4,292 results match your criteria Nature Cell Biology [Journal]


Serial genomic inversions induce tissue-specific architectural stripes, gene misexpression and congenital malformations.

Nat Cell Biol 2019 Feb 11. Epub 2019 Feb 11.

RG Development & Disease, Max Planck Institute for Molecular Genetics, Berlin, Germany.

Balanced chromosomal rearrangements such as inversions and translocations can cause congenital disease or cancer by inappropriately rewiring promoter-enhancer contacts. To study the potentially pathogenic consequences of balanced chromosomal rearrangements, we generated a series of genomic inversions by placing an active limb enhancer cluster from the Epha4 regulatory domain at different positions within a neighbouring gene-dense region and investigated their effects on gene regulation in vivo in mice. Expression studies and high-throughput chromosome conformation capture from embryonic limb buds showed that the enhancer cluster activated several genes downstream that are located within asymmetric regions of contact, the so-called architectural stripes. Read More

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http://dx.doi.org/10.1038/s41556-019-0273-xDOI Listing
February 2019
7 Reads

MicroRNA-dependent regulation of biomechanical genes establishes tissue stiffness homeostasis.

Nat Cell Biol 2019 Feb 11. Epub 2019 Feb 11.

Yale Cardiovascular Research Center, Department of Internal Medicine, Section of Cardiology, Yale University School of Medicine, New Haven, CT, USA.

Vertebrate tissues exhibit mechanical homeostasis, showing stable stiffness and tension over time and recovery after changes in mechanical stress. However, the regulatory pathways that mediate these effects are unknown. A comprehensive identification of Argonaute 2-associated microRNAs and mRNAs in endothelial cells identified a network of 122 microRNA families that target 73 mRNAs encoding cytoskeletal, contractile, adhesive and extracellular matrix (CAM) proteins. Read More

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http://dx.doi.org/10.1038/s41556-019-0272-yDOI Listing
February 2019
1 Read

Author Correction: CRISPR-Cas9-mediated base-editing screening in mice identifies DND1 amino acids that are critical for primordial germ cell development.

Nat Cell Biol 2019 Feb 4. Epub 2019 Feb 4.

State Key Laboratory of Cell Biology, Shanghai Key Laboratory of Molecular Andrology, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.

In Fig. 2a of this Technical Report originally published, the authors inadvertently used the same set of images for the 4B2N1 and 4B2N3 cells when preparing the figure. The three images (bright field, Oct4-EGFP and pCAG-mRFP) of 4B2N3 cells have now been replaced with the correct versions. Read More

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http://dx.doi.org/10.1038/s41556-018-0265-2DOI Listing
February 2019

Golgi mechanics controls lipid metabolism.

Nat Cell Biol 2019 Feb 4. Epub 2019 Feb 4.

Institut Necker-Enfants Malades, Paris, France.

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http://dx.doi.org/10.1038/s41556-019-0289-2DOI Listing
February 2019

Extracellular matrix mechanical cues regulate lipid metabolism through Lipin-1 and SREBP.

Nat Cell Biol 2019 Feb 4. Epub 2019 Feb 4.

Department of Molecular Medicine (DMM), University of Padua, Padua, Italy.

Extracellular matrix (ECM) mechanical cues have powerful effects on cell proliferation, differentiation and death. Here, starting from an unbiased metabolomics approach, we identify synthesis of neutral lipids as a general response to mechanical signals delivered by cell-matrix adhesions. Extracellular physical cues reverberate on the mechanical properties of the Golgi apparatus and regulate the Lipin-1 phosphatidate phosphatase. Read More

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http://dx.doi.org/10.1038/s41556-018-0270-5DOI Listing
February 2019

Recapitulating endocrine cell clustering in culture promotes maturation of human stem-cell-derived β cells.

Nat Cell Biol 2019 Feb 1;21(2):263-274. Epub 2019 Feb 1.

Diabetes Center, University of California San Francisco, San Francisco, CA, USA.

Despite advances in the differentiation of insulin-producing cells from human embryonic stem cells, the generation of mature functional β cells in vitro has remained elusive. To accomplish this goal, we have developed cell culture conditions to closely mimic events occurring during pancreatic islet organogenesis and β cell maturation. In particular, we have focused on recapitulating endocrine cell clustering by isolating and reaggregating immature β-like cells to form islet-sized enriched β-clusters (eBCs). Read More

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http://dx.doi.org/10.1038/s41556-018-0271-4DOI Listing
February 2019

Improving human β-cell maturation in vitro.

