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Brain and muscle Arnt-like protein-1 (BMAL1), a component of the molecular clock, regulates adipogenesis.
TLDR
Adenovirus-mediated expression of BMAL1 in 3T3-L1 adipocytes resulted in induction of several factors involved in lipogenesis and expression of these factors showed clear circadian rhythm in mice adipose tissue.
Characterization of the molecular clock in mouse peritoneal macrophages.
TLDR
The results obtained in this study indicate that the innate immunoreactions involving macrophages are at least partly regulated by the autonomous clock machinery.
Deficient of a Clock Gene, Brain and Muscle Arnt-Like Protein-1 (BMAL1), Induces Dyslipidemia and Ectopic Fat Formation
TLDR
BMAL1 is a crucial factor in the regulation of energy homeostasis, and disorders of the functions of BMAL1 lead to the development of metabolic syndrome.
EPAS1 Promotes Adipose Differentiation in 3T3-L1 Cells*
TLDR
The results suggest that EPAS1 plays several supporting roles in maintaining specific aspects of adipogenesis and adipocyte function including regulation of glucose uptake followed by lipid synthesis.
Occurrence and production of chloramines in the chlorination of creatinine in aqueous solution.
TLDR
Methylamine forms stable chloramines, which might be determined as mono- and/or di-chloramine fractions together with free chlorine by the DPD method in the reaction mixtures at higher molar ratios of chlorine.
Arylhydrocarbon receptor (AhR) is involved in negative regulation of adipose differentiation in 3T3-L1 cells: AhR inhibits adipose differentiation independently of dioxin.
TLDR
It is suggested that the arylhydrocarbon receptor is a negative regulator of adipose differentiation in 3T3 L1 cells.
Depletion of arylhydrocarbon receptor during adipose differentiation in 3T3-L1 cells.
TLDR
The results indicate that the depletion of AhR is a novel event associated with adipose differentiation in 3T3-L1 cells and that the magnitude of the depletion is sufficient for 3T 3-L 1 cells to lose the functional response to xenobiotics.
Aryl hydrocarbon receptor functions as a potent coactivator of E2F1-dependent trascription activity.
TLDR
The results in this study indicate the physiological function of AhR as a potent transcriptional coactivator of E2F1-dependent transcription and implicate the AhR-E2F 1 interaction as a part of the mechanism by which AhR/Arnt promotes cell proliferation.
DNA-strand breaks induced by dimethylarsinic acid, a metabolite of inorganic arsenics, are strongly enhanced by superoxide anion radicals.
TLDR
An experiment with UV-irradiation supported the possibility of DNA modification by DMAA exposure and indicated that O2- produced by paraquat in DMAA-exposed cells was more consumed than in non-exp exposed cells, assumingly through the reaction with the dimethylarsenic-modified region of DNA.
Transcriptional regulation of the AhR gene during adipose differentiation.
TLDR
The aryl hydrocarbon receptor protein is depleted during adipose differentiation, resulting in the loss of functional response to xenobiotics, and the mechanism by which the AhR is depleted is analyzed.
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