SCI杂志PPAR Research (IF: 2.93)特刊PPARs and Their Coactivators in Obesity and Metabolic Disease 约稿啦！ 本人和美国团队受邀作为special issue编辑开一期特刊。 杂志这几年影响因子稳步上升，今年很可能过3分！PPAR及其辅激活蛋白在代谢相关疾病，包括肿瘤中的机制和治疗均可！ http://www.hindawi.com/journals/PPAR/si/812927/cfp/ 欢迎投稿！欢迎转发！ PPARs and Their Coactivators in Obesity and Metabolic Disease Call for Papers Peroxisome proliferator-activated receptors (PPARs) are a subfamily of ligand-inducible nuclear hormone receptors including PPARα (NR1C1), PPARβ/δ (NR1C2), and PPARγ (NR1C3), which have distinct tissue distribution and specific functions in response to their agonists. PPARs have been recognized as master regulators of a number of physiological processes in multiple organs and cell types, participating in cellular differentiation, development, carbohydrate and lipid metabolism, energy homeostasis, tumorigenesis, and inflammation. Given that PPARs are known to play central functions in metabolic homeostasis, highly effective PPAR agonists have been developed and are widely used for the treatment of chronic metabolic diseases. Upon specific ligand-binding, PPARs heterodimerize with the retinoid X receptor (RXR) and bind to the peroxisome proliferator responsive element (PPRE) on target genes. Importantly, the transcriptional activation of specific target genes set in motion by liganded PPARs is also determined by a number of coactivators that partner with PPARs in a tissue- and cell type-specific manner. Three major categories of PPAR coactivators have been identified: (1) those with chromatin remodeling effects, such as those carrying histone acetyltransferase (HAT) or methyltransferase activity (i.e., members of the p160/SRC family); (2) anchoring coactivators, which serve as linkers between cofactor complexes and the basal transcriptional machinery (i.e., members of the mediator complex); (3) coactivators without intrinsic enzymatic activity which function by providing a scaffold to aggregate large transcriptional complexes on tissue specific target genes: these cofactors include PGC1 family members among others. These coactivators have also been shown to be recruited in response to ligand/agonist activation to a number of nuclear receptors and transcriptional factors in addition to PPARs. As one of the most serious public health problems of the 21st century, obesity is mainly caused by the combination of excessive caloric intake, sedentary lifestyle, and genetic susceptibility. Obesity is the leading risk factor for many physical disorders commonly known as the metabolic disease/syndrome which includes but is not limited to type 2 diabetes, hypertension, hyperlipidemia, cardiovascular diseases, hepatic steatosis, and certain types of cancer ultimately reducing life expectancy. Thus, understanding the molecular basis of PPARs and coactivator functions in controlling the expression of selective gene programs may be helpful for the development of possible strategies to prevent/treat obesity and metabolic comorbidities. We invite investigators to submit original research articles and review articles that aim to increase our knowledge on the molecular basis of the effects of PPARs and of cofactors on metabolism and on energy homeostasis, in a PPAR dependent or independent manner. Studies describing strategies targeting PPARs and cofactors to prevent/treat obesity and metabolic diseases are also highly welcomed. Potential topics include but are not limited to the following: Role of PPARs and cofactors (a) in energy homeostasis and metabolic disease, including obesity, type 2 diabetes, hypertension, hyperlipidemia, cardiovascular diseases, hepatic steatosis, and chronic inflammation; (b) in certain types of cancer and aging-related diseases; (c) in adipocyte biology Role of noncoding RNAs in the regulation of PPARs and cofactors in homeostasis and metabolic disease Epigenetic modifications of PPARs and cofactors affecting homeostasis and metabolic disease Mechanisms of preferential recruitment of cofactors to PPARs to specify lipid storage and thermogenic gene programs, under certain physiological conditions New PPARs ligands and/or cofactors agonists as therapeutic agents for metabolic diseases Novel strategies targeting PPARs and cofactors for preventing/treating metabolic disease Authors can submit their manuscripts through the Manuscript Tracking System at http://mts.hindawi.com/submit/journals/ppar/comd/. Manuscript Due Friday, 2 June 2017 First Round of Reviews Friday, 25 August 2017 Publication Date Friday, 20 October 2017 Lead Guest Editor Xinran Ma, East China Normal University, Shanghai, China Guest Editors Lingyan Xu, East China Normal University, Shanghai, China Elisabetta Mueller, New York University, New York, USA
Hijacked Journals Sometimes someone will create a counterfeit website that pretends to be the website of a legitimate scholarly journal. The website creators then solicit manuscript submissions for the hijacked version of the journal, pocketing the money. In some cases the legitimate versions of the journals are only published in print form and they may not have websites. In the table below, the hijacked journal is listed in the left column; the corresponding authentic version of the journal is on the right. In cases where no website can be found for the original journal, a link is made to a bibliographic record for the journal. 请详细看以下链接： http://scholarlyoa.com/other-pages/hijacked-journals/
1, 维基 WikiCFP : Call For Papers of Conferences, Workshops and Journals http://www.wikicfp.com/cfp/ 2, IEEE: Call for Papers Deadlines http://www.ieee.org/web/conferences/callforpapers/index.html 3, World's largest listing of Calls for Papers http://www.papersinvited.com/ 这三个基本上够用得了，很全。根据你的专业关键词，输入搜索选择适合你的。若是会议的话，如开会地点，时间，截稿日期等等
标签: 约稿