Nat Cell Biol 2019 Feb;21(2):119-121

Sarah W. Stedman Nutrition and Metabolism Center, Duke Molecular Physiology Institute, Department of Pharmacology & Cancer Biology and Department of Medicine, Endocrine Division, Duke University Medical Center, Durham, NC, USA.

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http://dx.doi.org/10.1038/s41556-019-0277-6DOI Listing
February 2019
1 Read

Championing scientist migration.

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Nat Cell Biol 2019 Feb;21(2):113

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http://dx.doi.org/10.1038/s41556-019-0283-8DOI Listing
February 2019

SETDB1-mediated methylation of Akt promotes its K63-linked ubiquitination and activation leading to tumorigenesis.

Nat Cell Biol 2019 Feb 28;21(2):214-225. Epub 2019 Jan 28.

Department of Cancer Biology, Wake Forest Baptist Medical Center, Wake Forest University, Winston Salem, NC, USA.

The serine/threonine kinase Akt plays a central role in cell proliferation, survival and metabolism, and its hyperactivation is linked to cancer progression. Here we report that Akt undergoes K64 methylation by SETDB1, which is crucial for cell membrane recruitment, phosphorylation and activation of Akt following growth factor stimulation. Furthermore, we reveal an adaptor function of histone demethylase JMJD2A, which is important for recognizing Akt K64 methylation and recruits E3 ligase TRAF6 and Skp2-SCF to the Akt complex, independently of its demethylase activity, thereby initiating K63-linked ubiquitination, cell membrane recruitment and activation of Akt. Read More

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http://dx.doi.org/10.1038/s41556-018-0266-1DOI Listing
February 2019
2 Reads

AKT methylation by SETDB1 promotes AKT kinase activity and oncogenic functions.

Nat Cell Biol 2019 Feb 28;21(2):226-237. Epub 2019 Jan 28.

Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.

Aberrant activation of AKT disturbs the proliferation, survival and metabolic homeostasis of various human cancers. Thus, it is critical to understand the upstream signalling pathways governing AKT activation. Here, we report that AKT undergoes SETDB1-mediated lysine methylation to promote its activation, which is antagonized by the Jumonji-family demethylase KDM4B. Read More

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http://dx.doi.org/10.1038/s41556-018-0261-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6377565PMC
February 2019
2 Reads
19.679 Impact Factor

Oncogenic AKTivation by methylation.

Nat Cell Biol 2019 Feb;21(2):114-115

Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, USA.

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http://dx.doi.org/10.1038/s41556-019-0275-8DOI Listing
February 2019

Snail-induced claudin-11 prompts collective migration for tumour progression.

Nat Cell Biol 2019 Feb 21;21(2):251-262. Epub 2019 Jan 21.

Program in Molecular Medicine, National Yang-Ming University and Academia Sinica, Taipei, Taiwan.

Epithelial-mesenchymal transition (EMT) is a pivotal mechanism for cancer dissemination. However, EMT-regulated individual cancer cell invasion is difficult to detect in clinical samples. Emerging evidence implies that EMT is correlated to collective cell migration and invasion with unknown mechanisms. Read More

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http://dx.doi.org/10.1038/s41556-018-0268-zDOI Listing
February 2019
6 Reads

ALK phosphorylates SMAD4 on tyrosine to disable TGF-β tumour suppressor functions.

Nat Cell Biol 2019 Feb 21;21(2):179-189. Epub 2019 Jan 21.

MOE Key Laboratory of Biosystems Homeostasis & Protection and Innovation Center for Cell Signaling Network, Life Sciences Institute, Zhejiang University, Hangzhou, China.

Loss of TGF-β tumour suppressive response is a hallmark of human cancers. As a central player in TGF-β signal transduction, SMAD4 (also known as DPC4) is frequently mutated or deleted in gastrointestinal and pancreatic cancer. However, such genetic alterations are rare in most cancer types and the underlying mechanism for TGF-β resistance is not understood. Read More

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http://www.nature.com/articles/s41556-018-0264-3
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February 2019
8 Reads

Targeting the perivascular niche sensitizes disseminated tumour cells to chemotherapy.

Nat Cell Biol 2019 Feb 21;21(2):238-250. Epub 2019 Jan 21.

Public Health Sciences Division/Translational Research Program, Fred Hutchinson Cancer Research Center, Seattle, WA, USA.

