Publications by authors named "Yaolai Wang"

Article Synopsis
  • Gene transcription occurs in sporadic bursts, but there's ongoing debate about whether the size or frequency of these bursts is influenced by transcriptional activators due to technical challenges in studying them individually.
  • This research introduces two theoretical methods to analyze transcriptional bursting, linking it to variations in transcriptional levels and addressing the uncertainty in gene expression.
  • By comparing theoretical predictions to experimental data, the study finds strong evidence supporting the idea that frequency modulation is the main factor, resolving previous debates on burst signaling in gene transcription.
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Hepatocellular carcinoma (HCC) is a common cancer of high mortality, mainly due to the difficulty in diagnosis during its clinical stage. Here we aim to find the gene biomarkers, which are of important significance for diagnosis and treatment. In this work, 3682 differentially expressed genes on HCC were firstly differentiated based on the Cancer Genome Atlas database (TCGA).

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Background: Lung adenocarcinoma is the most common type of lung cancer, with high mortality worldwide. Its occurrence and development were thoroughly studied by high-throughput expression microarray, which produced abundant data on gene expression, DNA methylation, and miRNA quantification. However, the hub genes, which can be served as bio-markers for discriminating cancer and healthy individuals, are not well screened.

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There is accumulating evidence that, from bacteria to mammalian cells, messenger RNAs (mRNAs) are produced in intermittent bursts - a much 'noisier' process than traditionally thought. Based on quantitative measurements at individual promoters, diverse phenomenological models have been proposed for transcriptional bursting. Nevertheless, the underlying molecular mechanisms and significance for cellular signalling remain elusive.

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Transcription initiation is orchestrated by dynamic molecular interactions, with kinetic steps difficult to detect. Utilizing a hybrid method, we aim to unravel essential kinetic steps of transcriptional regulation on the glnAp2 promoter, whose regulatory region includes two enhancers (sites I and II) and three low-affinity sequences (sites III-V), to which the transcriptional activator NtrC binds. By structure reconstruction, we analyze all possible organization architectures of the transcription apparatus (TA).

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During gene transcription, proteins appear to cycle on and off some gene promoters with both long (tens of minutes) and short periods (no more than several minutes). The essence of these phenomena still remains unclear. Here, we propose a stochastic model for the state evolution of promoters in terms of DNA-protein interactions.

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The transcription apparatus (TA) is a huge molecular machine. It detects the time-varying concentrations of transcriptional activators and initiates mRNA transcripts at appropriate rates. Based on the general structural organizations of the TA, we propose how the TA dynamically orchestrates transcriptional responses.

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