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https://www.readbyqxmd.com/read/27906079/muscle-specific-loss-of-bmal1-leads-to-disrupted-tissue-glucose-metabolism-and-systemic-glucose-homeostasis
#1
Brianna D Harfmann, Elizabeth A Schroder, Maureen T Kachman, Brian A Hodge, Xiping Zhang, Karyn A Esser
BACKGROUND: Diabetes is the seventh leading cause of death in the USA, and disruption of circadian rhythms is gaining recognition as a contributing factor to disease prevalence. This disease is characterized by hyperglycemia and glucose intolerance and symptoms caused by failure to produce and/or respond to insulin. The skeletal muscle is a key insulin-sensitive metabolic tissue, taking up ~80 % of postprandial glucose. To address the role of the skeletal muscle molecular clock to insulin sensitivity and glucose tolerance, we generated an inducible skeletal muscle-specific Bmal1 (-/-) mouse (iMSBmal1 (-/-))...
March 30, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27898346/amp-kinase-promotes-bcl6-expression-in-both-mouse-and-human-t-cells
#2
Markus M Xie, Tohti Amet, Hong Liu, Qigui Yu, Alexander L Dent
The transcription factor Bcl6 is a master regulator of follicular helper T (TFH) cells, and understanding the signaling pathway that induces Bcl6 and TFH cell differentiation is therefore critical. IL-2 produced during T cell activation inhibits Bcl6 expression but how TFH cells evade IL-2 inhibition is not completely understood. Here we show that Bcl6 is highly up-regulated in activated CD4 T cells following glucose deprivation (GD), and this pathway is insensitive to inhibition by IL-2. Similar to GD, the glucose analog 2-deoxyglucose (2DG) inhibits glycolysis, and 2DG induced Bcl6 expression in activated CD4 T cells...
November 26, 2016: Molecular Immunology
https://www.readbyqxmd.com/read/27878239/aicar-induces-mitochondrial-apoptosis-in-human-osteosarcoma-cells-through-an-ampk-dependent-pathway
#3
Masayuki Morishita, Teruya Kawamoto, Hitomi Hara, Yasuo Onishi, Takeshi Ueha, Masaya Minoda, Etsuko Katayama, Toshiyuki Takemori, Naomasa Fukase, Masahiro Kurosaka, Ryosuke Kuroda, Toshihiro Akisue
The AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) modulates cellular energy metabolism, and promotes mitochondrial proliferation and apoptosis. Previous studies have shown that AICAR has anticancer effects in various cancers, however the roles of AMPK and/or the effects of AICAR on osteosarcoma have not been reported. In the present study, we evaluated the effects of AICAR on tumor growth and mitochondrial apoptosis in human osteosarcoma both in vitro and in vivo...
November 21, 2016: International Journal of Oncology
https://www.readbyqxmd.com/read/27847321/aicar-activates-er-stress-dependent-apoptosis-in-gallbladder-cancer-cells
#4
Jifeng Nie, Aidong Liu, Qunya Tan, Kai Zhao, Kui Hu, Yong Li, Bin Yan, Lin Zhou
AICAR (5-Aminoimidazole-4-carboxamide riboside or acadesine) is an AMP-activated protein kinase (AMPK) agonist, its activity in human gallbladder cancer cells was evaluated here. We show that AICAR provoked significant apoptosis in human gallbladder cancer cell lines (Mz-ChA-1, QBC939 and GBC-SD) and primary gallbladder cancer cells. AICAR-induced cytotoxicity in gallbladder cancer cells appears independent of AMPK activation. Inhibition of AMPK, via AMPKα shRNA knockdown or dominant negative mutation (T172A), failed to rescue GBC-SD cells from AICAR...