The presence of disseminated tumour cells (DTCs) in bone marrow is predictive of poor metastasis-free survival of patients with breast cancer with localized disease. DTCs persist in distant tissues despite systemic administration of adjuvant chemotherapy. Many assume that this is because the majority of DTCs are quiescent. Read More

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http://www.nature.com/articles/s41556-018-0267-0
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February 2019
8 Reads
19.679 Impact Factor

Multicolour single-molecule tracking of mRNA interactions with RNP granules.

Nat Cell Biol 2019 Feb 21;21(2):162-168. Epub 2019 Jan 21.

Department of Biochemistry, Colorado State University, Fort Collins, CO, USA.

Ribonucleoprotein (RNP) granules are non-membrane-bound organelles that have critical roles in the stress response, maternal messenger RNA storage, synaptic plasticity, tumour progression and neurodegeneration. However, the dynamics of their mRNA components within and near the granule surface remain poorly characterized, particularly in the context and timing of mRNAs exiting translation. Herein, we used multicolour single-molecule tracking to quantify the precise timing and kinetics of single mRNAs as they exit translation and enter RNP granules during stress. Read More

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http://www.nature.com/articles/s41556-018-0263-4
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6375083PMC
February 2019
12 Reads

Dynamics of mRNA entry into stress granules.

Nat Cell Biol 2019 Feb;21(2):116-117

Department of Molecular Biology and Genetics, Johns Hopkins University, Baltimore, MD, USA.

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http://dx.doi.org/10.1038/s41556-019-0278-5DOI Listing
February 2019
1 Read

Therapy resistance beyond cellular dormancy.

Nat Cell Biol 2019 Feb;21(2):117-119

Experimental Medicine and Therapy Research, University of Regensburg, Regensburg, Germany.

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http://dx.doi.org/10.1038/s41556-019-0276-7DOI Listing
February 2019
1 Read

An IRAK1-PIN1 signalling axis drives intrinsic tumour resistance to radiation therapy.

Nat Cell Biol 2019 Feb 21;21(2):203-213. Epub 2019 Jan 21.

Department of Medicine, Division of Hematology and Medical Oncology, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Drug-based strategies to overcome tumour resistance to radiotherapy (R-RT) remain limited by the single-agent toxicity of traditional radiosensitizers (for example, platinums) and a lack of targeted alternatives. In a screen for compounds that restore radiosensitivity in p53 mutant zebrafish while tolerated in non-irradiated wild-type animals, we identified the benzimidazole anthelmintic oxfendazole. Surprisingly, oxfendazole acts via the inhibition of IRAK1, a kinase thus far implicated in interleukin-1 receptor (IL-1R) and Toll-like receptor (TLR) immune responses. Read More

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http://www.nature.com/articles/s41556-018-0260-7
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February 2019
6 Reads

Author Correction: ZSCAN10 expression corrects the genomic instability of iPSCs from aged donors.

Nat Cell Biol 2019 Jan 14. Epub 2019 Jan 14.

Cancer Biology and Genetics Program, Center for Cell Engineering, Center for Stem Cell Biology, Memorial Sloan Kettering Cancer Center, Sloan Kettering Institute for Cancer Research, and Department of Cell and Developmental Biology, Weill Medical College of Cornell University, New York, New York, 10065, USA.

In the version of this Article originally published, Supplementary Fig. 6j showed incorrect values for the LS and AG4 glutathione samples, and Fig. 5c and Supplementary Fig. Read More

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http://www.nature.com/articles/s41556-018-0269-y
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January 2019
3 Reads
19.679 Impact Factor

Super-resolution microscopy demystified.

Nat Cell Biol 2019 Jan 2;21(1):72-84. Epub 2019 Jan 2.

Advanced Bio-Imaging Program, Bio&Nano Solutions‒LAB3BIO, Bielefeld, Germany.

Super-resolution microscopy (SRM) bypasses the diffraction limit, a physical barrier that restricts the optical resolution to roughly 250 nm and was previously thought to be impenetrable. SRM techniques allow the visualization of subcellular organization with unprecedented detail, but also confront biologists with the challenge of selecting the best-suited approach for their particular research question. Here, we provide guidance on how to use SRM techniques advantageously for investigating cellular structures and dynamics to promote new discoveries. Read More

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http://www.nature.com/articles/s41556-018-0251-8
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January 2019
8 Reads

Celebrating 20 years of cell biology.

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Nat Cell Biol 2019 Jan;21(1)

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http://dx.doi.org/10.1038/s41556-018-0262-5DOI Listing
January 2019

Specificities of secretion and uptake of exosomes and other extracellular vesicles for cell-to-cell communication.

