Journal: Nature Cell Biology

Abbreviation

Nat Cell Biol

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Nature

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1465-7392
1476-4679

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Publications 1 - 10 of 59
  • Selective autophagy
    Item type: Journal Article
    Kraft, Claudine; Peter, Matthias; Hofmann, Kay (2010)
    Nature Cell Biology
  • A mechanism for chromosome segregation sensing by the NoCut checkpoint
    Item type: Journal Article
    Mendoza, Manuel; Norden, Caren; Durrer, Kathrin; et al. (2009)
    Nature Cell Biology
  • MyomiR-133 regulates brown fat differentiation through Prdm16
    Item type: Journal Article
    Trajkovski, Mirko; Ahmed, Kashan; Esau, Christine C.; et al. (2012)
    Nature Cell Biology
  • A guideline on the molecular ecosystem regulating ferroptosis
    Item type: Review Article
    Dai, Enyong; Chen, Xin; Linkermann, Andreas; et al. (2024)
    Nature Cell Biology
    Ferroptosis, an intricately regulated form of cell death characterized by uncontrolled lipid peroxidation, has garnered substantial interest since this term was first coined in 2012. Recent years have witnessed remarkable progress in elucidating the detailed molecular mechanisms that govern ferroptosis induction and defence, with particular emphasis on the roles of heterogeneity and plasticity. In this Review, we discuss the molecular ecosystem of ferroptosis, with implications that may inform and enable safe and effective therapeutic strategies across a broad spectrum of diseases.
  • Network plasticity of pluripotency transcription factors in embryonic stem cells
    Item type: Journal Article
    Filipczyk, Adam; Marr, Carsten; Hastreiter, Simon; et al. (2015)
    Nature Cell Biology
  • VHL loss causes spindle misorientation and chromosome instability
    Item type: Journal Article
    Thoma, Claudio R.; Toso, Alberto; Gutbrodt, Katrin L.; et al. (2009)
    Nature Cell Biology
    Error-free mitosis depends on fidelity-monitoring checkpoint systems that ensure correct temporal and spatial coordination of chromosome segregation by the microtubule spindle apparatus. Defects in these checkpoint systems can lead to genomic instability, an important aspect of tumorigenesis. Here we show that the von Hippel-Lindau (VHL) tumour suppressor protein, pVHL, which is inactivated in hereditary and sporadic forms of renal cell carcinoma, localizes to the mitotic spindle in mammalian cells and its functional inactivation provokes spindle misorientation, spindle checkpoint weakening and chromosomal instability. Spindle misorientation is linked to unstable astral microtubules and is supressed by the restoration of wild-type pVHL in pVHL-deficient cells, but not in naturally-occurring VHL disease mutants that are defective in microtubule stabilization. Impaired spindle checkpoint function and chromosomal instability are the result of reduced Mad2 (mitotic arrest deficient 2) levels actuated by pVHL-inactivation and are rescued by re-expression of either Mad2 or pVHL in VHL-defective cells. An association between VHL inactivation, reduced Mad2 levels and increased aneuploidy was also found in human renal cancer, implying that the newly identified functions of pVHL in promoting proper spindle orientation and chromosomal stability probably contribute to tumour suppression.
  • BTB proteins as henchmen of Cul3-based ubiquitin ligases
    Item type: Other Journal Item
    Krek, Wilhelm (2003)
    Nature Cell Biology
    The choice of ubiquitination substrates of Cul1- and Cul2-based E3 ubiquitin protein ligase complexes is dictated by the identity of their substrate-specific adaptors, known as F-box and BC-box proteins, respectively. Recent work suggests that members of the large family of BTB-domain proteins define a new class of substrate-specific adaptors of Cul3-based E3 complexes. This finding places many signalling pathways in which BTB-domain proteins participate under direct control of the ubiquitination pathway.
  • H3K9me selectively blocks transcription factor activity and ensures differentiated tissue integrity
    Item type: Journal Article
    Methot, Stephen P.; Padeken, Jan; Brancati, Giovanna; et al. (2021)
    Nature Cell Biology
    The developmental role of histone H3K9 methylation (H3K9me), which typifies heterochromatin, remains unclear. In Caenorhabditis elegans, loss of H3K9me leads to a highly divergent upregulation of genes with tissue and developmental-stage specificity. During development H3K9me is lost from differentiated cell type-specific genes and gained at genes expressed in earlier developmental stages or other tissues. The continuous deposition of H3K9me2 by the SETDB1 homolog MET-2 after terminal differentiation is necessary to maintain repression. In differentiated tissues, H3K9me ensures silencing by restricting the activity of a defined set of transcription factors at promoters and enhancers. Increased chromatin accessibility following the loss of H3K9me is neither sufficient nor necessary to drive transcription. Increased ATAC-seq signal and gene expression correlate at a subset of loci positioned away from the nuclear envelope, while derepressed genes at the nuclear periphery remain poorly accessible despite being transcribed. In conclusion, H3K9me deposition can confer tissue-specific gene expression and maintain the integrity of terminally differentiated muscle by restricting transcription factor activity.
  • Glucose controls lipolysis through Golgi PtdIns4P-mediated regulation of ATGL
    Item type: Journal Article
    Ding, Lianggong; Huwyler, Florian; Long, Fen; et al. (2024)
    Nature Cell Biology
    Metabolic crosstalk of the major nutrients glucose, amino acids and fatty acids (FAs) ensures systemic metabolic homeostasis. The coordination between the supply of glucose and FAs to meet various physiological demands is especially important as improper nutrient levels lead to metabolic disorders, such as diabetes and metabolic dysfunction-associated steatohepatitis (MASH). In response to the oscillations in blood glucose levels, lipolysis is thought to be mainly regulated hormonally to control FA liberation from lipid droplets by insulin, catecholamine and glucagon. However, whether general cell-intrinsic mechanisms exist to directly modulate lipolysis via glucose sensing remains largely unknown. Here we report the identification of such an intrinsic mechanism, which involves Golgi PtdIns4P-mediated regulation of adipose triglyceride lipase (ATGL)-driven lipolysis via intracellular glucose sensing. Mechanistically, depletion of intracellular glucose results in lower Golgi PtdIns4P levels, and thus reduced assembly of the E3 ligase complex CUL7FBXW8 in the Golgi apparatus. Decreased levels of the E3 ligase complex lead to reduced polyubiquitylation of ATGL in the Golgi and enhancement of ATGL-driven lipolysis. This cell-intrinsic mechanism regulates both the pool of intracellular FAs and their extracellular release to meet physiological demands during fasting and glucose deprivation. Moreover, genetic and pharmacological manipulation of the Golgi PtdIns4P-CUL7FBXW8-ATGL axis in mouse models of simple hepatic steatosis and MASH, as well as during ex vivo perfusion of a human steatotic liver graft leads to the amelioration of steatosis, suggesting that this pathway might be a promising target for metabolic dysfunction-associated steatotic liver disease and possibly MASH.
  • Absence of nucleolar disruption after impairment of 40S ribosome biogenesis reveals an rpL11-translation-dependent mechanism of p53 induction
    Item type: Journal Article
    Fumagalli, Stefano; Di Cara, Alessandro; Neb-Gulati, Arti; et al. (2009)
    Nature Cell Biology
Publications 1 - 10 of 59