TY - JOUR. T1 - Dissociation of diabetes and obesity in mice lacking orphan nuclear receptor small heterodimer partner. AU - Park, Young Joo. AU - Kim, Seong Chul. AU - Kim, Jeehee. AU - Anakk, Sayeepriyadarshini. AU - Lee, Jae Man. AU - Tseng, Hsiu Ting. AU - Yechoor, Vijay. AU - Park, Junchol. AU - Choi, June Seek. AU - Jang, Hak Chul. AU - Lee, Ki Up. AU - Novak, Colleen M.. AU - Moore, David D.. AU - Lee, Yoon Kwang. PY - 2011/12. Y1 - 2011/12. N2 - Mixed background SHP -/- mice are resistant to diet-induced obesity due to increased energy expenditure caused by enhanced PGC-1α expression in brown adipocytes. However, congenic SHP -/- mice on the C57BL/6 background showed normal expression of PGC-1α and other genes involved in brown adipose tissue thermogenesis. Thus, we reinvestigated the impact of small heterodimer partner (SHP) deletion on diet-induced obesity and insulin resistance using congenic SHP -/- mice. Compared with their C57BL/6 wild-type counterparts, SHP -/- mice subjected to ...

Background: Small heterodimer partner (SHP; NR0B2) is an atypical orphan nuclear receptor lacking DNA binding domain. SHP directly modulates the activities of other nuclear receptors and regulates a variety of cellular events such as cell differentiation, proliferation, and metabolism in various tissues. However, the role of SHP in heart has not yet been elucidated. Thus, in this study, we tried to investigate the functional roles of SHP in heart physiology and in the development of cardiac hypertrophy.. Methods and Results: We observed that SHP knock-out mice elicited cardiac hypertrophic features determined by heart weight to body weight or to tibia length ratios. Fetal genes, such as atrial natriuretic factor (ANF) or beta myosin heavy chain (βMHC) were significantly up-regulated in SHP knockout mice heart. In neonatal rat ventricular cardiomyocytes (NRVCs), phenylephrine (PE) reduced promoter activation of SHP and decreased protein level of SHP. Adenovirus-mediated over-expression of SHP ...

7 alpha-hydroxy-4-cholesten-3-one 12-alpha-hydroxylase7-alpha-hydroxy-4-cholesten-3-one 12-alpha-hydroxylase7-alpha-hydroxycholest-4-en-3-one 12-alpha-hydroxylaseCYPVIIIB1cytochrome P450 8B1cytochrome P450, subfamily VIIIB (sterol 12-alpha- ...

Small heterodimer partner interacting leucine zipper protein (SMILE) is an orphan nuclear receptor and a member of the bZIP family of proteins. We investigated the mechanism by which SMILE suppressed the development of inflammatory bowel disease (IBD) using a DSS-induced colitis mouse model and peripheral blood mononuclear cells (PBMCs) from patients with ulcerative colitis (UC). Metformin, an antidiabetic drug and an inducer of AMPK, upregulated the level of SMILE in human intestinal epithelial cells and the number of SMILE-expressing cells in colon tissues from DSS-induced colitis mice compared to control mice. Overexpression of SMILE using a DNA vector reduced the severity of DSS-induced colitis and colitis-associated intestinal fibrosis compared to mock vector. Furthermore, SMILE transgenic mice showed ameliorated DSS-induced colitis compared with wild-type mice. The mRNA levels of SMILE and Foxp3 were downregulated and SMILE expression was positively correlated with Foxp3 in PBMCs from patients

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FXR is expressed at high levels in the liver and intestine. Chenodeoxycholic acid and other bile acids are natural ligands for FXR. Similar to other nuclear receptors, when activated, FXR translocates to the cell nucleus, forms a dimer (in this case a heterodimer with RXR) and binds to hormone response elements on DNA, which up- or down-regulates the expression of certain genes.[6] One of the primary functions of FXR activation is the suppression of cholesterol 7 alpha-hydroxylase (CYP7A1), the rate-limiting enzyme in bile acid synthesis from cholesterol. FXR does not directly bind to the CYP7A1 promoter. Rather, FXR induces expression of small heterodimer partner (SHP), which then functions to inhibit transcription of the CYP7A1 gene. In this way, a negative feedback pathway is established in which synthesis of bile acids is inhibited when cellular levels are already high. FXR has also been found to be important in regulation of hepatic triglyceride levels.[7] Studies have also shown the FXR to ...

Endoplasmic reticulum (ER) stress is a common feature of Parkinsons disease (PD), and several PD-related genes are responsible for ER dysfunction. Recent studies suggested LRRK2-G2019S, a pathogenic mutation in the PD-associated gene LRRK2, cause ER dysfunction, and could thereby contribute to the development of PD. It remains unclear, however, how mutant LRRK2 influence ER stress to control cellular outcome. In this study, we identified the mechanism by which LRRK2-G2019S accelerates ER stress and cell death in astrocytes. To investigate changes in ER stress response genes, we treated LRRK2-wild type and LRRK2-G2019S astrocytes with tunicamycin, an ER stress-inducing agent, and performed gene expression profiling with microarrays. The XBP1 SUMOylation and PIAS1 ubiquitination were performed using immunoprecipitation assay. The effect of astrocyte to neuronal survival were assessed by astrocytes-neuron coculture and slice culture systems. To provide in vivo proof-of-concept of our approach, we measured

Sigma-Aldrich offers abstracts and full-text articles by [Janin Lehmann, Christina Seebode, Sabine Smolorz, Steffen Schubert, Steffen Emmert].

Creative-Proteomics offer cas 81-25-4 CHOLIC ACID (2,2,4,4-D4, 98%). We are specialized in manufacturing Stabel Isotope Labeled Analytical Standard products.

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SHP2兔多克隆抗体(ab10555)可与大鼠样本反应并经WB实验严格验证，被5篇文献引用并得到1个独立的用户反馈。所有产品均提供质保服务，中国75%以上现货。