Gotowa bibliografia na temat „Acyl-CoAs metabolome”
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 „Acyl-CoAs metabolome”.
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 "Acyl-CoAs metabolome"
Tokarska-Schlattner, Malgorzata, Nour Zeaiter, Valérie Cunin, Stéphane Attia, Cécile Meunier, Laurence Kay, Amel Achouri i in. "Multi-Method Quantification of Acetyl-Coenzyme A and Further Acyl-Coenzyme A Species in Normal and Ischemic Rat Liver". International Journal of Molecular Sciences 24, nr 19 (6.10.2023): 14957. http://dx.doi.org/10.3390/ijms241914957.
Pełny tekst źródłaHan, Lijuan, Ling Zhao, Yong Zhou, Chao Yang, Teng Xiong, Lin Lu, Yusheng Deng i in. "Altered metabolome and microbiome features provide clues in understanding irritable bowel syndrome and depression comorbidity". ISME Journal 16, nr 4 (8.11.2021): 983–96. http://dx.doi.org/10.1038/s41396-021-01123-5.
Pełny tekst źródłaIGAL, R. Ariel, Ping WANG i Rosalind A. COLEMAN. "Triacsin C blocks de novo synthesis of glycerolipids and cholesterol esters but not recycling of fatty acid into phospholipid: evidence for functionally separate pools of acyl-CoA". Biochemical Journal 324, nr 2 (1.06.1997): 529–34. http://dx.doi.org/10.1042/bj3240529.
Pełny tekst źródłaPons, Roser, i Darryl C. De Vivo. "Primary and Secondary Carnitine Deficiency Syndromes". Journal of Child Neurology 10, nr 2_suppl (listopad 1995): 2S8–2S24. http://dx.doi.org/10.1177/0883073895010002s03.
Pełny tekst źródłaYu, Wenfeng, Xiquan Liang, Regina E. Ensenauer, Jerry Vockley, Lawrence Sweetman i Horst Schulz. "Leaky β-Oxidation of atrans-Fatty Acid". Journal of Biological Chemistry 279, nr 50 (4.10.2004): 52160–67. http://dx.doi.org/10.1074/jbc.m409640200.
Pełny tekst źródłaVarner, Erika L., Sophie Trefely, David Bartee, Eliana von Krusenstiern, Luke Izzo, Carmen Bekeova, Roddy S. O'Connor i in. "Quantification of lactoyl-CoA (lactyl-CoA) by liquid chromatography mass spectrometry in mammalian cells and tissues". Open Biology 10, nr 9 (wrzesień 2020): 200187. http://dx.doi.org/10.1098/rsob.200187.
Pełny tekst źródłaXia, Chuanwu, Zhuji Fu, Kevin P. Battaile i Jung-Ja P. Kim. "Crystal structure of human mitochondrial trifunctional protein, a fatty acid β-oxidation metabolon". Proceedings of the National Academy of Sciences 116, nr 13 (8.03.2019): 6069–74. http://dx.doi.org/10.1073/pnas.1816317116.
Pełny tekst źródłaLone, Museer A., Andreas J. Hülsmeier, Essa M. Saied, Gergely Karsai, Christoph Arenz, Arnold von Eckardstein i Thorsten Hornemann. "Subunit composition of the mammalian serine-palmitoyltransferase defines the spectrum of straight and methyl-branched long-chain bases". Proceedings of the National Academy of Sciences 117, nr 27 (23.06.2020): 15591–98. http://dx.doi.org/10.1073/pnas.2002391117.
Pełny tekst źródłaCarrer, Alessandro, Joshua L. D. Parris, Sophie Trefely, Ryan A. Henry, David C. Montgomery, AnnMarie Torres, John M. Viola i in. "Impact of a High-fat Diet on Tissue Acyl-CoA and Histone Acetylation Levels". Journal of Biological Chemistry 292, nr 8 (11.01.2017): 3312–22. http://dx.doi.org/10.1074/jbc.m116.750620.
Pełny tekst źródłaWu, Hao, Jingdan Liang, Lixia Gou, Qiulin Wu, Wei-Jun Liang, Xiufen Zhou, Ian J. Bruce, Zixin Deng i Zhijun Wang. "Recycling of Overactivated Acyls by a Type II Thioesterase during Calcimycin Biosynthesis in Streptomyces chartreusis NRRL 3882". Applied and Environmental Microbiology 84, nr 12 (13.04.2018): e00587-18. http://dx.doi.org/10.1128/aem.00587-18.
Pełny tekst źródłaRozprawy doktorskie na temat "Acyl-CoAs metabolome"
Zeaiter, Nour. "Les effets des changements métaboliques sur le métabolome des acyl-CoAs et l'acylation d'histone épigénétique". Electronic Thesis or Diss., Université Grenoble Alpes, 2024. http://www.theses.fr/2024GRALV013.
Pełny tekst źródłaAccumulating evidence suggests that metabolism can affect epigenetic post-translational modifications of histones, thus potentially linking nutrient availability or environmental conditions to gene expression and human physiopathology. However, there is still a lack of more detailed insight into this relationship. Here we study the role of short-chain (sc)-acyl-CoAs, generated in various metabolic pathways, as substrates for histone acylation. Analyzing acyl-CoAs is challenging due to their diverging (sub)cellular concentrations and physico-chemical properties. First, we applied a panel of analytical methods to establish reliable acyl-CoAs quantification, using liver ischemia as a model for inducing a metabolic shift. HPLC and MS emerged as the most suitable methods for unbiased analysis of sc-acyl-CoAs. Second, we employed HepG2 cells as a model system to explore the role of metabolic key enzymes and nutrient-induced metabolic shifts on acyl-CoA levels and histone acylation. Here and in the following, sc-acyl-CoAs were quantified by MS, and histone acylation was assessed at H4K5 and H4K8 by immunoblotting. Knockdown (KD) of enzymes involved in nucleocytosolic generation of acetyl-CoA (and potentially other acyl-CoAs) confirmed that ATP citrate lyase (ACLY) and acetyl-CoA synthetase short chain 2 (ACSS2) are the two major sources for nucleo-cytosolic acetyl-CoA. Moreover, we demonstrated that contrary to widespread believe, ACSS2 is not involved in biosynthesis of sc-acyl-CoAs other than acetyl-CoA. Further, KD of carnitine palmitoyltransferase 1A (CPT1A) did not yield clear evidence for its involvement in the export of mitochondrial sc-acyl-CoAs. Among the metabolic shifts studied, changes in acyl-CoA levels correlated with altered histone acylation only in some cases, namely octanoate fatty acid supplementation and glucose deprivation. These data suggest that substrate availability can be a determining factor for histone acylation, but that other factors can also be involved. Third, a transgenerational rat model for the effects of an environmental pollutant, endocrine disruptors (ED), revealed altered histone acylation patterns. Here we developed a HepG2 cell model that recapitulates direct ED effects on histone acylation, in particular an increased level of acetylation, together with increased acetyl-CoA levels. These data suggest HepG2 cells as a suitable model to study epigenetic ED effects mechanistically. In summary, this work established a basis to study epigenetic effects of nutrients and environmental pollutants in more detail
Knoll, Anja. "Etude du métabolisme des acides gras à très longues chaînes dans le cerveau du rat : activités enzymatiques d'élongation des acyl-CoAs, expression des gènes de la béta-oxydation peroxysomale". Bordeaux 2, 2000. http://www.theses.fr/2000BOR28756.
Pełny tekst źródła