Josep Tarragó‐Celada

ORCID: 0000-0001-7322-9736
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Research Areas
  • Cancer, Hypoxia, and Metabolism
  • Microbial Metabolic Engineering and Bioproduction
  • Metabolism, Diabetes, and Cancer
  • Metabolomics and Mass Spectrometry Studies
  • Cancer-related Molecular Pathways
  • Nitric Oxide and Endothelin Effects
  • Advanced Proteomics Techniques and Applications
  • Advanced Breast Cancer Therapies
  • Gene Regulatory Network Analysis
  • Selenium in Biological Systems
  • Cancer-related cognitive impairment studies
  • Radiomics and Machine Learning in Medical Imaging
  • Diet and metabolism studies
  • Biological Research and Disease Studies
  • Histone Deacetylase Inhibitors Research
  • Folate and B Vitamins Research
  • Machine Learning in Bioinformatics
  • Ubiquitin and proteasome pathways
  • Mitochondrial Function and Pathology
  • Artificial Intelligence in Healthcare
  • Synthesis and Biological Evaluation
  • Cancer, Lipids, and Metabolism
  • Genomics, phytochemicals, and oxidative stress
  • Advanced Control Systems Optimization
  • Computational Drug Discovery Methods

Universitat de Barcelona
2015-2024

The Francis Crick Institute
2024

Article4 October 2017Open Access Source DataTransparent process De novo MYC addiction as an adaptive response of cancer cells to CDK4/6 inhibition Míriam Tarrado-Castellarnau Department Biochemistry and Molecular Biomedicine, Faculty Biology, Universitat de Barcelona, Spain Institute Biomedicine Barcelona (IBUB) CSIC-Associated Unit, Search for more papers by this author Pedro Atauri orcid.org/0000-0002-7754-7851 Josep Tarragó-Celada Jordi Perarnau Mariia Yuneva The Francis Crick Institute,...

10.15252/msb.20167321 article EN cc-by Molecular Systems Biology 2017-10-01

With most cancer-related deaths resulting from metastasis, the development of new therapeutic approaches against metastatic colorectal cancer (mCRC) is essential to increasing patient survival. The metabolic adaptations that support mCRC remain undefined and their elucidation crucial identify potential targets. Here, we employed a strategy for rational identification targetable vulnerabilities. This involved first thorough characterisation same-patient-derived cell lines primary colon...

10.3390/cancers13030425 article EN Cancers 2021-01-23

Compelling evidence has accumulated on the role of oxidative stress endothelial cell (EC) dysfunction in acute coronary syndrome. Unveiling underlying metabolic determinants been hampered by scarcity appropriate models to address cell-autonomous mechanisms EC dysfunction. We have generated cells derived from thrombectomy specimens patients affected with myocardial infarction (AMI) and conducted phenotypical characterizations. AMI-derived (AMIECs) display impaired growth, migration,...

10.7554/elife.86260 article EN cc-by eLife 2023-11-28

Growing evidence is showing that acetylation plays an essential role in cancer, but studies on the impact of KDAC inhibition (KDACi) metabolic profile are still their infancy. Here, we analyzed, by using iTRAQ-based quantitative proteomics approach, changes proteome KRAS-mutated non-small cell lung cancer (NSCLC) A549 cells response to trichostatin-A (TSA) and nicotinamide (NAM) under normoxia hypoxia. Part this was further validated molecular biochemical analyses correlated with...

10.3390/ijms22073378 article EN International Journal of Molecular Sciences 2021-03-25

Summary Several mechanisms of resistance cancer cells to cyclin-dependent kinase inhibitors (CDKi) have been identified, including the upregulation metabolic regulators such as glutaminase. However, whether and targets are optimal has not determined. Here, we systematically analyzed reprogramming in colorectal exposed Palbociclib, a CDKi selectively targeting CDK4/6, or Telaglenestat, selective glutaminase inhibitor. Through multiple approaches, show that Palbociclib Telaglenestat elicit...

10.1101/2024.01.04.574237 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-01-05

Metabolic adaptations to complex perturbations, like the response pharmacological treatments in multifactorial diseases such as cancer, can be described through measurements of part fluxes and concentrations at systemic level individual transporter enzyme activities molecular level. In framework Control Analysis (MCA), ensembles linear constraints built integrating these both levels, which are expressed relative differences or changes produced metabolic adaptation. Here, combining MCA with...

10.1371/journal.pcbi.1009234 article EN cc-by PLoS Computational Biology 2021-07-23

Abstract Compelling evidence has accumulated for the role of oxidative stress on endothelial cell (EC) dysfunction underlying acute coronary syndromes. However, understanding metabolic determinants EC been hampered by scarcity appropriate models. Here, we have generated and phenotypically characterized derived from thrombectomy specimens in patients with myocardial infarction (AMI). We found that AMI-derived cells (AMIECs), but not control health arteries, display impaired growth, migration...

10.1101/2023.02.28.530418 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2023-03-01
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