Related papers: Gene Copy Number and Cell Cycle Arrest
The biological processes that execute complex multiple functions, such as cell cycle, must ensure the order of sequential events and keep the dynamic robustness against various fluctuations. Here, we examine the dynamic mechanism and the…
Ionizing radiation is known to delay the cell cycle progression. In particular after particle exposure significant delays have been observed and it has been shown that the extent of delay affects the expression of damage such as chromosome…
A mechanism of double strand breaking (DSB) in DNA due to the action of two electrons is considered. These are the electrons produced in the vicinity of DNA molecules due to ionization of water molecules with a consecutive emission of two…
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…
The prediction plays the important role in detecting efficient protection and therapy of cancer. The prediction of mutations in gene needs a diagnostic and classification, which is based on the whole database (big dataset), to reach…
Effective wound repair treatments rely on a clear picture of how cell proliferation and migration are coordinated during tissue restoration. Fibroblasts are key contributors to tissue restoration in the dermis, and modern imaging tools…
Individual cancer cells carry a bewildering number of distinct genomic alterations i.e., copy number variations and mutations, making it a challenge to uncover genomic-driven mechanisms governing tumorigenesis. Here we performed…
Electronic properties of DNA are believed to play a crucial role in many phenomena in living organisms, for example the location of DNA lesions by base excision repair (BER) glycosylases and the regulation of tumor-suppressor genes such as…
DNA double-strand breaks (DSBs) represent a serious source of damage for all living things and thus there have been many quantitative studies of DSBs both in vivo and in vitro. Despite this fact, the processes that lead to their production…
Breakage-Fusion-Bridge cycles in cancer arise when a broken segment of DNA is duplicated and an end from each copy joined together. This structure then `unfolds' into a new piece of palindromic DNA. This is one mechanism responsible for the…
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…
Bacterial DNA gyrase introduces negative supercoils into chromosomal DNA and relaxes positive supercoils introduced by replication and transiently by transcription. Removal of these positive supercoils is essential for replication fork…
A four-node network consisting of a negative loop controlling a positive one is studied. It models some of the features of the p53 gene network. Using piecewise linear dynamics with thresholds, the allowed dynamical classes are fully…
Tumor recurrence, driven by the evolution of drug resistance is a major barrier to therapeutic success in cancer. Resistance is often caused by genetic alterations such as point mutation, which refers to the modification of a single genomic…
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…
Accurate subtyping or classification of breast cancer is important for ensuring proper treatment of patients and also for understanding the molecular mechanisms driving this disease. While there have been several gene signatures proposed in…
Cellular reprogramming, the conversion of one cell type to another, has fundamentally transformed our conception of cell types. Cellular reprogramming induces global changes in gene expression involving hundreds of transcription factors and…
Mutations can arise from the chance misincorporation of nucleotides during DNA replication or from DNA lesions that are not repaired correctly. We introduce a model that relates the source of mutations to their accumulation with cell…
Evolving genomes increase a number of their genes by gene duplications. To escape degradation in a functionless pseudogene, any gene duplicate needs to be guarded by negative (purifying) selection from otherwise inevitable fixation of…
We construct a model of cell reprogramming (the conversion of fully differentiated cells to a state of pluripotency, known as induced pluripotent stem cells, or iPSCs) which builds on key elements of cell biology viz. cell cycles and cell…