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Showing 1–16 of 16 results
Advanced filters: Author: Maria Kost-Alimova Clear advanced filters

  • This Resource presents the genetic subset of the 136,000 chemical and genetic perturbations tested by the Joint Undertaking for Morphological Profiling (JUMP) Cell Painting Consortium and associated analysis of phenotypic profiles.

    • Srinivas Niranj Chandrasekaran
    • Eric Alix
    • Anne E. Carpenter
    Research
    Nature Methods
    Volume: 22, P: 1742-1752

  • The molecular circuitry that drives dendrite formation during osteocytogenesis remains poorly understood. Here the authors show that deletion of Sp7, a gene linked to rare and common skeletal disease, in mature osteoblasts and osteocytes causes severe defects in osteocyte dendrites.

    • Jialiang S. Wang
    • Tushar Kamath
    • Marc N. Wein
    ResearchOpen Access
    Nature Communications
    Volume: 12, P: 1-20

  • Clear-cell carcinomas are aggressive tumours characterised by high accumulation of lipids and glycogen. Here, the authors report that these cancers have a common vulnerability to GPX4 inhibition-induced ferroptosis and using CRISPR screen and lipodomic profiling, they identify HIF-2α- HILPDA axis promotes ferroptosis via enrichment of PUFA lipids.

    • Yilong Zou
    • Michael J. Palte
    • Stuart L. Schreiber
    ResearchOpen Access
    Nature Communications
    Volume: 10, P: 1-13

  • How reproducible human kidney organoids derived from different iPSC lines are, and how faithful they are to human kidney tissue remain unclear. Here, the authors use four human iPSC lines to derive kidney organoids and show how organoid composition is reproducible, comparable to human tissue and of improved quality after transplantation.

    • Ayshwarya Subramanian
    • Eriene-Heidi Sidhom
    • Anna Greka
    ResearchOpen Access
    Nature Communications
    Volume: 10, P: 1-15

  • Here it is shown that telomere dysfunction drives metabolic and mitochondrial compromise. Mice with dysfunctional telomeres activate p53, which in turn represses PGC-1α and PGC-1β, master regulators of metabolic and mitochondrial processes. This results in reduced mitochondrial mass, mitochondrial dysfunction and reduced ATP generation, impaired gluconeogenesis, cariomyopathy and increased reactive oxygen species. This telomere–p53–PGC pathway shows how telomere dysfunction may compromise organ function and contribute to age-related disorders.

    • Ergün Sahin
    • Simona Colla
    • Ronald A. DePinho
    Research
    Nature
    Volume: 470, P: 359-365

  • Deficiency in dystrophin leads to death with cardiorespiratory failure in humans, but mice lacking dystrophin have minimal heart defects. Blau and colleagues find that mice that lack dystrophin and have shorter telomeres exhibit cardiac defects similar to human patients, with an increase in oxidative stress. The authors also found that onset of cardiac defects could be delayed by antioxidant treatments and that, strikingly, patients also have shortened telomeres.

    • Foteini Mourkioti
    • Jackie Kustan
    • Helen M. Blau
    Research
    Nature Cell Biology
    Volume: 15, P: 895-904

  • The CPJUMP1 Resource comprises Cell Painting images and profiles of 75 million cells treated with hundreds of chemical and genetic perturbations. The dataset enables exploration of their relationships and lays the foundation for the development of advanced methods to match perturbations.

    • Srinivas Niranj Chandrasekaran
    • Beth A. Cimini
    • Anne E. Carpenter
    ResearchOpen Access
    Nature Methods
    Volume: 21, P: 1114-1121

  • KRAS mutations are a driver event of pancreatic ductal adenocarcinoma; here, a subpopulation of dormant tumour cells, relying on oxidative phosphorylation for survival, is shown to be responsible for tumour relapse after treatment targeting the KRAS pathway.

    • Andrea Viale
    • Piergiorgio Pettazzoni
    • Giulio F. Draetta
    Research
    Nature
    Volume: 514, P: 628-632

  • Here it is shown that reactivation of endogenous telomerase activity in mice extends telomeres, reduces DNA damage signalling, allows resumption of proliferation in quiescent cultures, and eliminates degenerative phenotypes across multiple organs including testes, spleens and intestines. Accumulating evidence implicating telomere damage as a driver of age-associated organ decline and disease and the reversal of damage observed here support the development of regenerative strategies designed to restore telomere integrity.

    • Mariela Jaskelioff
    • Florian L. Muller
    • Ronald A. DePinho
    Research
    Nature
    Volume: 469, P: 102-106

  • We provide an updated protocol for image-based profiling with Cell Painting. A detailed procedure, with standardized conditions for the assay, is presented, along with a comprehensive description of parameters to be considered when optimizing the assay.

    • Beth A. Cimini
    • Srinivas Niranj Chandrasekaran
    • Anne E. Carpenter
    Protocols
    Nature Protocols
    Volume: 18, P: 1981-2013