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相关论文: A p53 Oscillator Model of DNA Break Repair Control

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The protein p53 has a well established role in protecting genomic integrity in human cells. When DNA is damaged p53 induces the cell cycle arrest to prevent the transmission of the damage to cell progeny, triggers the production of proteins…

分子网络 · 定量生物学 2012-11-22 Lídice Cruz-Rodríguez , Nuris Figueroa-Morales , Roberto Mulet

The tumor suppressor p53 plays a central role in cell fate decisions after DNA damage. Programmed Cell Death 5 (PDCD5) is known to interact with the p53 pathway to promote cell apoptosis. Recombinant human PDCD5 can significantly sensitize…

分子网络 · 定量生物学 2015-03-31 Changjing Zhuge , Xiaojuan Sun , Yingyu Chen , Jinzhi Lei

The cell cycle is an orderly sequence of events which ultimately lead to the division of a single cell into two daughter cells. In the case of DNA damage by radiation or chemicals, the damage checkpoints in the $G_{1}$ and $G_{2}$ phases of…

分子网络 · 定量生物学 2009-11-11 Bhaswar Ghosh , Indrani Bose

The p53 protein is well-known for its tumour suppressor function. The p53-MDM2 negative feedback loop constitutes the core module of a network of regulatory interactions activated under cellular stress. In normal cells, the level of p53…

分子网络 · 定量生物学 2007-08-24 Indrani Bose , Bhaswar Ghosh

Cells are constantly exposed to DNA damaging insults. To protect the organism, cells developed a complex molecular response coordinated by P53, the master regulator of DNA repair, cell division and cell fate. DNA damage accumulation and…

Dynamics of p53 is known to play important roles in the regulation of cell fate decisions in response to various stresses, and PDCD5 functions as a co-activator of p53 to modulate the p53 dynamics. In the present paper, we investigate how…

分子网络 · 定量生物学 2015-03-31 Yuanhong Bi , Zhuoqin Yang , Changjing Zhuge , Jinzhi Lei

A feedback mechanism that involves the proteins p53 and mdm2, induces cell death as a controled response to severe DNA damage. A minimal model for this mechanism demonstrates that the respone may be dynamic and connected with the time…

无序系统与神经网络 · 物理学 2009-11-07 G. Tiana , M. H. Jensen , K. Sneppen

We study the regulating mechanism of p53 on the properties of cell cycle dynamics in the light of the proposed model of interacting p53 and cell cycle networks via p53. Irradiation (IR) introduce to p53 compel p53 dynamics to suffer…

分子网络 · 定量生物学 2014-10-14 Md. Jahoor Alam , Sanjay Kumar , Vikram Singh , R. K. Brojen Singh

The transition from a normal to cancerous cell requires a number of highly specific mutations that affect cell cycle regulation, apoptosis, differentiation, and many other cell functions. One hallmark of cancerous genomes is genomic…

基因组学 · 定量生物学 2009-11-10 Yisroel Brumer , Eugene I. Shakhnovich

TP53 is the most frequently mutated tumor suppressor gene in human cancers, with mutations primarily in its DNA-binding domain (p53-DBD). Mutations in p53-DBD are categorized into hotspot mutations (resulting in complete loss-of-function)…

生物物理 · 物理学 2026-01-19 Han Zhou , Tao Zhou , Shiwei Yan

Specific activator and repressor transcription factors which bind to specific regulator DNA sequences, play an important role in gene activity control. Interactions between genes coding such transcription factors should explain the…

动力系统 · 数学 2015-06-26 Gh. I. Mihalas , M. Neamtu , D. Opris , F. Horhat

Gene regulatory networks, i.e. DNA segments in a cell which interact with each other indirectly through their RNA and protein products, lie at the heart of many important intracellular signal transduction processes. In this paper we analyse…

偏微分方程分析 · 数学 2014-04-03 Mark Chaplain , Mariya Ptashnyk , Marc Sturrock

Recently, some authors have shown that a DNA molecule produces electromagnetic signals and communicates with other DNA molecules or other molecules. In fact, a DNA acts like a receiver or transmitter of radio waves. In this paper, we…

生物物理 · 物理学 2018-08-03 Alireza Sepehri

We present the mechanism of interaction of Wnt network module, which is responsible for periodic sometogenesis, with p53 regulatory network, which is one of the main regulators of various cellular functions, and switching of various…

亚细胞过程 · 定量生物学 2015-03-17 Md. Zubbair Malik , Shahnawaz Ali , Md. Jahoor Alam , Romana Ishrat , R. K. Brojen Singh

Specific activator and repressor transcription factors which bind to specific regulator DNA sequences, play an important role in gene activity control. Interactions between genes coding such transcripion factors should explain the different…

动力系统 · 数学 2007-05-23 R. F. Horhat , M. Neamtu , D. Opris

Recent studies suggest that PML (Promyelocytic Leukemia) suppresses p53 protein degradation by inhibiting MDM2 protein in the nucleus [1], and regulates a number of biological functions [2]. We modeled a PML-MDM2-p53 regulatory network by…

分子网络 · 定量生物学 2015-04-21 Md. Jahoor Alam , Eyad M. AlShammari , R. K. Brojen Singh

Cancer cells exhibit significant alterations in their metabolism, characterised by a reduction in oxidative phosphorylation (OXPHOS) and an increased reliance on glycolysis, even in the presence of oxygen. This metabolic shift, known as the…

分子网络 · 定量生物学 2024-08-05 Roba Abukwaik , Elias Vera-Siguenza , Daniel Tennant , Fabian Spill

We develop and study the evolution of a model of radiation induced apoptosis in cells using stochastic simulations, and identified key protein targets for effective mitigation of radiation damage. We identified several key proteins…

生物物理 · 物理学 2011-09-06 Divesh Bhatt , Zoltan Oltvai , Ivet Bahar

DNA inversion is an important mechanism by which bacteria and bacteriophage switch reversibly between phenotypic states. In such switches, the orientation of a short DNA element is flipped by a site-specific recombinase enzyme. We propose a…

分子网络 · 定量生物学 2008-09-12 Paolo Visco , Rosalind J. Allen , Martin R. Evans

Recent data support the notion that a group of key transcriptional regulators involved in tumorigenesis, including MYC, p53, E2F1, and BMI1, share an intriguing capacity to simultaneously regulate metabolism and cell cycle. Here, we show…

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