Gotowa bibliografia na temat „Inactivation de l'X”
Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych
Spis treści
Zobacz listy aktualnych artykułów, książek, rozpraw, streszczeń i innych źródeł naukowych na temat „Inactivation de l'X”.
Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.
Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.
Artykuły w czasopismach na temat "Inactivation de l'X"
Gilgenkrantz, H. "Inactivation de l'X : un gène actif spécifique de l'X inactif ?" médecine/sciences 7, nr 4 (1991): 375. http://dx.doi.org/10.4267/10608/4363.
Pełny tekst źródłaFontés, M. "Empreinte génomique parentale et inactivation de l'X : l'antisens a t-il un sens ?" médecine/sciences 15, nr 11 (1999): 1277. http://dx.doi.org/10.4267/10608/1256.
Pełny tekst źródłaByun, Do-Sun, Naseem Ahmed, Shannon Nasser, Joongho Shin, Sheren Al-Obaidi, Sanjay Goel, Georgia A. Corner i in. "Intestinal epithelial-specific PTEN inactivation results in tumor formation". American Journal of Physiology-Gastrointestinal and Liver Physiology 301, nr 5 (listopad 2011): G856—G864. http://dx.doi.org/10.1152/ajpgi.00178.2011.
Pełny tekst źródłaStaiculescu, Marius Catalin, Jungsil Kim, Robert P. Mecham i Jessica E. Wagenseil. "Mechanical behavior and matrisome gene expression in the aneurysm-prone thoracic aorta of newborn lysyl oxidase knockout mice". American Journal of Physiology-Heart and Circulatory Physiology 313, nr 2 (1.08.2017): H446—H456. http://dx.doi.org/10.1152/ajpheart.00712.2016.
Pełny tekst źródłaAppelmelk, Ben J., M. Celeste Martino, Eveline Veenhof, Mario A. Monteiro, Janneke J. Maaskant, Riccardo Negrini, Frank Lindh, Malcolm Perry, Giuseppe Del Giudice i Christina M. J. E. Vandenbroucke-Grauls. "Phase Variation in H Type I and Lewis a Epitopes ofHelicobacter pylori Lipopolysaccharide". Infection and Immunity 68, nr 10 (1.10.2000): 5928–32. http://dx.doi.org/10.1128/iai.68.10.5928-5932.2000.
Pełny tekst źródłaGao, Xiquan, Marion Brodhagen, Tom Isakeit, Sigal Horowitz Brown, Cornelia Göbel, Javier Betran, Ivo Feussner, Nancy P. Keller i Michael V. Kolomiets. "Inactivation of the Lipoxygenase ZmLOX3 Increases Susceptibility of Maize to Aspergillus spp." Molecular Plant-Microbe Interactions® 22, nr 2 (luty 2009): 222–31. http://dx.doi.org/10.1094/mpmi-22-2-0222.
Pełny tekst źródłaMcGrail, Maura, Fang Liu, Sekhar Kambakam i Zhitao Ming. "Abstract PR-010: Asc1lb progenitor-specific RB conditional inactivation in zebrafish models rare CNS primitive neuroectodermal tumors". Cancer Research 84, nr 5_Supplement_1 (4.03.2024): PR—010—PR—010. http://dx.doi.org/10.1158/1538-7445.brain23-pr-010.
Pełny tekst źródłaEpp, Nikolas, Gerhard Fürstenberger, Karsten Müller, Silvia de Juanes, Michael Leitges, Ingrid Hausser, Florian Thieme, Gerhard Liebisch, Gerd Schmitz i Peter Krieg. "12R-lipoxygenase deficiency disrupts epidermal barrier function". Journal of Cell Biology 177, nr 1 (2.04.2007): 173–82. http://dx.doi.org/10.1083/jcb.200612116.
Pełny tekst źródłaDionellis, Vasilis S., Maxim Norkin, Angeliki Karamichali, Giacomo G. Rossetti, Joerg Huelsken, Paloma Ordonez-Moran i Thanos D. Halazonetis. "Genomic Instability Profiles at the Single Cell Level in Mouse Colorectal Cancers of Defined Genotypes". Cancers 13, nr 6 (12.03.2021): 1267. http://dx.doi.org/10.3390/cancers13061267.
Pełny tekst źródłaLiu, Lei, Huichun Tong i Xiuzhu Dong. "Function of the Pyruvate Oxidase-Lactate Oxidase Cascade in Interspecies Competition between Streptococcus oligofermentans and Streptococcus mutans". Applied and Environmental Microbiology 78, nr 7 (27.01.2012): 2120–27. http://dx.doi.org/10.1128/aem.07539-11.
Pełny tekst źródłaRozprawy doktorskie na temat "Inactivation de l'X"
Raas, Quentin. "Inactivation génique des transporteurs ABC peroxysomaux ABCD1 et ABCD2 dans les cellules microgliales BV-2 : étude de la physiopathogenèse de l’adrénoleucodystrophie liée à l’X". Thesis, Bourgogne Franche-Comté, 2018. http://www.theses.fr/2018UBFCI011/document.
Pełny tekst źródłaX-linked adrenoleukodystrophy (X-ALD) is a severe neurodegenerative disorder characterized by very-long-chain fatty acid (VLCFA) accumulation resulting from a peroxisomal β-oxidation defect. The disease is caused by mutations in the ABCD1 gene, which encodes for a peroxisomal half ABC transporter predicted, like its closest homologue ABCD2, to participate in the entry of VLCFA-CoA into the peroxisome, the unique site of their β-oxidation. Progress in understanding the physiopathogenesis of X-ALD suffers from the lack of appropriate cell and animal models. Since peroxisomal defects in microglia seem to be a key element of the onset of the disease, we generated four microglial cell lines unable to transport and/or β-oxidize VLCFA into the peroxisome. BV-2 microglial cells were engineered with CRISPR-Cas9 to generate four microglial cell lines deficient in ABCD1, ABCD2, both ABCD1 and ABCD2 or ACOX-1 (the first rate-limiting enzyme of the peroxisomal β-oxidation system). Biochemical defects and lipid content changes associated with VLCFA accumulation but also fatty acids and cholesterol changes were identified in deficient microglia. Ultrastructural investigations confirmed cytosolic lipid inclusions and an increased number of peroxisome and mitochondria. Transcriptomic profiles of deficient microglia are indicative of an impaired plasticity and an impaired capacity to operate the metabolic shift required upon an inflammatory stimulation. Peroxisomal defect is likely to affect phagocytosis and antigen presentation capacity of microglia. Peroxisomal lipid metabolism defect is also suggested to modify cell membranes organization. Altogether, these novel mutant cell lines represent a promising model that should permit identification of new therapeutic targets for this complex neurodegenerative disease
Sourrouille, Christophe. "Inactivation de l'α(1. 3)-fucosyltransférase et de la β(1. 2)-xylotransférase, en vue de la production de protéines recombinantes d'intérêt thérapeutique chez la luzerne". Rouen, 2005. http://www.theses.fr/2005ROUES046.
Pełny tekst źródłaThis work develops the strategy of PTGS with the aim of inhibiting α(1. 3)-fucosyltransferase (FucT) and β(1. 2)-xylotransferase (XylT) activities in Medicago sativa. From this perspective, the cDNAs coding for these two glycoltransferases have been cloned and characterized. To induce the PTGS in M. Sativa, we have transformed plants with sens, antisens and intron-hairpin ARN (ihpARN) constructs targeting either α(1. 3)-FucT or β(1. 2)-XylT. Then, we have selected one transformant presenting a decrease in α(1. 3)-fucosylation of its glycoproteins and two plants presenting a reduction in the β(1. 2)-xylosylation. In addition, in these plants, we have shown a strong diminution in the amount of α(1. 3)-FucT and β(1. 2)-XylT transcripts respectively. Furthermore, we have demonstrated the “inhibiting” constructs realized from the M. Sativa β(1. 2)-XylT cDNA are able to induce the PTGS in a heterologous system: tobacco BY-2 cells