@WolfmannotJack @Immuno_Alex @ewyler @Sander_Lab @TheBinderLab @pelagicbird @_b_meyer @EckerleIsabella @BrinkmannLab Interessant, würde ich aber nicht zu hoch hängen, denn -meiste Daten nur mit ACE2-A549-Zellen gemacht -OC43-Kontrolle wächst wahrsch schwächer --viele Viren fummeln irgendwie am Chromatin rum, zB influenza oder Erkältungscorona 229E (nicht zitiert
The NF-κB-dependent and -independent transcriptome and chromatin landscapes of human coronavirus 229E-infected cells.
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Apr 2020 – Apr 2023Where it's discussed
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X / Twitter4 posts
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News4 articles
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Facebook2 posts
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Reddit2 posts
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YouTube1 videos
AI synopsis
What people are saying
The overall tone indicates cautious interest, with some posts highlighting the data limitations such as reliance on specific cell lines, like ACE2-A549 cells, and references to other viruses not directly cited. Words like 'Interessant' (interesting) and comments about viral interactions with chromatin show curiosity but not strong enthusiasm, reflecting a nuanced and moderate perspective on the research's significance.
The discussions express mixed reactions, some acknowledging the research but with reservations, reflecting balanced opinions.
The posts show mild interest, with some findings noted but not elaborated upon deeply.
Commenters neither dismiss nor thoroughly analyze the research, indicating a neutral engagement level.
Comments suggest the publication's impact is recognized but not viewed as transformative or highly influential at this stage.
Abstract in brief
- The study explores how human coronavirus 229E (HCoV229E) affects gene expression and chromatin structure in infected cells, showing that the virus can suppress inflammatory responses typically driven by the NF-κB pathway, partly by degrading specific signaling proteins.
- Researchers identified specific genomic regions and enhancers that are activated during infection, noting that some genes are turned on independently of the usual NF-κB (p65) recruitment, which suggests alternative mechanisms of gene regulation.
- The findings highlight both common and unique genetic and epigenetic responses to HCoV229E and inflammatory signals like IL-1, deepening our understanding of how coronavirus infection modulates host cell processes at the molecular level.]
Top posts
Most liked on X and BlueskyAn alternative hypothesis for Vulnerability to Coronavirus pathogenicity; aging and tissue stiffness https://t.co/JBoqkwLnhZ via @YouTube #COVID_19 #coronavirus #aging #biochemistry #scicomm
RT @Friedemann1: @WolfmannotJack @Immuno_Alex @ewyler @Sander_Lab @TheBinderLab @pelagicbird @_b_meyer @EckerleIsabella @BrinkmannLab Inter…
RT @EleanorSheekey: An alternative hypothesis for Vulnerability to Coronavirus pathogenicity; aging and tissue stiffness https://t.co/JBoqk…
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Impact of Tissue Stiffness and Aging on Coronavirus Pathogenicity
This video explores how tissue stiffness and aging may influence coronavirus infection severity, discussing mechanotransduction and gene regulation mechanisms that affect immune response and pathogenicity.
RT @Friedemann1: @WolfmannotJack @Immuno_Alex @ewyler @Sander_Lab @TheBinderLab @pelagicbird @_b_meyer @EckerleIsabella @BrinkmannLab Inter…
@WolfmannotJack @Immuno_Alex @ewyler @Sander_Lab @TheBinderLab @pelagicbird @_b_meyer @EckerleIsabella @BrinkmannLab Interessant, würde ich aber nicht zu hoch hängen, denn -meiste Daten nur mit ACE2-A549-Zellen gemacht -OC43-Kontrolle wächst wahrsch schwächer --viele Viren fummeln irgendwie am Chromatin rum, zB influenza oder Erkältungscorona 229E (nicht zitiert
RT @EleanorSheekey: An alternative hypothesis for Vulnerability to Coronavirus pathogenicity; aging and tissue stiffness https://t.co/JBoqk…
An alternative hypothesis for Vulnerability to Coronavirus pathogenicity; aging and tissue stiffness https://t.co/JBoqkwLnhZ via @YouTube #COVID_19 #coronavirus #aging #biochemistry #scicomm
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