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Relevant bibliographies by topics / SIRT2-KO mice

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Academic literature on the topic 'SIRT2-KO mice'

Author: Grafiati

Published: 6 September 2023

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Journal articles on the topic "SIRT2-KO mice"

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Jung, Yu Jin, Woong Park, Kyung Pyo Kang, and Won Kim. "SIRT2 is involved in cisplatin-induced acute kidney injury through regulation of mitogen-activated protein kinase phosphatase-1." Nephrology Dialysis Transplantation 35, no. 7 (2020): 1145–56. http://dx.doi.org/10.1093/ndt/gfaa042.

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Abstract Background Activation of mitogen-activated protein kinase phosphatase-1 (MKP-1), a dual-specificity protein phosphatase, regulates mitogen-activated protein kinase signaling. C-Jun N-terminal kinase (JNK) and p38 are activated in cisplatin-induced renal injury. However, the change of MKP-1 expression in cisplatin-induced renal injury and the regulatory effect of sirtuin 2 (SIRT2), a nicotinamide adenine dinucleotide–dependent deacetylase, on MKP-1 remains unknown. Methods To address these issues, we used constitutional Sirt2 knockout (KO) mice, transgenic (TG) mice with increased expr

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Leal, Helena, João Cardoso, Patrícia Valério, et al. "SIRT2 Deficiency Exacerbates Hepatic Steatosis via a Putative Role of the ER Stress Pathway." International Journal of Molecular Sciences 23, no. 12 (2022): 6790. http://dx.doi.org/10.3390/ijms23126790.

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Nonalcoholic fatty liver disease (NAFLD), a condition strongly associated with obesity and insulin resistance, is characterized by hepatic lipid accumulation and activation of the endoplasmic reticulum (ER) stress response. The sirtuin 2 (SIRT2) protein deacetylase is emerging as a new player in metabolic homeostasis, but its role in the development of hepatic steatosis and its link with ER stress activation remains unknown. SIRT2-knockout (SIRT2-KO) and wild-type mice were fed either a control or a high-fat diet (HFD) for 4 weeks. Genetic manipulation of SIRT2 levels was performed in human he

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3

Li, Xingyu, Yimeng Du, Chunyuan Xue, et al. "SIRT2 Deficiency Aggravates Diet-Induced Nonalcoholic Fatty Liver Disease through Modulating Gut Microbiota and Metabolites." International Journal of Molecular Sciences 24, no. 10 (2023): 8970. http://dx.doi.org/10.3390/ijms24108970.

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Non-alcoholic fatty liver disease (NAFLD), characterized by excessive lipid accumulation in hepatocytes, is an increasing global healthcare burden. Sirtuin 2 (SIRT2) functions as a preventive molecule for NAFLD with incompletely clarified regulatory mechanisms. Metabolic changes and gut microbiota imbalance are critical to the pathogenesis of NAFLD. However, their association with SIRT2 in NAFLD progression is still unknown. Here, we report that SIRT2 knockout (KO) mice are susceptible to HFCS (high-fat/high-cholesterol/high-sucrose)-induced obesity and hepatic steatosis accompanied with an ag

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Sato, Teruki, Xiaoyan Yan, Hsiang-Chun Chang, Chen Chunlei, Jason S. Shapiro, and Hossein Ardehali. "Abstract 424: Loss of Sirt2 Protects Against Pressure Overload- and Ischemic Reperfusion Injury-induced Cardiac Dysfunction." Circulation Research 127, Suppl_1 (2020). http://dx.doi.org/10.1161/res.127.suppl_1.424.

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Introduction: Sirtuins are NAD+ dependent deacetylases and critical regulators of energy metabolism and response to oxidative stress. Sirtuin2 (SIRT2) is a cytoplasmic member of the sirtuin family, and has been shown to regulate cellular iron homeostasis through deacetylation of nuclear factor erythroid-derived 2-related factor 2 (NRF2). However, whether SIRT2-NRF2 pathway is involved in the development of heart failure remains unknown. Methods and results: To investigate the functional role of SIRT2 in the response to cardiac stress, SIRT2 knockout (KO) mice and their littermate controls were

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Dissertations / Theses on the topic "SIRT2-KO mice"

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Sarikhani, Mohsen. "Understanding the Role of SIRT2 in Cardiac Hypertrophy, Cell Death and Glucose Homeostasis." Thesis, 2018. https://etd.iisc.ac.in/handle/2005/5424.

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Over the last century the major causes of human deaths and ailments has shifted from acute infectious diseases to chronic aging related disorders like cancer and type-2 diabetes. The aging process is a universal property of most organisms, accompanied by a subtle, progressive, and often irreversible decline of physiological and reproductive functions resulting in an increased vulnerability to environmental challenge and a growing risk of disease and death. In molecular terms, it can be understood as a decline of the homeostatic mechanisms that ensure the function of cells, tissues, organs, and

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