Aleksey Lazarenkov

ORCID: 0000-0003-0652-8116
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About
Contact & Profiles
Research Areas
  • Epigenetics and DNA Methylation
  • CRISPR and Genetic Engineering
  • Pluripotent Stem Cells Research
  • Genomics and Chromatin Dynamics
  • Cancer-related Molecular Pathways
  • Cytomegalovirus and herpesvirus research
  • Genetics, Aging, and Longevity in Model Organisms
  • RNA modifications and cancer
  • Childhood Cancer Survivors' Quality of Life
  • Genetic Syndromes and Imprinting
  • Acute Myeloid Leukemia Research
  • Immune responses and vaccinations
  • Acute Lymphoblastic Leukemia research

Josep Carreras Leukaemia Research Institute
2018-2024

Universitat Autònoma de Barcelona
2018

Abstract Activation of the p53 tumor suppressor triggers a transcriptional program to control cellular response stress. However, molecular mechanisms by which controls gene transcription are not completely understood. Here, we uncover critical role spatio-temporal genome architecture in this process. We demonstrate that drives direct and indirect changes compartments, topologically associating domains, DNA loops prior one hour its activation, escort program. Focusing on p53-bound enhancers,...

10.1038/s41467-024-46666-1 article EN cc-by Nature Communications 2024-04-01

ABSTRACT DNA methylation is traditionally associated with gene silencing, but its causal relationship and role in shaping cell fate decisions still need to be fully elucidated. Here, we conducted a genome-wide analysis investigate the between expression at regulatory regions human immune cells. By utilizing CRISPR-dCas9 editing tools, successfully established cause-and-effect levels of promoter Interleukin1-receptor antagonist ( IL1RN ) expression. Notably, observed that modifying status...

10.1101/2024.07.10.599183 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-07-10

Reprogramming somatic cells into induced pluripotent stem (iPSCs) requires activation of the pluripotency network and resetting epigenome by erasing epigenetic memory state. In female mouse cells, a critical reprogramming step is reactivation inactive X chromosome. Despite its importance, systematic understanding regulatory networks linking X-reactivation missing. Here, we reveal important pathways for acquisition using genome-wide CRISPR screen during neural precursor to iPSC reprogramming....

10.1126/sciadv.adj8862 article EN cc-by-nc Science Advances 2024-08-07

Abstract Reprogramming somatic cells into induced pluripotent stem (iPSCs) requires activation of the pluripotency network and resetting epigenome by erasing epigenetic memory state. In female mouse cells, a critical reprogramming step is reactivation inactive X chromosome. Despite its importance, systematic understanding regulatory networks linking X-reactivation missing. Here we reveal pathways important for iPSC using genome-wide CRISPR screen. particular, discover that interferon γ...

10.1101/2023.07.31.551297 preprint EN cc-by-nc bioRxiv (Cold Spring Harbor Laboratory) 2023-08-02

Activation of the p53 tumor suppressor triggers a transcriptional program to control cellular response stress. However, molecular mechanisms by which controls gene transcription are not completely understood. Here, using multi-omics integration framework, we uncover critical role spatio-temporal genome architecture in this process. We demonstrate that drives direct and indirect changes compartments, topologically associating domains DNA loops within minutes its activation, escort along time....

10.1101/2023.10.10.561663 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-10-11
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