November 12, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27826658/a-tbc1d1-ser231ala-knockin-mutation-partially-impairs-aicar-but-not-exercise-induced-muscle-glucose-uptake-in-mice
#5
Qiaoli Chen, Bingxian Xie, Sangsang Zhu, Ping Rong, Yang Sheng, Serge Ducommun, Liang Chen, Chao Quan, Min Li, Kei Sakamoto, Carol MacKintosh, Shuai Chen, Hong Yu Wang
AIMS/HYPOTHESIS: TBC1D1 (tre-2/USP6, BUB2, cdc16 domain family member 1) is a Rab GTPase-activating protein (RabGAP) that has been implicated in regulating GLUT4 trafficking. TBC1D1 can be phosphorylated by the AMP-activated protein kinase (AMPK) on Ser(231), which consequently interacts with 14-3-3 proteins. Given the key role for AMPK in regulating insulin-independent muscle glucose uptake, we hypothesised that TBC1D1-Ser(231) phosphorylation and/or 14-3-3 binding may mediate AMPK-governed glucose homeostasis...
November 8, 2016: Diabetologia
https://www.readbyqxmd.com/read/27809464/hat-inhibitors-antagonize-ampk-in-postmortem-glycolysis
#6
Qiong Li, Zhongwen Li, Aihua Lou, Zhenyu Wang, Dequan Zhang, Qingwu Shen
Objective: The purpose of this study was to investigate the influence of AMP-activated protein kinase (AMPK) activation on protein acetylation and glycolysis in postmortem muscle to better understand the mechanism by which AMPK regulates postmortem glycolysis and meat quality. Methods: A total of 32 mice were randomly assigned to four groups and intraperitoneally injected with 5-Aminoimidazole-4-carboxamide1-β-D-ribofuranoside (AICAR, a specific activator of AMPK), AICAR and histone acetyltransferase inhibitor II, or AICAR, Trichostatin A (TSA, an inhibitor of histone deacetylase I and II) and Nicotinamide (NAM, an inhibitor of the Sirt family deacetylases)...
October 28, 2016: Asian-Australasian Journal of Animal Sciences
https://www.readbyqxmd.com/read/27798331/glycine-regulates-protein-turnover-by-activating-akt-mtor-and-by-inhibiting-murf1-and-atrogin-1-gene-expression-in-c2c12-myoblasts
#7
KaiJi Sun, Zhenlong Wu, Yun Ji, Guoyao Wu
BACKGROUND: The regulation of protein turnover in skeletal muscle is essential for the maintenance of integrity, growth, and function of this tissue. We recently reported that glycine enhances skeletal muscle growth in young pigs. However, the underlying mechanisms remain unknown. OBJECTIVE: This study was conducted with a mouse myoblast cell line, C2C12, to test the hypothesis that glycine activates protein kinase B/mammalian target of rapamycin (Akt/mTOR), as well as inhibits 5'-adenosine monophosphate-activated protein kinase (AMPK) and the expression of genes for proteolysis...
October 26, 2016: Journal of Nutrition
https://www.readbyqxmd.com/read/27797909/enhanced-muscle-insulin-sensitivity-after-contraction-exercise-is-mediated-by-ampk
#8
Rasmus Kjøbsted, Nanna Munk-Hansen, Jesper B Birk, Marc Foretz, Benoit Viollet, Marie Björnholm, Juleen R Zierath, Jonas T Treebak, Jørgen F P Wojtaszewski
Earlier studies have demonstrated that muscle insulin sensitivity to stimulate glucose uptake is enhanced several hours after an acute bout of exercise. Using 5-aminoimidazole-4-carboxamide-ribonucleotide (AICAR), we recently demonstrated that prior activation of AMPK is sufficient to increase insulin sensitivity in mouse skeletal muscle. Here we aimed to determine whether activation of AMPK is also a prerequisite for the ability of muscle contraction to increase insulin sensitivity. We found that prior in situ contraction of m...