Nat Cell Biol 2019 Jan 2;21(1):9-17. Epub 2019 Jan 2.

Institut Curie, PSL Research University, INSERM U932, Paris, France.

The ability of exosomes to transfer cargo from donor to acceptor cells, thereby triggering phenotypic changes in the latter, has generated substantial interest in the scientific community. However, the extent to which exosomes differ from other extracellular vesicles in terms of their biogenesis and functions remains ill-defined. Here, we discuss the current knowledge on the specificities of exosomes and other types of extracellular vesicles, and their roles as important agents of cell-to-cell communication. Read More

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http://www.nature.com/articles/s41556-018-0250-9
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http://dx.doi.org/10.1038/s41556-018-0250-9DOI Listing
January 2019
5 Reads

The diverse consequences of aneuploidy.

Nat Cell Biol 2019 Jan 2;21(1):54-62. Epub 2019 Jan 2.

Department of Molecular Genetics, TU Kaiserslautern, Kaiserslautern, Germany.

Aneuploidy, or imbalanced chromosome number, has profound effects on eukaryotic cells. In humans, aneuploidy is associated with various pathologies, including cancer, which suggests that it mediates a proliferative advantage under these conditions. Here, we discuss physiological changes triggered by aneuploidy, such as altered cell growth, transcriptional changes, proteotoxic stress, genomic instability and response to interferons, and how cancer cells adapt to the changing aneuploid genome. Read More

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http://dx.doi.org/10.1038/s41556-018-0243-8DOI Listing
January 2019

The dynamic nature of senescence in cancer.

Nat Cell Biol 2019 Jan 2;21(1):94-101. Epub 2019 Jan 2.

Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health; Medical Department of Hematology, Oncology and Tumor Immunology, Virchow Campus, and Molekulares Krebsforschungszentrum, Berlin, Germany.

Cellular senescence is implicated in physiological and pathological processes spanning development, wound healing, age-related decline in organ functions and cancer. Here, we discuss cell-autonomous and non-cell-autonomous properties of senescence in the context of tumour formation and anticancer therapy, and characterize these properties, such as reprogramming into stemness, tissue remodelling and immune crosstalk, as far more dynamic than suggested by the common view of senescence as an irreversible, static condition. Read More

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http://www.nature.com/articles/s41556-018-0249-2
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January 2019
14 Reads

Stem cell dynamics, migration and plasticity during wound healing.

Nat Cell Biol 2019 Jan 2;21(1):18-24. Epub 2019 Jan 2.

Laboratory of Stem Cells and Cancer, Université Libre de Bruxelles, Brussels, Belgium.

Tissue repair is critical for animal survival. The skin epidermis is particularly exposed to injuries, which necessitates rapid repair. The coordinated action of distinct epidermal stem cells recruited from various skin regions together with other cell types, including fibroblasts and immune cells, is required to ensure efficient and harmonious wound healing. Read More

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http://www.nature.com/articles/s41556-018-0237-6
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January 2019
9 Reads

Integrin activation by talin, kindlin and mechanical forces.

Nat Cell Biol 2019 Jan 2;21(1):25-31. Epub 2019 Jan 2.

Max Planck Institute of Biochemistry, Martinsried, Germany.

Integrins are the major family of adhesion molecules that mediate cell adhesion to the extracellular matrix. They are essential for embryonic development and influence numerous diseases, including inflammation, cancer cell invasion and metastasis. In this Perspective, we discuss the current understanding of how talin, kindlin and mechanical forces regulate integrin affinity and avidity, and how integrin inactivators function in this framework. Read More

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http://dx.doi.org/10.1038/s41556-018-0234-9DOI Listing
January 2019
1 Read

Haematopoiesis in the era of advanced single-cell technologies.

Nat Cell Biol 2019 Jan 2;21(1):2-8. Epub 2019 Jan 2.

MRC Molecular Haematology Unit, MRC Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford, UK.

The molecular and functional characterization of single cells at scale has emerged as a key driver to unravel tissue biology. Thus, it is important to understand the strengths and limitations of transcriptomic approaches, molecular barcoding and functional assays used to study cellular properties at the single-cell level. Here, we review recent relevant work from the haematopoietic system and discuss how to interpret and integrate data obtained with different technologies. Read More

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http://dx.doi.org/10.1038/s41556-018-0227-8DOI Listing
January 2019

Metabolism as a guiding force for immunity.

