Nikolaus Dietlein

ORCID: 0000-0003-2154-9492
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Ubiquitin and proteasome pathways
  • interferon and immune responses
  • Immunotherapy and Immune Responses
  • Immune cells in cancer
  • Adipokines, Inflammation, and Metabolic Diseases
  • T-cell and B-cell Immunology
  • Mesenchymal stem cell research
  • Acute Myeloid Leukemia Research
  • Adipose Tissue and Metabolism
  • Single-cell and spatial transcriptomics
  • CRISPR and Genetic Engineering
  • NF-κB Signaling Pathways
  • Immune Cell Function and Interaction

German Cancer Research Center
2017-2023

Heidelberg University
2017-2023

Emergency hematopoiesis is a concerted response aimed toward enhanced protection from infection, involving multiple cell types and developmental stages across the immune system. Despite its importance, underlying molecular regulation remains poorly understood. The deubiquitinase USP22 regulates levels of monoubiquitinated histone H2B (H2Bub1), which associated with activation interferon responses upon viral infection. Here, we show that in absence infection or inflammation, mice lacking...

10.1126/sciimmunol.abq2061 article EN Science Immunology 2022-12-09

Ubiquitin-specific peptidase 22 (Usp22) cleaves ubiquitin moieties from numerous proteins, including histone H2B and transcription factors. Recently, it was reported that Usp22 acts as a negative regulator of interferon-dependent responses. In the current study, we investigated role deficiency in acute viral infection with lymphocytic choriomeningitis virus (LCMV). We found lack on bone marrow-derived cells (Usp22fl/fl Vav1-Cre mice) reduced induction type I II interferons. A limited...

10.3390/vaccines11101563 article EN cc-by Vaccines 2023-10-05

Ubiquitin-Specific-peptidase 22 (Usp22) cleaves ubiquitin moieties from numerous proteins, in particular transcription factors. Recently, it was reported that Usp22 acts as negative regulator of interferon-dependent responses. In the current study, we investigated role deficiency upon acute viral infection with lymphocytic choriomeningitis (LCMV) virus. We found lack on bone marrow derived cells (Usp22 fl/fl Vav1-Cre mice) reduced induction type I and II interferons. Limited interferon...

10.20944/preprints202308.0878.v1 preprint EN 2023-08-11

Abstract Interferons protect from virus infections by inducing hundreds of interferon-stimulated genes (ISG) which orchestrate anti-viral adaptive and innate immunity. Upon viral infection or type I interferon (IFN) stimulation cell lines, a histone modification, monoubiquitinated 2B (H2Bub1), increases at ISG loci, raising the possibility that specific chromatin state can broadly stimulate IFN immunity in vivo. Here we show that, absence elevated levels, mice lacking relevant...

10.1101/2021.04.09.439190 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2021-04-11
Coming Soon ...