Tim Liebner

ORCID: 0000-0003-0868-0859
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About
Contact & Profiles
Research Areas
  • Genomics and Chromatin Dynamics
  • RNA Research and Splicing
  • Ubiquitin and proteasome pathways
  • Histone Deacetylase Inhibitors Research
  • Signaling Pathways in Disease
  • Peptidase Inhibition and Analysis
  • RNA and protein synthesis mechanisms
  • HIV/AIDS Research and Interventions
  • HIV/AIDS drug development and treatment
  • HIV Research and Treatment
  • Epigenetics and DNA Methylation

Novo Nordisk Foundation
2020-2024

University of Copenhagen
2020-2024

Abstract Chromatin features are widely used for genome-scale mapping of enhancers. However, discriminating active enhancers from other cis -regulatory elements, predicting enhancer strength and identifying their target genes is challenging. Here we establish histone H2B N-terminus multisite lysine acetylation (H2BNTac) as a signature H2BNTac prominently marks candidate subset promoters discriminates them ubiquitously promoters. Two mechanisms underlie the distinct specificity: (1) unlike...

10.1038/s41588-023-01348-4 article EN cc-by Nature Genetics 2023-04-01

In all eukaryotes, acetylation of histone lysine residues correlates with transcription activation. Whether is a cause or consequence debated. One model suggests that promotes the recruitment and/or activation acetyltransferases, and occurs as ongoing transcription. However, extent to which shapes global protein landscapes not known. Here, we show remains virtually unaltered after acute inhibition. Transcription inhibition ablates co-transcriptionally occurring ubiquitylation H2BK120 but...

10.1038/s41467-024-49370-2 article EN cc-by Nature Communications 2024-06-11

Passive stiffness of the heart is determined largely by extracellular matrix and titin, which functions as a molecular spring within sarcomeres. Titin stiffening associated with development diastolic dysfunction (DD), while augmented titin compliance appears to impair systolic performance in dilated cardiomyopathy. We found that myofibril was elevated mice lacking histone deacetylase 6 (HDAC6). Cultured adult murine ventricular myocytes treated selective HDAC6 inhibitor also exhibited...

10.1172/jci148333 article EN cc-by Journal of Clinical Investigation 2022-05-15

Abstract Chromatin features are widely used for genome-scale mapping of enhancers. However, discriminating active enhancers from other cis-regulatory elements, predicting enhancer strength, and identifying their target genes remains challenging. Here we establish histone H2B N-terminus multisite lysine acetylation (H2BNTac) as a genuine signature H2BNTac prominently marks candidate promoters discriminates them ubiquitously promoters. Two mechanisms afford the distinct specificity. (1) Unlike...

10.1101/2022.07.18.500459 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2022-07-19

Abstract While current combined antiretroviral therapy (cART) allows control of HIV replication in patients and effectively suppresses plasma viral loads, it is unable to target latent reservoirs, which are responsible for virus rebound after discontinuation therapy. Several histone deacetylase inhibitors (HDACIs) have been shown reservoirs reactivate HIV. this effect highly desired, carries the risk that HIV-1 may be reactivated tissue compartments were cART concentrations insufficient thus...

10.1101/2020.04.29.067884 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2020-05-01
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