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Titlebook: RUNX Proteins in Development and Cancer; Yoram Groner,Yoshiaki Ito,Andre van Wijnen Book 2017 This is a U.S. Government work and not under

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發(fā)表于 2025-3-21 16:43:58 | 只看該作者 |倒序瀏覽 |閱讀模式
書目名稱RUNX Proteins in Development and Cancer
編輯Yoram Groner,Yoshiaki Ito,Andre van Wijnen
視頻videohttp://file.papertrans.cn/821/820246/820246.mp4
概述Provides readers with an overview of the diverse functions of the RUNX family genes.Is a compendium and reference source that will be of broad interest to cancer researchers, developmental biologists
叢書名稱Advances in Experimental Medicine and Biology
圖書封面Titlebook: RUNX Proteins in Development and Cancer;  Yoram Groner,Yoshiaki Ito,Andre van Wijnen Book 2017 This is a U.S. Government work and not under
描述.This volume provides the reader with an overview of the diverse functions of the RUNX family of genes. As highlighted in the introduction and several of the 29 chapters, humans and other mammals have three .RUNX. genes that are known to play specific roles in blood, bone and neuronal development. However, their evolutionary history has recently been traced back to unicellular organisms and their involvement in many well-known signaling pathways (Wnt, TGFb, Notch, Hippo) is indicative of a more general function in cell biology. Their documented roles in cell fate decisions include control of proliferation, differentiation, survival, senescence and autophagy...The pleiotropic effects of RUNX in development are mirrored in cancer, where RUNX genes can function as oncogenes that collaborate strongly with Myc family oncogenes or as tumour suppressor genes. In the latter role, they display hallmarks of both ‘gatekeepers’ that modulate p53 responses and ‘caretakers’ that protect the genome from DNA damage. Several chapters focus on the importance of these genes in leukemia research, where .RUNX1. and .CBFB. are frequently affected by chromosomal translocations that generate fusion oncopr
出版日期Book 2017
關(guān)鍵詞CBFb; DNA damage response; RUNX; epigenetic memory; lineage-specific developmental regulators
版次1
doihttps://doi.org/10.1007/978-981-10-3233-2
isbn_softcover978-981-10-9822-2
isbn_ebook978-981-10-3233-2Series ISSN 0065-2598 Series E-ISSN 2214-8019
issn_series 0065-2598
copyrightThis is a U.S. Government work and not under copyright protection in the U.S.; foreign copyright pro
The information of publication is updating

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沙發(fā)
發(fā)表于 2025-3-21 23:06:06 | 只看該作者
Advances in Experimental Medicine and Biologyhttp://image.papertrans.cn/r/image/820246.jpg
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發(fā)表于 2025-3-22 03:37:56 | 只看該作者
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發(fā)表于 2025-3-22 05:30:05 | 只看該作者
978-981-10-9822-2This is a U.S. Government work and not under copyright protection in the U.S.; foreign copyright pro
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發(fā)表于 2025-3-22 09:47:33 | 只看該作者
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發(fā)表于 2025-3-22 16:28:37 | 只看該作者
0065-2598 ad interest to cancer researchers, developmental biologists .This volume provides the reader with an overview of the diverse functions of the RUNX family of genes. As highlighted in the introduction and several of the 29 chapters, humans and other mammals have three .RUNX. genes that are known to pl
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發(fā)表于 2025-3-22 18:26:02 | 只看該作者
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發(fā)表于 2025-3-23 00:04:49 | 只看該作者
The Role of Runx1 in Embryonic Blood Cell Formationtopoiesis because it plays an essential function during specification of the hematopoietic lineage during embryogenesis. Here we review the role of Runx1 in embryonic HSPC formation, with a particular focus on its role in hemogenic endothelium.
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發(fā)表于 2025-3-23 03:57:33 | 只看該作者
Runx1 Structure and Function in Blood Cell Developmenthape the epigenetic landscape and the three-dimensional structure of gene loci within the nucleus. Finally, we review how aberrant forms of RUNX1 deregulate blood cell development and cause hematopoietic malignancies.
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發(fā)表于 2025-3-23 08:14:34 | 只看該作者
RUNX1-ETO Leukemiacquisition of cooperating secondary events. Furthermore, it has become increasingly apparent that a delicate balance of AML1-ETO and native AML1 is important to sustain the malignant cell phenotype. Translation of these findings into the clinical setting is just beginning.
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