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Titlebook: Glucocorticoid Signaling; From Molecules to Mi Jen-Chywan Wang,Charles Harris Book 2015 The Editor(s) (if applicable) and The Author(s), un

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發(fā)表于 2025-3-21 16:10:26 | 只看該作者 |倒序?yàn)g覽 |閱讀模式
書(shū)目名稱(chēng)Glucocorticoid Signaling
副標(biāo)題From Molecules to Mi
編輯Jen-Chywan Wang,Charles Harris
視頻videohttp://file.papertrans.cn/388/387046/387046.mp4
概述Fills a need in the market for comprehensive coverage on glucocorticoids.Includes the most up-to-date mechanistic information about the receptor that mediates glucocorticoid action?.Written by leading
叢書(shū)名稱(chēng)Advances in Experimental Medicine and Biology
圖書(shū)封面Titlebook: Glucocorticoid Signaling; From Molecules to Mi Jen-Chywan Wang,Charles Harris Book 2015 The Editor(s) (if applicable) and The Author(s), un
描述.This timely volume provides a comprehensive overview of glucocorticoids and their role in regulating many aspects of physiology and their use in the treatment of disease. The book is broken into four sections that begin by giving a general introduction to glucocorticoids and a brief history of the field. The second section will discuss the effects of glucocorticoids on metabolism, while the third section will cover the effects of glucocorticoids on key tissues. The final section will discuss general topics, such as animal models in glucocorticoid research and clinical implications of glucocorticoid research. Featuring chapters from leaders in the field, this volume will be of interest to both researchers and clinicians..
出版日期Book 2015
關(guān)鍵詞gene expression; glucocorticoid receptor; glucocorticoids; nuclear receptors; steroid hormones
版次1
doihttps://doi.org/10.1007/978-1-4939-2895-8
isbn_softcover978-1-4939-4997-7
isbn_ebook978-1-4939-2895-8Series ISSN 0065-2598 Series E-ISSN 2214-8019
issn_series 0065-2598
copyrightThe Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Science+Busines
The information of publication is updating

書(shū)目名稱(chēng)Glucocorticoid Signaling影響因子(影響力)




書(shū)目名稱(chēng)Glucocorticoid Signaling影響因子(影響力)學(xué)科排名




書(shū)目名稱(chēng)Glucocorticoid Signaling網(wǎng)絡(luò)公開(kāi)度




書(shū)目名稱(chēng)Glucocorticoid Signaling網(wǎng)絡(luò)公開(kāi)度學(xué)科排名




書(shū)目名稱(chēng)Glucocorticoid Signaling被引頻次




書(shū)目名稱(chēng)Glucocorticoid Signaling被引頻次學(xué)科排名




書(shū)目名稱(chēng)Glucocorticoid Signaling年度引用




書(shū)目名稱(chēng)Glucocorticoid Signaling年度引用學(xué)科排名




書(shū)目名稱(chēng)Glucocorticoid Signaling讀者反饋




書(shū)目名稱(chēng)Glucocorticoid Signaling讀者反饋學(xué)科排名




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Mechanisms of Glucocorticoid-Regulated Gene Transcriptionrt a consequence of transcriptional regulation by the glucocorticoid receptor (GR). Activation of GR by glucocorticoids results in tissue-specific changes in gene expression levels with some genes being activated whereas others are repressed. This raises two questions: First, how does GR regulate di
地板
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Regulation of Glucose Homeostasis by Glucocorticoidsin skeletal muscle and white adipose tissue they decrease glucose uptake and utilization by antagonizing insulin response. Therefore, excess glucocorticoid exposure causes hyperglycemia and insulin resistance. Glucocorticoids also regulate glycogen metabolism. In liver, glucocorticoids increase glyc
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Glucocorticoid-Induced Osteoporosisidence from both humans and mice indicate deleterious skeletal effects within weeks of pharmacological GC administration, both related and unrelated to a decrease in bone mineral density (BMD). Osteoclast numbers and bone resorption are also rapidly increased, and together with osteoblast inactivati
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Effects of Glucocorticoids in the Immune Systemmobilize amino acids from extra hepatic tissues, inhibit glucose uptake in muscle and adipose tissue, and stimulate fat breakdown in adipose tissue. They also mediate stress response. They exert potent immune-suppressive and anti-inflammatory effects particularly when administered pharmacologically.
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Glucocorticoid Regulation of Reproductioncorticoids activate many parts of the fight or flight response, mobilizing energy and enhancing survival, while inhibiting metabolic processes that are not necessary for survival in the moment. This includes reproduction, an energetically costly procedure that is very finely regulated. In the short
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