Search results for: ACOX2
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Effect of hyperoside on cervical cancer cells and transcriptome analysis of differentially expressed genes.Hyperoside (Hy) is a plant-derived quercetin 3-d-galactoside that exhibits inhibitory activities on various tumor types. The objective of the current study was to explore Hy effects on cervical cancer cell proliferation, and to perform a transcriptome analysis of differentially expressed genes.
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Hypoxia exacerbates nonalcoholic fatty liver disease via the HIF-2α/PPARα pathway.This study aimed to investigate whether hypoxia can affect nonalcoholic fatty liver disease (NAFLD) progression and the associated mechanisms, specifically regarding the hypoxia-inducible factor (HIF)-2α/peroxisome proliferator-activated receptor (PPAR)α pathway in vitro and in vivo. Recent studies have reported that, compared with HIF-1α, HIF-2α has different effects on lipid metabolism. We propose hypoxia may exacerbate NAFLD by the HIF-2α upregulation-induced suppression of PPARα in the liver. To verify this hypothesis, a steatotic human hepatocyte (L02) cell line treated with free fatty acids and a mouse model of NAFLD fed a high-fat diet were used. Steatotic hepatocytes were treated with hypoxia, HIF-2α siRNA, PPARα agonists, and inhibitors, respectively. Meanwhile, the NAFLD mice were exposed to intermittent hypoxia or intermittent hypoxia with PPARα agonists. The relative gene expression levels of HIF-1α, HIF-2α, mitochondrial function, fatty acid β-oxidation and lipogenesis were examined. Evidence of lipid accumulation was observed, which demonstrated that, compared with normal hepatocytes, steatotic hepatocytes exhibited higher sensitivity to hypoxia. This phenomenon was closely associated with HIF-2α. Moreover, lipid accumulation in hepatocytes was ameliorated by HIF-2α silencing or a PPARα agonist, despite the hypoxia treatment. HIF-2α overexpression under hypoxic conditions suppressed PPARα, leading to PGC-1α, NRF-1, ESRRα downregulation, and mitochondrial impairment. Additionally, β-oxidation genes such as CPT1α, CPT2α, ACOX1, and ACOX2 were downregulated and lipogenesis genes including LXRα, FAS, and SCD1 were upregulated by hypoxia. Therefore, we concluded that HIF-2α overexpression induced by hypoxia aggravated NAFLD progression by suppressing fatty acid β-oxidation and inducing lipogenesis in the liver via PPARα.
2772 related Products with: Hypoxia exacerbates nonalcoholic fatty liver disease via the HIF-2α/PPARα pathway.LIVER DISEASES TBA (Color LIVER DISEASES TBA (Color Multiple diseases of live Liver disease spectrum (h LIVER DISEASES Adenosine Liver disease spectrum ti ENZYMATIC ASSAY KITS (CH LIVER DISEASES 5' Nucleot LIVER DISEASES Total Bile LIVER DISEASES Total Bile Hepatic disease spectrum ENZYMATIC ASSAY KITS (CH
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Endometrial genome-wide DNA methylation patterns of Guanzhong dairy goats at days 5 and 15 of the gestation period.Uterine receptivity for the embryo is established and maintained through a series of precise cellular and molecular events, such as DNA methylation. There have been no studies to elucidate entire genome DNA methylation changes associated with embryo receptivity development of the endometrium (RE). In the present study, there was development of a complete genome-wide DNA methylome maps of the RE using whole-genome bisulphite sequencing and bioinformatics analysis. As many as 163.06 Gb of sequencing data averaging 81.53 Gb per sample were obtained for genome bisulphite sequencing of endometrium samples. There were distinct genome-wide DNA methylation patterns in pre-receptive endometrium (PE; Day 5 of gestation) and RE (Day 15 of gestation). There were as many as 16,467 differentially methylated regions (DMRs); 21,391 DMRs were less methylated in RE samples compared with PE samples (P-values ≤ 0.05 and |log2 (fold change)| ≥ 2). Compared with PE samples, methylation ratios of IGF2BP2, ACOX2, PTGDS, VEGFB and PTGDR2 genes were markedly less in RE samples (P-value ≤ 0.05 and |log2 (fold change)| ≥ 2). Conversely, in RE samples there was a markedly greater methylation ratio of IGFBP3 and IGF1R genes. The results of KEGG analysis indicated that these genes were involved in the signalling pathways for insulin, mitogen-activated protein kinase, gonadotropin-releasing hormone, vascular endothelial growth factor and progesterone-mediated oocyte maturation, which participated in differential regulation of goat endometrial development during receptive and prereceptive phases. The results of previous and the present study indicate resulting proteins of IGF2BP2, PTGDS, VEGFB, PGR, IGFBP3 and IGF1R gene expression may have important functions in regulating endometrial receptivity for the embryo.
