Filter By:

Journal Check one or more journals to show results from those journals only.

Choose more journals

Article type Check one or more article types to show results from those article types only.
Subject Check one or more subjects to show results from those subjects only.
Date Choose a date option to show results from those dates only.

Custom date range

Clear all filters
Sort by:
Showing 1–16 of 16 results
Advanced filters: Author: Issam Ben-Sahra Clear advanced filters
  • The mode of action of eukaryotic initiation factor 5A (eIF5A), a translation factor activated by hypusination, remains to be characterized. Here, the authors suggest that hypusinated eIF5A is involved in mitochondrial metabolism and translation promoting prostate cancer progression.

    • Michel Kahi
    • Abigail Mazzu′
    • Frédéric Bost
    ResearchOpen Access
    Nature Communications
    P: 1-20
  • Gliocidin can target brain tumours by disrupting the production of nucleotides needed for cell growth. The molecule’s unusual ability to cross the blood–brain barrier suggests a promising way to develop therapies.

    • Mushtaq A. Nengroo
    • Issam Ben-Sahra
    News & Views
    Nature
    Volume: 636, P: 307-308
  • Dihydroorotate dehydrogenase (DHODH) is the only core de novo pyrimidine enzyme in the mitochondrial inner membrane, coupling nucleotide production to electron transport. Curtabbi et al. show that a cytosolic, fumarate-dependent DHODH orthologue can bypass this dependence, sustaining pyrimidine synthesis and supporting cell growth during respiration failure.

    • Olivia Vidal-Cruchez
    • Issam Ben-Sahra
    News & Views
    Nature Metabolism
    Volume: 8, P: 290-292
  • Nucleotides are essential for different biological processes and have been also associated to cancer development. Depleting cellular nucleotides is a strategy commonly employed to target cancers. Here, the authors show that purine depletion induces serine synthesis to promote cancer cell migration and metastasis.

    • Mona Hoseini Soflaee
    • Rushendhiran Kesavan
    • Gerta Hoxhaj
    ResearchOpen Access
    Nature Communications
    Volume: 13, P: 1-14
  • The mechanistic target of rapamycin complex 1 (mTORC1) network integrates nutrient and energy signals that regulate metabolism and cell growth. Orozco et al. now show that the glycolytic intermediate dihydroxyacetone phosphate (DHAP) relays glycolytic activity to mTORC1 signalling.

    • Gerta Hoxhaj
    • Jason W. Locasale
    • Issam Ben-Sahra
    News & Views
    Nature Metabolism
    Volume: 2, P: 801-802
  • Cell division is a highly regulated process and requires a concurrent supply of energy and nutrients. Shin et al. provide critical insights into the allosteric mechanisms by which UTP regulates CAD activity and pyrimidine synthesis during the cell cycle.

    • Umakant Sahu
    • Issam Ben-Sahra
    News & Views
    Nature Metabolism
    Volume: 5, P: 199-200
  • The urea cycle enzyme argininosuccinate synthase 1 (ASS1) is upregulated in some cancer types. A study now shows that tumor cells with elevated urea cycle activity due to high ASS1 expression enhance gluconeogenesis, enabling a metabolic shift toward serine synthesis and causing purine synthesis addiction for growth and proliferation.

    • Elodie Villa
    • Issam Ben-Sahra
    News & Views
    Nature Cancer
    Volume: 1, P: 862-863
  • Shapiro, Chang, et al. identify a conserved role for the iron-binding histone demethylase KDM3B in sensing iron levels and regulating mTORC1 through transcriptional repression of key mTORC1 pathway components.

    • Jason S. Shapiro
    • Hsiang-Chun Chang
    • Hossein Ardehali
    Research
    Nature Cell Biology
    Volume: 25, P: 1478-1494
  • Distinct macrophage phenotypes are associated with their polarization to a proinflammatory or alternative state, but it is not well understood how metabolic status affects this process. Here, Byles et al.demonstrate that the mTOR metabolic pathway regulates macrophage differentiation.

    • Vanessa Byles
    • Anthony J. Covarrubias
    • Tiffany Horng
    Research
    Nature Communications
    Volume: 4, P: 1-11
  • Mitochondrial interaction of HKDC1 is essential for its pro-proliferative role in LC. When HKDC1 is ablated in liver cancer cells, mitochondrial dysfunction occurs which results in decrease ATP in the cells. The cancer cells react to decreased cellular energy by increasing glucose uptake. Also due to mitochondrial dysfunction there is enhanced ER stress and ER-mitochondrial interaction, leading to more calcium flux into the mitochondria. This multi-pronged effects of HKDC1 ablation leads to decreased cellular proliferation in LC.

    • Md. Wasim Khan
    • Alexander R. Terry
    • Brian T. Layden
    ResearchOpen Access
    Cell Death & Disease
    Volume: 13, P: 1-17