Adam Karoutas

ORCID: 0000-0003-4264-8203
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About
Contact & Profiles
Research Areas
  • Nuclear Structure and Function
  • Cancer Cells and Metastasis
  • Genomics and Chromatin Dynamics
  • Cancer, Hypoxia, and Metabolism
  • Neonatal Respiratory Health Research
  • Glioma Diagnosis and Treatment
  • Ubiquitin and proteasome pathways
  • Chemical Synthesis and Analysis
  • Microtubule and mitosis dynamics
  • Effects of Radiation Exposure
  • ATP Synthase and ATPases Research
  • Immune cells in cancer
  • Neuroblastoma Research and Treatments
  • Mitochondrial Function and Pathology
  • RNA modifications and cancer
  • Epigenetics and DNA Methylation
  • Management of metastatic bone disease
  • Protein Degradation and Inhibitors
  • RNA Research and Splicing
  • Muscle Physiology and Disorders
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Chronic Obstructive Pulmonary Disease (COPD) Research

The Francis Crick Institute
2022-2024

Max Planck Institute of Immunobiology and Epigenetics
2019-2023

University of Freiburg
2023

Institut Gustave Roussy
2015

Abstract Reversible acetylation of mitochondrial proteins is a regulatory mechanism central to adaptive metabolic responses. Yet, how such functionally relevant protein achieved remains unexplored. Here we reveal an unprecedented role the MYST family lysine acetyltransferase MOF in energy metabolism via acetylation. Loss MOF–KANSL complex members leads defects including fragmentation, reduced cristae density and impaired electron transport chain IV integrity primary mouse embryonic...

10.1038/s42255-023-00904-w article EN cc-by Nature Metabolism 2023-10-09

A key step for metastatic outgrowth involves the generation of a deeply altered microenvironment (niche) that supports malignant behavior cancer cells. The complexity niche has posed significant challenge in elucidating underlying programs driving its origin. Here, by focusing on early stages breast metastasis to lung mice, we describe cancer-dependent chromatin remodeling and activation developmental alveolar type 2 (AT2) cells within niche. We show can prime AT2 into reprogrammed...

10.1016/j.devcel.2024.05.020 article EN cc-by Developmental Cell 2024-06-01

Facioscapulohumeral dystrophy (FSHD) is an epi/genetic satellite disease associated with at least two sequences in 4q35: (i) D4Z4 macrosatellite and (ii) β-satellite repeats (BSR), a prevalent part of the 4qA allele. Most recent FSHD studies have been focused on DUX4 transcript inside its tandem contraction patients. However, D4Z4-contraction alone not pathological, which would also require Since little known about BSR, we investigated BSR functional role transcriptional control region 4q35....

10.1093/nar/gkv721 article EN cc-by-nc Nucleic Acids Research 2015-07-15

<title>Abstract</title> Metastatic relapse can occur months to years after the cancer is first diagnosed, and it relies on reactivation of disseminated tumour cells (DTCs) that have lied dormant in secondary organs. The acquisition maintenance a dormancy phenotype are tightly regulated by interaction DTCs with their microenvironment. In bone, program activated metastatic competent how induced largely unknown. We here present strategy engineer mouse-to-mouse extramedullary (EM) which...

10.21203/rs.3.rs-3173228/v1 preprint EN cc-by Research Square (Research Square) 2023-07-27

A key step for metastatic outgrowth involves the generation of a deeply altered microenvironment (niche) that supports malignant behavior cancer cells. However, it is unclear whether fundamental program driving this de novo cellular environment can be identified. Here, by focusing on breast metastasis to lung, we describe cancer-dependent activation developmental programs in alveolar epithelial We have identified relationship linking high competency lung with induction multilineage state AT2...

10.2139/ssrn.4540765 preprint EN 2023-01-01
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