1080 related Products with: Endometrial genome-wide DNA methylation patterns of Guanzhong dairy goats at days 5 and 15 of the gestation period.Attractin (ATRN), Human A Andrographolide C20H30O5 Recombinant E. coli HSP70 Protease, DNASE free hea Attractin (ATRN), Human Atropine sulfate monohydr Recombinant Human DNase P (3S,5S)-Atorvastatin Sodi Attractin (ATRN), Human A 5HT1A, WB control Protease, DNASE free heat ∆1-Androstene-3β,17β-
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[Glucagon-like peptide-1 regulates lipid metabolism in hepatocytes through Foxo1/3].Glucagon-like peptide-1 (GLP-1) has been reported to be effective in the treatment of nonalcoholic fatty liver disease (NAFLD). However, the molecular mechanism of GLP-1 on NAFLD is remained unclear. The present study was to detect whether the effect of GLP-1 on triglyceride (TG) content in hepatocytes is dependent on Foxos. HepG2 cells were treated with palmitic/oleic acid for 24 h. The knockdown of Foxo1, Foxo3 was conducted through small interfering RNA (siRNA). Real time PCT (RT-PCR) was used to detect the changes of the SREBP1c and Aco genes in HepG2 cells after Foxo1/3 knockdown. As expected, palmitic/oleic acid increased TG concentration in HepG2 cells [(12.65 ± 1.32) μg/mg vs. (4.32±0.54) μg/mg, 0.05]. Addition of GLP-1 dose (10, 50, 100nmol/L) dependently lowered the TG content and reached plateau at 100 nmol/L of GLP-1 [TG(8.38±1.47) μg/mg]. The GLP-1 effect on TG remained after knocking down either Foxo1 [(9.09±1.34)μg/mg] or Foxo3 [(8.90±1.60) μg/mg] alone, but not when knocking down Foxo1 and Foxo3 (Foxo1/3) together [(14.66±1.77)μg/mg]. Moreover, knocking down Foxo1/3 also abolished GLP-1 effect on SREBP1c and Aco expression. GLP-1 can inhibit the synthesis of TG in hepatocytes depending on Foxo1 and Foxo3. Further studies are needed to explore the specific mechanisms.
1922 related Products with: [Glucagon-like peptide-1 regulates lipid metabolism in hepatocytes through Foxo1/3].Polyclonal Antibody Recep GLP 1 ELISA Kit, Rat Gluc Glucagon ELISA KIT, Rat G Trypsin EDTA (1 250) UV i Rabbit Anti-Integrin β2 ILP-2 Blocking Peptide;Ap superSf9-3 insect cells Anti-human C-peptide Anti Rabbit Anti-Integrin beta Hsp105 Blocking Peptide;A Rabbit Anti-G protein alp Rabbit Anti-Integrin alph
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and Are Affected by Stretch in HL-1 Atrial Myocytes.Lipid expression is increased in the atrial myocytes of mitral regurgitation (MR) patients. This study aimed to investigate key regulatory genes and mechanisms of atrial lipotoxic myopathy in MR.
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Loss of Enzymes in the Bile Acid Synthesis Pathway Explains Differences in Bile Composition among Mammals.Bile acids are important for absorbing nutrients. Most mammals produce cholic and chenodeoxycholic bile acids. Here, we investigated genes in the bile acid synthesis pathway in four mammals that deviate from the usual mammalian bile composition. First, we show that naked-mole rats, elephants, and manatees repeatedly inactivated CYP8B1, an enzyme uniquely required for cholic acid synthesis, which explains the absence of cholic acid in these species. Second, no gene-inactivating mutations were found in any pathway gene in the rhinoceros, a species that lacks bile acids, indicating an evolutionarily recent change in its bile composition. Third, elephants and/or manatees that also lack bile acids altogether have lost additional nonessential enzymes (SLC27A5, ACOX2). Apart from uncovering genomic differences explaining deviations in bile composition, our analysis of bile acid enzymes in bile acid-lacking species suggests that essentiality prevents gene loss, while loss of pleiotropic genes is permitted if their other functions are compensated by functionally related proteins.
