Publications by authors named "Yanheng Chen"

Article Synopsis
  • Metabolic reprogramming is crucial for macrophage functions like fighting bacteria and producing cytokines, with BRD4 playing a significant role in these processes during infections like Helicobacter pylori.
  • In experiments with macrophages from mice lacking BRD4, it was found that BRD4 deficiency impaired the glycolysis process necessary for combating H pylori and resulted in lower nitric oxide production for bacterial killing.
  • The study concludes that BRD4 not only regulates glycolysis in macrophages but also enhances their ability to fight infections by stabilizing messenger RNA needed for nitric oxide production, thus highlighting its importance in the immune response.
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Converting solar energy into hydrogen energy using conjugated polymers (CP) is a promising solution to the energy crisis. Improving water solubility plays one of the critical factors in enhancing the hydrogen evolution rate (HER) of CP photocatalysts. In this study, a novel concept of incorporating hydrophilic side chains to connect the backbones of CPs to improve their HER is proposed.

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This paper studies the dynamical characteristics of discrete analogue of impulsive recurrent neural networks with both discrete and finite distributed asynchronous time-varying delays. Firstly, the discrete impulsive system of the corresponding continuous-time model is reformed by impulsive maps and semi-discrete method. Secondly, by employing a famous delay impulsive differential inequality, several novel sufficient conditions are derived to ensure the uniqueness of equilibrium point and its global exponential stability in Lagrange sense for the discussed discrete-time impulsive system.

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P-TEFb modulates RNA polymerase II elongation through alternative interaction with negative and positive regulation factors. While inactive P-TEFbs are mainly sequestered in the 7SK snRNP complex in a chromatin-free state, most of its active forms are in complex with its recruitment factors, Brd4 and SEC, in a chromatin-associated state. Thus, switching from inactive 7SK snRNP to active P-TEFb (Brd4/P-TEFb or SEC/P-TEFb) is essential for global gene expression.

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Macrophage-mediated inflammatory response has been implicated in the pathogenesis of obesity and insulin resistance. Brd4 has emerged as a key regulator in the innate immune response. However, the role of Brd4 in obesity-associated inflammation and insulin resistance remains uncharacterized.

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H. pylori infection is one of the leading causes of gastric cancer and the pathogenicity of H. pylori infection is associated with its ability to induce chronic inflammation and apoptosis resistance.

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In the past decade, much emphasis has been put on the transcriptional activation of HIV-1, which is proposed as a promised strategy for eradicating latent HIV-1 provirus. Two drugs, prostratin and hexamethylene bisacetamide (HMBA), have shown potent effects as inducers for releasing HIV-1 latency when used alone or in combination, although their cellular target(s) are currently not well understood, especially under drug combination. Here, we have shown that HMBA and prostratin synergistically release HIV-1 latency via different mechanisms.

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The association of DSIF and NELF with initiated RNA Polymerase II (Pol II) is the general mechanism for inducing promoter-proximal pausing of Pol II. However, it remains largely unclear how the paused Pol II is released in response to stimulation. Here, we show that the release of the paused Pol II is cooperatively regulated by multiple P-TEFbs which are recruited by bromodomain-containing protein Brd4 and super elongation complex (SEC) via different recruitment mechanisms.

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The adenovirus early region 1A (E1A) oncoprotein hijacks host cells via direct interactions with many key cellular proteins, such as KAT2B, also known as PCAF (p300/CBP associated factor). E1A binds the histone acetyltransferase (HAT) domain of KAT2B to repress its transcriptional activation. However, the molecular mechanism by which E1A inhibits the HAT activity is not known.

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Prostratin has been proposed as a promising reagent for eradicating the latent HIV-1 provirus by inducing HIV-1 transcription activation. The molecular mechanism of this activation, however, is far from clear. Here, we show that the protein kinase D3 (PKD3) is essential for prostratin-induced transcription activation of latent HIV-1 provirus.

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