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Titlebook: Recent Advances in Prolactin Research; Maria Diakonova, PhD Book 2015 The Editor(s) (if applicable) and The Author(s), under exclusive lic

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发表于 2025-3-21 19:04:21 | 显示全部楼层 |阅读模式
书目名称Recent Advances in Prolactin Research
编辑Maria Diakonova, PhD
视频videohttp://file.papertrans.cn/823/822961/822961.mp4
概述Serves a large number of scientists and clinicians who are interested in the normal and patho physiology of prolactin.Gives an overview of major advances in the field of prolactin signaling pathways a
丛书名称Advances in Experimental Medicine and Biology
图书封面Titlebook: Recent Advances in Prolactin Research;  Maria Diakonova, PhD Book 2015 The Editor(s) (if applicable) and The Author(s), under exclusive lic
描述.Recent Advances in Prolactin Research. summarizes the current knowledge of prolactin (PRL), PRL receptor, PRL-dependent signaling pathways, the role of PRL in oncogenesis and PRL crosstalk with other oncogenic factors. The chapters are written by experts in these fields and focus on identifying and reviewing timely experimental findings that provide new insights into the expanding role of PRL in the pathophysiology associated with a variety of human conditions..Prolactin is a peptide hormone that is best known for its role in lactation. Prolactin also has an influence on hematopoiesis and angiogenesis, and is involved in the regulation of blood clotting through several pathways. Although PRL was discovered more than 80 years ago, the understanding of PRL signaling and its relationship to various pathologies is still very incomplete. PRL is not only a pituitary hormone with an important role in reproduction, but PRL also acts as a cytokine, modulating a wide variety of physiological processes. For example, data gathered during the last decade have demonstrated that locally produced PRL acts as the autocrine/paracrine factor and plays a contributory role during breast oncogenesis. I
出版日期Book 2015
关键词Cytokine; Pituitary; Prolactin; breast cancer; signaling pathways
版次1
doihttps://doi.org/10.1007/978-3-319-12114-7
isbn_softcover978-3-319-35276-3
isbn_ebook978-3-319-12114-7Series 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 Nature Switzerl
The information of publication is updating

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发表于 2025-3-21 22:47:20 | 显示全部楼层
Tyrosyl Phosphorylated Serine-Threonine Kinase PAK1 is a Novel Regulator of Prolactin-Dependent Breeases actin-regulating activity to facilitate cell motility. Tyrosyl phosphorylated PAK1 also stimulates invasion of breast cancer cells in response to PRL and three-dimensional (3D) collagen IV via transcription and secretion of MMP-1 and MMP-3 in a MAPK-dependent manner. These data illustrate the
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Prolactin-Induced Protein in Breast Cancer,grin-β1 with integrin-linked kinase 1 (ILK1) and ErbB2. Furthermore, the importance of PIP in cell proliferation has been demonstrated by the fact that purified PIP promotes growth of breast cancer cells and PIP expression is necessary for the proliferation of T-47D and MDA-MB-453 cell lines. In add
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A Positive Feedback Loop Between Prolactin and Stat5 Promotes Angiogenesis,ronment. Thus, PRL may stimulate tumor angiogenesis via autocrine, paracrine, and endocrine pathways. The disruption of tumor angiogenesis by interfering with PRL signaling may offer an attractive target for therapeutic intervention.
发表于 2025-3-22 18:47:52 | 显示全部楼层
Book 2015role in reproduction, but PRL also acts as a cytokine, modulating a wide variety of physiological processes. For example, data gathered during the last decade have demonstrated that locally produced PRL acts as the autocrine/paracrine factor and plays a contributory role during breast oncogenesis. I
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Allyson K. Booth,Arthur Gutierrez-Hartmannanty, warranting ethnobotanical surveys in these countries to fill the existing data gaps. The study further shows that less than 50% of ethnoveterinary plants have been validated scientifically, opening up opportunities for interesting pharmacological investigation. The study also highlights the ne
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