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Combined effects of (E404D) and (R409H) cause metabolic defects in primary cardiac malignant tumor.Primary malignant cardiac tumors (PMCTs) are extremely rare. The apparent immunity of the heart to invasive cancer has attracted considerable interest given the continuously rising incidence of cancer in other organs. This study aims to determine the conditions that could result in cardiac carcinoma and expand our understanding of cardiac tumor occurrence. We report two cases: a male (Patient-1) with primary cardiac malignant fibrous histiocytoma (MFH) and a female (Patient-2) with primary cardiac angiosarcoma. Merged genome-wide analyses of aCGH, Exome sequencing, and RNA-sequencing were performed on Patient-1 using peripheral blood, carcinoma tissue, and samples of adjacent normal tissue. Only whole-transcriptome analysis was carried out on Patient-2, due to insufficient quantities of sample from Patient-2. We identified a novel inherited loss of functional mutation of (Glu404Asp), a recurrent somatic hotspot mutation of (His1047Arg) and a somatic duplication in copy number of . (E404D) severely compromised FH enzyme activity and lead to decreased protein expression in cardiac tumor tissues. We previously reported a functional mutation (R409H), which is potentially associated with decreased β-oxidation of fatty acids in the cardiac tumor tissue. Results of transcriptome analyses on two patients further revealed that the RNA expression of genes in the TCA cycle and beta-oxidation were uniformly downregulated. In this study, combined effects of (E404D) and (R409H) on metabolic switch from fatty acids to glucose were remarkably distinct, which might be an essential precondition to trigger the occurrence of PMCTs and mimic the Warburg effect, a hallmark of cancer metabolism.
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Experimental Nonalcoholic Steatohepatitis and Liver Fibrosis Are Ameliorated by Pharmacologic Activation of Nrf2 (NF-E2 p45-Related Factor 2).Nonalcoholic steatohepatitis (NASH) is associated with oxidative stress. We surmised that pharmacologic activation of NF-E2 p45-related factor 2 (Nrf2) using the acetylenic tricyclic bis(cyano enone) TBE-31 would suppress NASH because Nrf2 is a transcriptional master regulator of intracellular redox homeostasis.
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Organelle-Derived Acetyl-CoA Promotes Prostate Cancer Cell Survival, Migration, and Metastasis via Activation of Calmodulin Kinase II.Although emerging evidence suggests a potential role of calcium/calmodulin-dependent kinase II (CaMKII) in prostate cancer, its role in prostate cancer tumorigenesis is largely unknown. Here, we examine whether the acetyl CoA-CaMKII pathway, first described in frog oocytes, promotes prostate cancer tumorigenesis. In human prostate cancer specimens, metastatic prostate cancer expressed higher levels of active CaMKII compared with localized prostate cancer. Correspondingly, basal CaMKII activity was significantly higher in the more tumorigenic PC3 and PC3-mm2 cells relative to the less tumorigenic LNCaP and C4-2B4 cells. Deletion of CaMKII by CRISPR/Cas9 in PC3-mm2 cells abrogated cell survival under low-serum conditions, anchorage-independent growth and cell migration; overexpression of constitutively active CaMKII in C4-2B4 cells promoted these phenotypes. In an animal model of prostate cancer metastasis, genetic ablation of CaMKII reduced PC3-mm2 cell metastasis from the prostate to the lymph nodes. Knockdown of the acetyl-CoA transporter carnitine acetyltransferase abolished CaMKII activation, providing evidence that acetyl-CoA generated from organelles is a major activator of CaMKII. Genetic deletion of the β-oxidation rate-limiting enzyme ACOX family proteins decreased CaMKII activation, whereas overexpression of ACOXI increased CaMKII activation. Overall, our studies identify active CaMKII as a novel connection between organelle β-oxidation and acetyl-CoA transport with cell survival, migration, and prostate cancer metastasis. This study identifies a cell metabolic pathway that promotes prostate cancer metastasis and suggests prostate cancer may be susceptible to β-oxidation inhibitors. .
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