Lipids Reprogram Metabolism to Become a Major Carbon Source for Histone Acetylation.
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Metabolic interactions in cancer: cellular metabolism at the interface between the microenvironment, the cancer cell phenotype and the epigenetic landscape.Nicotinamide mononucleotide requires SIRT3 to improve cardiac function and bioenergetics in a Friedreich's ataxia cardiomyopathy modelMetabolism and Skeletal Muscle Homeostasis in Lung Disease.Multi-dimensional Roles of Ketone Bodies in Fuel Metabolism, Signaling, and Therapeutics.Mitochondria control acute and chronic responses to hypoxia.HDAC3 is a molecular brake of the metabolic switch supporting white adipose tissue browningSodium Octanoate Modulates the Innate Immune Response of Bovine Mammary Epithelial Cells through the TLR2/P38/JNK/ERK1/2 Pathway: Implications during Staphylococcus aureus Internalization.Fatty acid oxidation by the osteoblast is required for normal bone acquisition in a sex- and diet-dependent manner.The mitochondrial respiratory chain is essential for haematopoietic stem cell function.Brown Fat AKT2 Is a Cold-Induced Kinase that Stimulates ChREBP-Mediated De Novo Lipogenesis to Optimize Fuel Storage and Thermogenesis.Metabolic Signaling to Epigenetic Alterations in Cancer.Cofactors As Metabolic Sensors Driving Cell Adaptation in Physiology and Disease.Metabolic pathways at the crossroads of diabetes and inborn errors.Metabolism and Transcription in Cancer: Merging Two Classic Tales.Cancer Associated Fibroblasts: The Architects of Stroma Remodeling.Spatiotemporal Control of Acetyl-CoA Metabolism in Chromatin Regulation.Endothelial Cell Metabolism.Fatty acid synthase (FASN) as a therapeutic target in breast cancer.The carnitine system and cancer metabolic plasticity.Insulin action and resistance in obesity and type 2 diabetes.Metabolic recoding of epigenetics in cancerReciprocal Regulation of Metabolic Reprogramming and Epigenetic Modifications in CancerFatty acid metabolism complements glycolysis in the selective regulatory T cell expansion during tumor growthThe contributions of cancer cell metabolism to metastasisEpigenetic-Transcriptional Regulation of Fatty Acid Metabolism and Its Alterations in LeukaemiaMetabolism and Epigenetic Interplay in Cancer: Regulation and Putative Therapeutic Targets
P2860
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P2860
Lipids Reprogram Metabolism to Become a Major Carbon Source for Histone Acetylation.
description
2016 nî lūn-bûn
@nan
2016年の論文
@ja
2016年学术文章
@wuu
2016年学术文章
@zh-cn
2016年学术文章
@zh-hans
2016年学术文章
@zh-my
2016年学术文章
@zh-sg
2016年學術文章
@yue
2016年學術文章
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2016年學術文章
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name
Lipids Reprogram Metabolism to Become a Major Carbon Source for Histone Acetylation.
@en
Lipids Reprogram Metabolism to Become a Major Carbon Source for Histone Acetylation.
@nl
type
label
Lipids Reprogram Metabolism to Become a Major Carbon Source for Histone Acetylation.
@en
Lipids Reprogram Metabolism to Become a Major Carbon Source for Histone Acetylation.
@nl
prefLabel
Lipids Reprogram Metabolism to Become a Major Carbon Source for Histone Acetylation.
@en
Lipids Reprogram Metabolism to Become a Major Carbon Source for Histone Acetylation.
@nl
P2093
P2860
P1433
P1476
Lipids Reprogram Metabolism to Become a Major Carbon Source for Histone Acetylation.
@en
P2093
Betül Kitir
Douglas B Fox
Eoin McDonnell
Olga R Ilkayeva
Paul A Grimsrud
Scott B Crown
P2860
P304
P356
10.1016/J.CELREP.2016.10.012
P577
2016-11-01T00:00:00Z