Konstantin Slobodnyuk

ORCID: 0000-0002-7766-971X
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About
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Research Areas
  • Autophagy in Disease and Therapy
  • Endoplasmic Reticulum Stress and Disease
  • Melanoma and MAPK Pathways
  • Telomeres, Telomerase, and Senescence
  • Cancer Cells and Metastasis
  • Histone Deacetylase Inhibitors Research
  • Protein Kinase Regulation and GTPase Signaling
  • Glutathione Transferases and Polymorphisms
  • Protein Tyrosine Phosphatases
  • Cancer-related Molecular Pathways
  • Cell death mechanisms and regulation
  • CRISPR and Genetic Engineering
  • Mitochondrial Function and Pathology
  • Advanced Breast Cancer Therapies
  • Estrogen and related hormone effects
  • Toxoplasma gondii Research Studies

Universitat Autònoma de Barcelona
2022

Vall d'Hebron Institut de Recerca
2022

Centro de Investigación Biomédica en Red de Cáncer
2022

Institute for Research in Biomedicine
2017-2019

Abstract Apoptosis and senescence are two mutually exclusive cell fate programs that can be activated by stress. The factors instruct cells to enter into or apoptosis not fully understood, but both regulated the stress kinase p38α. Using an inducible system specifically activates this pathway, we show sustained p38α activation suffices trigger massive autophagosome formation enhance basal autophagic flux. This requires concurrent effect of increased mitochondrial reactive oxygen species...

10.1038/s41419-019-1607-0 article EN cc-by Cell Death and Disease 2019-05-15

Adequate responses to environmental stresses are essential for cell survival. The regulation of cellular energetics that involves mitochondrial energy production and oxidative stress is central in the process adaptation response. p38α signalling pathway plays a key role response stimuli by orchestrating multiple processes. However, prolonged activation results impaired proliferation can lead death. Here we use system specifically activate show sustained this suffices induce important...

10.1038/s41598-017-11309-7 article EN cc-by Scientific Reports 2017-09-06

Targeting the kinases MNK1 and MNK2 has emerged as a valuable strategy in oncology. However, most of advanced inhibitors are acting an adenosine triphosphate (ATP)-competitive mode, precluding evaluation different binding modes preclinical settings. Using rational design, we identified validated 4,6-diaryl-pyrazolo[3,4-

10.1021/acs.jmedchem.1c01941 article EN cc-by-nc-nd Journal of Medicinal Chemistry 2022-04-13

Highlights•Luminal progenitor cell fate in the mammary gland is regulated by p38α•p38α controls ER transcriptional program modulating RUNX1•p38α regulates H3 phosphorylation at RUNX1 promoter through kinase MSK1•p38α promotes tumorigenesis maintaining luminal tumor-initiating cellsSummaryMammary stem and cells are essential for homeostasis also candidates of origin tumors. Here, we have investigated function protein p38α using mice that delete this epithelial cells. We show modulation...

10.1016/j.stemcr.2017.11.021 article EN cc-by-nc-nd Stem Cell Reports 2017-12-28
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