相关实验视频
Updated: Jul 1, 2025

08:40
Methyl-binding DNA capture Sequencing for Patient Tissues
Published on: October 31, 2016
8.6K
TP63-TRIM29轴调节前列腺癌中的增强器甲基化和染色体不稳定性
R Sultanov1,2, A Mulyukina3, O Zubkova3
1Center for Precision Genome Editing and Genetic Technologies for Biomedicine, Lopukhin Federal Research and Clinical Center of Physical-Chemical Medicine of Federal Medical Biological Agency, Moscow, Russia. rhenium112@gmail.com.
Epigenetics & chromatin
|March 14, 2024
概括
前列腺癌 (PRAD) 由于基因组不稳定性而表现出很高的变异性. 研究人员将TP63和TRIM29确定为关键调节剂,揭示了TRIM29在PRAD发展中的作用.
科学领域:
- 在瘤学瘤学.
- 基因组学就是基因组学.
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
背景情况:
- 前列腺腺癌 (PRAD) 是男性癌症死亡的主要原因.
- PRAD的特点是显著的DNA甲基化变异性和基因组不稳定性.
- 了解PRAD异质性的分子驱动因素至关重要.
研究的目的:
- 调查PRAD中基因组和表观基因组不稳定的分子基础.
- 确定与PRAD发展相关的关键调节基因.
- 阐明前列腺癌中已识别的调节者的功能性作用.
主要方法:
- 综合分析DNA甲基化,RNA测序和副本数量改变数据从癌症基因组图谱 (TCGA) 的PRAD.
- 应用权重基因共同表达网络分析 (WGCNA) 来识别与不稳定性相关的基因集群.
- 研究了候选基因TP63和TRIM29的调节功能.
主要成果:
- 在PRAD中,单个共同表达基因集群与基因组和表观基因组不稳定性有显著的关联.
- 在这个群体中,TP63和TRIM29被确定为关键的转录调节剂,显示了PRAD的下调.
- TP63调节增强剂甲基化,而TRIM29与TP63形成复合体,以保持前列腺基础上皮质的同一性并防止TMPRSS2:ERG融合.
结论:
- 在正常情况下,TRIM29和TP63对于维持前列腺基底上皮质标识至关重要.
- TRIM29在前列腺腺癌的发展中起着重要作用.
- 这些发现突出了PRAD的潜在治疗目标.
相关概念视频
Epigenetic Regulation
3.0K
Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
X-chromosome...
3.0K
Abnormal Proliferation
4.5K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.5K
Spreading of Chromatin Modifications
8.3K
The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
Writers
The writer...
Writers
The writer...
8.3K
Negative Regulator Molecules
35.4K
Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
35.4K
Chromatin Modification in iPS Cells
1.7K
Chromatin modification alters gene expression; therefore, scientists can add histone-modifying enzymes, histone variants, and chromatin remodeling complexes to somatic cells to aid reprogramming into pluripotent stem (iPS) cells.
Compact chromatin makes reprogramming difficult. Enzymes, such as histone demethylases and acetyltransferases, are often added during reprogramming to loosen the chromatin, making the DNA more accessible to transcription factors. Molecules that inhibit histone...
Compact chromatin makes reprogramming difficult. Enzymes, such as histone demethylases and acetyltransferases, are often added during reprogramming to loosen the chromatin, making the DNA more accessible to transcription factors. Molecules that inhibit histone...
1.7K