October 26, 2016: Diabetes
https://www.readbyqxmd.com/read/27792760/ampk-activation-prevents-and-reverses-drug-induced-mitochondrial-and-hepatocyte-injury-by-promoting-mitochondrial-fusion-and-function
#9
Sun Woo Sophie Kang, Ghada Haydar, Caitlin Taniane, Geoffrey Farrell, Irwin M Arias, Jennifer Lippincott-Schwartz, Dong Fu
Mitochondrial damage is the major factor underlying drug-induced liver disease but whether conditions that thwart mitochondrial injury can prevent or reverse drug-induced liver damage is unclear. A key molecule regulating mitochondria quality control is AMP activated kinase (AMPK). When activated, AMPK causes mitochondria to elongate/fuse and proliferate, with mitochondria now producing more ATP and less reactive oxygen species. Autophagy is also triggered, a process capable of removing damaged/defective mitochondria...
2016: PloS One
https://www.readbyqxmd.com/read/27783307/therapeutic-effects-of-aicar-and-dox-conjugated-multifunctional-nanoparticles-in-sensitization-and-elimination-of-cancer-cells-via-survivin-targeting
#10
Cenk Daglioglu, Burcu Okutucu
PURPOSE: Resistance to chemotherapy is one of the major problems facing current cancer research. Enhancing tumor cell response to anticancer agents increases chemotherapeutic effectiveness. We have recently addressed this issue and reported on producing multifunctional nanoparticles (Fe3O4@SiO2(FITC)-FA/AICAR/DOX) aiming to overcome chemoresistance with synergetic effect of AICAR and DOX. In the present study, we demonstrated that these nanoparticles not only show enhanced cellular uptake and cytotoxic effect but can also show enhanced pro-apoptotic and anti-proliferative effects in five different tumor-derived cell lines (A549, HCT-116, HeLa, Jurkat and MIA PaCa-2)...
October 25, 2016: Pharmaceutical Research
https://www.readbyqxmd.com/read/27751888/signaling-involved-in-ptth-stimulated-4e-bp-phosphorylation-in-prothoracic-gland-cells-of-bombyx-mori
#11
Shi-Hong Gu, Yun-Chih Hsieh, Pei-Ling Lin
Our previous studies showed that adenosine 5'-monophosphate-activated protein kinase (AMPK)/the target of rapamycin (TOR) signaling is involved in prothoracicotropic hormone (PTTH)-stimulated ecdysteroidogenesis in Bombyx mori prothoracic glands (PGs). In the present study, we further investigated the signaling involved in PTTH-stimulated phosphorylation of 4E-BP. We found that 4E-BP phosphorylation stimulated by PTTH was partially reduced in Ca(2+)-free medium, indicating the involvement of Ca(2+). In addition, we found that a potent and specific inhibitor of phospholipase C (PLC), U73122, greatly inhibited 4E-BP phosphorylation...
October 14, 2016: Journal of Insect Physiology
https://www.readbyqxmd.com/read/27751863/impact-of-genetic-variants-of-atp-binding-cassette-b1-aicar-transformylase-imp-cyclohydrolase-folyl-polyglutamatesynthetase-and-methylenetetrahydrofolatereductase-on-methotrexate-toxicity
#12
Luis Sala-Icardo, Amalia Lamana, Ana María Ortiz, Elena García Lorenzo, Pablo Moreno Fresneda, Rosario García-Vicuña, Isidoro González-Álvaro
OBJECTIVE: To analyze the effect of single nucleotide polymorphisms (SNPs) with well-known functional impact of methylenetetrahydrofolatereductase (MTHFR; rs1801131 and rs1801133), the membrane transporter ABCB1 (rs1045642), the AICAR transformylase/IMP cyclohydrolase (ATIC; rs2372536) and folyl-polyglutamatesynthetase (FPGS; rs1544105), on liver and bone marrow toxicity of methotrexate (MTX). PATIENTS AND METHODS: We analyzed 1415 visits from 350 patients of the PEARL (Princesa Early Arthritis Register Longitudinal) study: (732 with MTX, 683 without MTX)...
October 14, 2016: Reumatología Clinica
https://www.readbyqxmd.com/read/27751856/ampk-activation-by-gsk621-inhibits-human-melanoma-cells-in-vitro-and-in-vivo
#13
Lezi Chen, Quan Chen, Guosan Deng, Wenbin Xie, Jihong Lian, Mian Wang, Huilan Zhu
Recent studies suggest that forced activation of AMP-activated protein kinase (AMPK) could inhibit melanoma cell proliferation. In this report, we evaluated the anti-melanoma cell activity by a novel small-molecular AMPK activator, GSK621. Treatment of GSK621 decreased survival and proliferation of human melanoma cells (A375, WM-115 and SK-Mel-2 lines), which was accompanied by activation of caspase-3/-9 and apoptosis. Reversely, caspase inhibitors attenuated GSK621-induced cytotoxicity against melanoma cells...
October 14, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27733682/activation-of-amp-activated-protein-kinase-by-metformin-induces-protein-acetylation-in-prostate-and-ovarian-cancer-cells
#14
Luciano Galdieri, Himavanth Gatla, Ivana Vancurova, Ales Vancura
AMP-activated protein kinase (AMPK) is an energy sensor and master regulator of metabolism. AMPK functions as a fuel gauge monitoring systemic and cellular energy status. Activation of AMPK occurs when the intracellular AMP/ATP ratio increases and leads to a metabolic switch from anabolism to catabolism. AMPK phosphorylates and inhibits acetyl-CoA carboxylase (ACC), which catalyzes carboxylation of acetyl-CoA to malonyl-CoA, the first and rate-limiting reaction in de novo synthesis of fatty acids. AMPK thus regulates homeostasis of acetyl-CoA, a key metabolite at the crossroads of metabolism, signaling, chromatin structure, and transcription...
November 25, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27707786/chemo-genetic-interactions-between-histone-modification-and-the-anti-proliferation-drug-aicar-are-conserved-in-yeast-and-humans
#15
Delphine Albrecht, Johanna Ceschin, Jim Dompierre, Florian Gueniot, Benoît Pinson, Bertrand Daignan-Fornier
Identifying synthetic lethal interactions has emerged as a promising new therapeutic approach aimed at targeting cancer cells directly. Here, we used the yeast Saccharomyces cerevisiae as a simple eukaryotic model to screen for mutations resulting in a synthetic lethality with 5-Amino-4-Imidazole CarboxAmide Ribonucleoside (AICAR) treatment. Indeed, AICAR has been reported to inhibit the proliferation of multiple cancer cell lines. Here, we found that loss of several histone-modifying enzymes, including Bre1 (histone H2B ubiquitination) and Set1 (histone H3 lysine 4 methylation), greatly enhanced AICAR inhibition on growth via combined-effects of both the drug and the mutations on G1 cyclins...
October 5, 2016: Genetics
https://www.readbyqxmd.com/read/27706018/controls-of-nuclear-factor-kappa-b-signaling-activity-by-5-amp-activated-protein-kinase-activation-with-examples-in-human-bladder-cancer-cells
#16
Bo-Hwa Choi, Da-Hyun Lee, Jin Kim, Ju-Hee Kang, Chang-Shin Park
Generally, both lipopolysaccharide (LPS)- and hypoxia-induced nuclear factor kappa B (NF-κB) effects are alleviated through differential posttranslational modification of NF-κB phosphorylation after pretreatment with 5´-AMP-activated protein kinase (AMPK) activators such as 5´-aminoimidazole-4-carboxamide ribonucleotide (AICAR) or the hypoglycemic agent metformin. We found that AICAR or metformin acts as a regulator of LPS/NF-κB-or hypoxia/NF-κB-mediated cyclooxygenase induction by an AMPK-dependent mechanism with interactions between p65-NF-κB phosphorylation and acetylation, including in a human bladder cancer cell line (T24)...
