摘要
I类同源基因(小鼠和人类中的HOX基因),编码39种转录因子和显示一个独特的主要涉及胚胎发育调控的细胞记忆程序的基因组网络组织。HOX基因网络控制着涉及细胞记忆程序的异常表观遗传修饰。具体的来说,HOX基因簇和多种疾病的生成起着至关重要的作用:同类畸形、肿瘤、代谢过程、细胞周期失调。在本文中,我讨论了在心血管发育过程中控制HOX基因网络的作用。
关键词: 同源基因,血管再生术,存储器程序,Rosetta stone线索。
Current Medicinal Chemistry
Title:Class I Homeobox Genes, “The Rosetta Stone of the Cell Biology”, in the Regulation of Cardiovascular Development
Volume: 23 Issue: 3
Author(s): Alfredo Procino
Affiliation:
关键词: 同源基因,血管再生术,存储器程序,Rosetta stone线索。
摘要: Class I homeobox genes (Hox in mice and HOX in humans), encode for 39 transcription factors and display a unique genomic network organization mainly involved in the regulation of embryonic development and in the cell memory program. The HOX network controls the aberrant epigenetic modifications involving in the cell memory program. In details, the HOX cluster plays a crucial role in the generation and evolution of several diseases: congenic malformation, oncogenesis, metabolic processes and deregulation of cell cycle. In this review, I discussed about the role of HOX gene network in the control of cardiovascular development.
Export Options
About this article
Cite this article as:
Alfredo Procino , Class I Homeobox Genes, “The Rosetta Stone of the Cell Biology”, in the Regulation of Cardiovascular Development, Current Medicinal Chemistry 2016; 23 (3) . https://dx.doi.org/10.2174/0929867323666151207111302
DOI https://dx.doi.org/10.2174/0929867323666151207111302 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |

- Author Guidelines
- Bentham Author Support Services (BASS)
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements