It is well known that protein kinase C (PKC) shows different translocation depending on subtype and stimulation, contributing to the physiological importance of the enzyme. However, molecular mechanism causing the different translocation has been unknown. Therefore, using GFP-tagged mutant εPKC, we attempted to identify the intramolecular domains required for saturated fatty acid-induced translocation of εPKC to the plasma membrane, and compared with those necessary for unsaturated fatty acid-induced translocation to the Golgi complex. We found that, unlike in the case of unsaturated fatty-acid induced translocation, both C1B domain and pseudosubstrate region are necessary for the saturated fatty acid-induced translocation of εPKC to the plasma membrane. The results suggest that different domains of PKC mediate distinct translocation depending on different stimulations, contributing to their subtype- and stimulation-specific functions.
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http://dx.doi.org/10.1016/j.bbrc.2013.01.048 | DOI Listing |
J Med Food
December 2024
Department of Food Science and Biotechnology, Andong National University, Andong, Korea.
In this study, two high-content flavonoid derivatives [3-8 biapigenin (HM 104) and quercetin-3--β--galactopyranoside (HM 111)] were obtained through the bioactivity-guided isolation of antidiabetic compounds from flowers. HM 104 and HM 111 exhibited good glucose consumption in fatty acid-induced insulin-resistant HepG2 cells. Moreover, both active compounds enhanced glucose uptake by restoring the expression of key regulators of glucose metabolism, including insulin receptor substrate 1, phosphoinositide 3-kinase, protein kinase B, and glucose transporter type 4, and by mitigating the expression of forkhead box O1 and the factors involved in gluconeogenesis.
View Article and Find Full Text PDFJ Appl Microbiol
December 2024
Centro de Excelencia en Productos y Procesos de Córdoba-CEPROCOR- Complejo Hospitalario, Santa María de Punilla, X6154 Córdoba, Argentina.
Aims: Thecaphora frezzii, the causal agent of peanut smut, causes significant grain losses in Argentina. Current control strategies are insufficient to manage this pathogen. We investigate the effect of antioxidants on the in vitro development of T.
View Article and Find Full Text PDFBiochem Biophys Res Commun
January 2025
Department of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, 226014, Lucknow, India. Electronic address:
Lipotoxicity is a key pathological feature in the development of non-alcoholic steatohepatitis (NASH), which is characterized by liver injury, inflammation, and fibrosis. Although lipotoxicity has been shown to induce transcriptomic alterations in liver cells, the specific role of epigenetic regulators in NASH remains elusive. In this study, we demonstrate that pharmacological inhibition of histone methyltransferase G9a significantly worsens NASH progression in mice, as evidenced by increased hepatic cell death, inflammation, and fibrosis.
View Article and Find Full Text PDFTissue Eng Regen Med
December 2024
Department of Biological Science, College of Natural Sciences, Chosun University, 309 Pilmun-Daero, Dong-Gu, Gwangju, 501-759, Korea.
Background: Non-alcoholic fatty liver disease (NAFLD) is a pathological condition that increase the risk of simple steatosis to hepatocellular carcinoma. This study aimed to investigate the biological effects of camphorquinone (CQ) in a high-fat diet (HFD)-fed and low dose streptozotocin (STZ)-induced mouse model, widely used to mimic the concurrent development of NAFLD pathological conditions in vivo, and a free fatty acid-induced hepatic steatosis cell model in vitro.
Methods: CQ (10 or 30 mg/kg/day; i.
World J Gastrointest Oncol
December 2024
Department of Gastroenterology, Ningbo Medical Center Lihuili Hospital, Ningbo 315000, Zhejiang Province, China.
Background: Non-alcoholic fatty liver disease (NAFLD), which is a significant liver condition associated with metabolic syndrome, is the leading cause of liver diseases globally and its prevalence is on the rise in most nations. The protective impact of vitamin D on NAFLD and its specific mechanism remains unclear.
Aim: To examine the role of vitamin D in NAFLD and how vitamin D affects the polarization of hepatic macrophages in NAFLD through the vitamin D receptor (VDR)-peroxisome proliferator activated receptor (PPAR)γ pathway.
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