R. Schermbrucker et R. Viljoen. Sephiri (Children's Stories). Juta Gariep, 2004.

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Chapitres de livres sur le sujet "Sephin1"

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ALEKSANDER, N. « Sephira ». Dans Digital Art Masters, 126–31. Elsevier, 2009. http://dx.doi.org/10.1016/b978-0-240-52170-1.50024-2.

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Actes de conférences sur le sujet "Sephin1"

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Almeida, Jamile Aislin Silva de, et Carla Yasmym De Carvalho Lima. « NUTRIGENÔMICA E AS DOENÇAS CRÔNICAS NÃO TRANSMISSÍVEIS : UMA REVISÃO BIBLIOGRÁFICA ENTRE OS POLIFORMISMOS E COMPOSTOS BIOATIVOS ». Dans II Congresso Brasileiro de Biologia Molecular On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/2323.

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Introdução: A presença de poliformismos associados ao risco de Doenças Crônicas Não Transmissíveis (DCNTs) se tornou um despertar de interesse para a genômica nutricional, que tem como foco o estudo da relação gene-nutriente, uma vez que vários nutrientes e compostos bioativos podem ter um papel importante na diminuição de tais doenças nos indivíduos. Objetivo: Analisar a contribuição da nutrigenômica para precaver os casos de DCNT, como obesidade, Diabetes Mellitus II, câncer, doenças inflamatórias intestinais e outras complicações, durante os últimos 3 anos. Material e Métodos: A pesquisa foi realizada a partir de 7 estudos retirados nas bases de dados SciElo, Web of, Science e Scopus. Publicados no período de 2018 e 2020, utilizando as palavras-chaves: “doenças crônicas não transmissíveis”, “nutrição”, “nutrigenômica” e “poliformismo”. Resultados: Estudos demonstraram que existem em nosso genoma diversos tipos de poliformismos, associados a incidência de DCNTs. Dentre eles temos os Poliformismos de Nucleotídeo Único (SNps) nos genes FTO; FADS1, ADRB2, LEPR, IL-6, LPIN1, AdipoR1, PPARγ, ZnT8, TCF7L2, BRCA1, PPM1K, RVD, DIO1-2, GPX-1,3, SEPHS1, SEPSECS e TXNRD2 e FOXO3. Com relação aos alimentos, temos aqueles à base de plantas, especialmente as frutas e hortaliças, que são fontes de uma variedade de compostos bioativos, como terpenóides, polifenóis, compostos de enxofre, alcalóides e poliaminas, em que a ingestão está ligado à proteção contra doenças crônicas. Compostos polifenóis, por exemplo, quando entram na via do fator nuclear κB (NF-κB) exercem a função de transcrição de vários genes, incluindo os que se relacionam com a produção de citocinas pró-inflamatórias, quimiocinas e moléculas essenciais para a resposta inflamatória, que irão exerce importante ação no retardo de DCNTs. Conclusão: Os resultados nutrigenômicos servem como parâmetro para a análise das DCNTs no período de três anos. Mas, é necessário corroborar que elas são resultado de uma rede de fatores, não apenas genéticos e nutricionais, mas também, ambientais, como a prática de atividade física, uso de álcool e tabaco e fatores individuais. Sendo de grande relevância entender melhor a interação gene-nutriente e seu papel para a saúde da população portadora de DCNTs ou em processo de tratamento.
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Rapports d'organisations sur le sujet "Sephin1"

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Kyser, E. A. Validation of the SEPHIS Program for the Modeling of the HM Process. Office of Scientific and Technical Information (OSTI), décembre 1998. http://dx.doi.org/10.2172/4836.

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