September 2016: International Neurourology Journal
https://www.readbyqxmd.com/read/27688165/upregulation-of-sirt1-ampk-by-thymoquinone-in-hepatic-stellate-cells-ameliorates-liver-injury
#17
Yong Yang, Ting Bai, You-Li Yao, De-Quan Zhang, Yan-Ling Wu, Li-Hua Lian, Ji-Xing Nan
Thymoquinone (TQ) is a biologically active compound isolated from the seeds of Nigella sativa L. (Ranuculaceae). This study investigated the hepato-protective effect of TQ on liver injury through AMP-activated protein kinase (AMPK) signaling in hepatic stellate cells (HSCs). In vitro, TGF-β time-dependently attenuated liver kinase B-1 (LKB1) and AMPK phosphorylation, which were blocked by pretreatment with TQ and AICAR (an activator of AMPK). TQ significantly inhibited collagen-Ι, α-SMA, TIMP-1 and enhanced MMP-13 expression, contributing to prevent TGF-β-induced human HSCs activation...
November 16, 2016: Toxicology Letters
https://www.readbyqxmd.com/read/27688041/orphan-nuclear-receptor-shp-regulates-iron-metabolism-through-inhibition-of-bmp6-mediated-hepcidin-expression
#18
Don-Kyu Kim, Yong-Hoon Kim, Yoon Seok Jung, Ki-Sun Kim, Jae-Ho Jeong, Yong-Soo Lee, Jae-Min Yuk, Byung-Chul Oh, Hyon E Choy, Steven Dooley, Martina U Muckenthaler, Chul-Ho Lee, Hueng-Sik Choi
Small heterodimer partner (SHP) is a transcriptional corepressor regulating diverse metabolic processes. Here, we show that SHP acts as an intrinsic negative regulator of iron homeostasis. SHP-deficient mice maintained on a high-iron diet showed increased serum hepcidin levels, decreased expression of the iron exporter ferroportin as well as iron accumulation compared to WT mice. Conversely, overexpression of either SHP or AMP-activated protein kinase (AMPK), a metabolic sensor inducing SHP expression, suppressed BMP6-induced hepcidin expression...
September 30, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27641099/ampk-%C3%AE-ketoglutarate-axis-dynamically-mediates-dna-demethylation-in-the-prdm16-promoter-and-brown-adipogenesis
#19
Qiyuan Yang, Xingwei Liang, Xiaofei Sun, Lupei Zhang, Xing Fu, Carl J Rogers, Anna Berim, Shuming Zhang, Songbo Wang, Bo Wang, Marc Foretz, Benoit Viollet, David R Gang, Buel D Rodgers, Mei-Jun Zhu, Min Du
Promoting brown adipose tissue (BAT) development is an attractive strategy for the treatment of obesity, as activated BAT dissipates energy through thermogenesis; however, the mechanisms controlling BAT formation are not fully understood. We hypothesized that as a master regulator of energy metabolism, AMP-activated protein kinase (AMPK) may play a direct role in the process and found that AMPKα1 (PRKAA1) ablation reduced Prdm16 expression and impaired BAT development. During early brown adipogenesis, the cellular levels of α-ketoglutarate (αKG), a key metabolite required for TET-mediated DNA demethylation, were profoundly increased and required for active DNA demethylation of the Prdm16 promoter...
October 11, 2016: Cell Metabolism
https://www.readbyqxmd.com/read/27638620/ampkalpha2-regulates-bladder-cancer-growth-through-skp2-mediated-degradation-of-p27
#20
Stavros Kopsiaftis, Katie L Sullivan, Isha Garg, John A Taylor, Kevin P Claffey
: AMP-activated protein kinase (AMPK) is the central metabolic regulator of the cell and controls energy consumption based upon nutrient availability. Due to its role in energy regulation, AMPK has been implicated as a barrier for cancer progression and is suppressed in multiple cancers. To examine whether AMPK regulates bladder cancer cell growth, HTB2 and HT1376 bladder cells were treated with an AMPK activator, AICAR. AICAR treatment reduced proliferation and induced the expression of p27Kip1 (CDKN1B), which was mediated through an mTOR-dependent mechanism...
September 16, 2016: Molecular Cancer Research: MCR
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