Results 11 to 20 of about 77,206 (307)
MicroRNA Regulation of SIRT1 [PDF]
SIRT1 is an NAD-dependent deacetylase that regulates stress response pathways. By deacetylating transcription factors and co-factors, SIRT1 modulates metabolism, inflammation, hypoxic responses, circadian rhythms, cell survival, and longevity. Since SIRT1 plays a key role in regulating pathways involved in cardiovascular diseases and metabolic diseases
Munekazu eYamakuchi, Munekazu Yamakuchi
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Rejuvenating SIRT1 Activators [PDF]
Whether the red wine component resveratrol directly activates the NAD(+)-dependent protein deacetylase SIRT1 has been debated. A recent study by Hubbard et al. (2013) strengthens the case that SIRT1-activating compounds (STACs) function as positive allosteric regulators of SIRT1 and thereby regulate mitochondrial function.
Gut, Philipp, Verdin, Eric
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SIRT1 impacts upon diverse cellular processes via its roles in the determination of chromatin structure, chromatin remodelling and gene expression. This review covers the recent discoveries linking SIRT1 with the regulation of mammalian metabolism and considers ways in which abnormal metabolism in disease may, in turn, impact upon SIRT1 because of ...
John R P, Knight, Jo, Milner
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LncRNA Sirt1-AS Protects Against Cardiac Hypertrophy by Modulating Sirt1
Background LncRNAs are pivotal regulators in cardiovascular diseases. Sirt1-AS, a lncRNA, has been shown to play a role in cardiovascular diseases. This study aimed to explore the role of Sirt1-AS in cardiac hypertrophy and the underlying molecular mechanism.
Xuejiao Wei +5 more
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Fibrillarin Resists Cellular Senescence Via SIRT1-Dependent Nicotinamide Metabolism and Its Inhibition Sensitizes Senolytic Therapy in Esophageal Squamous Cell Carcinoma. [PDF]
FBL directly binds to and stabilizes SIRT1 by blocking its ubiquitin‐proteasome degradation, thereby sustaining nicotinamide metabolism and redox homeostasis to counteract cellular senescence in ESCC. Genetic and pharmacological suppression of FBL sensitizes tumor cells to senolytic therapy.
Jin X +9 more
europepmc +2 more sources
Nicotinamide Metabolism Constrains Memory CD8<sup>+</sup> T Cell Formation Through a Putative HS1BP3-SIRT1-FOXO3-BCL6 Axis. [PDF]
ABSTRACT Memory T cells exhibit long‐term persistence, a defining feature that underpins durable clinical responses to adoptive immunotherapies. The mechanisms that integrate metabolic cues with transcriptional control of memory fate remain undetermined. Here, we identify HS1‐binding protein 3 (HS1BP3) is preferentially expressed in memory CD8+ T cells.
Wang S +13 more
europepmc +2 more sources
Regulation of SIRT1 by MicroRNAs [PDF]
Sirtuin 1 (SIRT1) is an NAD(+)-dependent deacetylase that connects cellular energy levels to homeostatic responses by deacetylating and modulating the activities of many transcriptional regulators. Discovered as a longevity protein in yeast, the mammalian SIRT1 has been intensively studied because of its great potential as a therapeutic target to ...
Sung-E, Choi, Jongsook Kim, Kemper
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SIRT1 and Kidney Function [PDF]
<b><i>Background:</i></b> SIRT1 is a nicotinamide adenine dinucleotide-dependent deacetylase belonging to the class III histone deacetylases. Abundantly expressed in the kidney, especially in the renal medulla, SIRT1 is closely involved in renal physiology and pathology.
Yi, Guan, Chuan-Ming, Hao
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The Role of Sirt1 in Epileptogenesis [PDF]
AbstractThe mechanisms by which brain insults lead to subsequent epilepsy remain unclear. Insults, including trauma, stroke, tumors, infections, and long seizures [status epilepticus (SE)], create a neuronal state of increased metabolic demand or decreased energy supply.
Alicia M. Hall +6 more
openaire +4 more sources
MiR-138 promotes apoptosis of colon cancer cells by targeting SIRT1
Objective To investigate the mechanism of miR-138 involving in the apoptosis of colon cancer cells by regulating SIRT1. Methods RT-qPCR was used to detect the expression of miR-138 in colon cancer cell lines HCT 116, SW480, Caco-2, HT29 and SW1116.
YANG Yang, PENG Wenli
doaj +1 more source

