Caroline C. Friedel

The paper identifies a co-dependency between CDK12 and the BAF chromatin-remodeling complex in TNBC, showing that their co-inhibition synergistically reduces cancer cell viability.

This study identifies ISG20 as an antiviral factor against HCMV by inducing an innate immune defense signature that enhances IFN production and response.

The paper presents a pipeline to identify viral variants from functional genomics data, showing it can accurately recover introduced mutations in HSV-1 mutants.

This study shows HSV-1 infection causes a downstream shift of +1 nucleosomes by depleting RNA Polymerase II from host genes, similar to Pol II depletion in yeast.

This study uses human hair-bearing skin organoids to investigate HSV-1 infection and host responses, revealing cell-type-specific susceptibility and spatially organized immune reactions.

This study identifies the HUSH complex as a host factor that restricts HAdV infection through epigenetic silencing, and shows HAdV proteins inhibit this complex to promote viral replication.

This study identifies a novel function of MCPyV small T antigen in suppressing the type I interferon response by reducing IRF9 levels, impacting immune evasion and tumor progression.

This study shows that CMTR1-mediated N1-2'O-methylation prevents antiviral recognition and regulates NVL2 mRNA splicing, affecting cell size, division, and ribosome biogenesis.

This study shows HSV-1 infection causes a downstream shift in promoter-proximal Pol II pausing for most host genes, more pronounced than NELF depletion.

This paper identifies M35 as a viral protein that binds DNA and inhibits IRF3-mediated gene expression, including Ifnb1, thereby suppressing the antiviral type I IFN response.

The paper shows HSV-1 and influenza infection induce circular and linear splicing of the NEAT1_2 isoform, independent of vhs and linked to transcription termination disruption.

This study shows HSV-1 infection causes widespread changes in host mRNA alternative polyadenylation, with ICP27 playing a role in shifting polyadenylation to intronic sites and affecting mRNA export and expression.