Nat Cell Biol 2019 Jan 2;21(1):85-93. Epub 2019 Jan 2.

Department of Genetics & Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA.

Recent studies indicate that cellular metabolism plays a key role in supporting immune cell maintenance and development. Here, we review how metabolism guides immune cell activation and differentiation to distinct cellular states, and how differential regulation of metabolism allows for context-dependent support during activation and lineage commitment. We discuss emerging principles of metabolic support of immune cell function in physiology and disease, as well as their general relevance to the field of cell biology. Read More

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http://dx.doi.org/10.1038/s41556-018-0217-xDOI Listing
January 2019

Turning back time with emerging rejuvenation strategies.

Nat Cell Biol 2019 Jan 2;21(1):32-43. Epub 2019 Jan 2.

Department of Genetics, Stanford University, Stanford, CA, USA.

Ageing is associated with the functional decline of all tissues and a striking increase in many diseases. Although ageing has long been considered a one-way street, strategies to delay and potentially even reverse the ageing process have recently been developed. Here, we review four emerging rejuvenation strategies-systemic factors, metabolic manipulations, senescent cell ablation and cellular reprogramming-and discuss their mechanisms of action, cellular targets, potential trade-offs and application to human ageing. Read More

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http://dx.doi.org/10.1038/s41556-018-0206-0DOI Listing
January 2019

Mesenchymal-epithelial transition in development and reprogramming.

Nat Cell Biol 2019 Jan 2;21(1):44-53. Epub 2019 Jan 2.

CAS Key Laboratory of Regenerative Biology, Guangdong Provincial Key Laboratory of Stem Cell and Regenerative Medicine, South China Institute for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.

During organogenesis, epithelial cells can give rise to mesenchymal cells through epithelial-mesenchymal transition. The reverse process, mesenchymal-epithelial transition (MET), can similarly generate epithelial cells. Transitions between epithelial and mesenchymal states are also critical for the induction of pluripotent stem cells from somatic cells. Read More

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http://dx.doi.org/10.1038/s41556-018-0195-zDOI Listing
January 2019

mTOR as a central hub of nutrient signalling and cell growth.

Nat Cell Biol 2019 Jan 2;21(1):63-71. Epub 2019 Jan 2.

Department of Pharmacology and Moores Cancer Center, University of California, San Diego, La Jolla, CA, USA.

The highly conserved protein kinase mechanistic target of rapamycin (mTOR; originally known as mammalian target of rapamycin) is a central cell growth regulator connecting cellular metabolism and growth with a wide range of environmental inputs as part of mTOR complex 1 (mTORC1) and mTORC2. In this Review, we introduce the landmark discoveries in the mTOR field, starting from the isolation of rapamycin to the molecular characterizations of key components of the mTORC signalling network with an emphasis on amino acid sensing, and discuss the perspectives of mTORC inhibitors in therapeutic applications. Read More

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http://www.nature.com/articles/s41556-018-0205-1
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January 2019
5 Reads

Non-redundant functions of EMT transcription factors.

Nat Cell Biol 2019 Jan 2;21(1):102-112. Epub 2019 Jan 2.

Department of Experimental Medicine 1, Nikolaus-Fiebiger-Center for Molecular Medicine, FAU University Erlangen-Nürnberg, Erlangen, Germany.

Epithelial-mesenchymal transition (EMT) is a crucial embryonic programme that is executed by various EMT transcription factors (EMT-TFs) and is aberrantly activated in cancer and other diseases. However, the causal role of EMT and EMT-TFs in different disease processes, especially cancer and metastasis, continues to be debated. In this Review, we identify and describe specific, non-redundant functions of the different EMT-TFs and discuss the reasons that may underlie disputes about EMT in cancer. Read More

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http://dx.doi.org/10.1038/s41556-018-0196-yDOI Listing
January 2019
2 Reads

Chromatin regulatory mechanisms and therapeutic opportunities in cancer.

Nat Cell Biol 2019 Feb 2;21(2):152-161. Epub 2019 Jan 2.

Department of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA.

Research over the past several decades has unmasked a major contribution of disrupted chromatin regulatory processes to human disease, particularly cancer. Advances in genome-wide technologies have highlighted frequent mutations in genes encoding chromatin-associated proteins, identified unexpected synthetic lethal opportunities and enabled increasingly comprehensive structural and functional dissection. Here, we review recent progress in our understanding of oncogenic mechanisms at each level of chromatin organization and regulation, and discuss new strategies towards therapeutic intervention. Read More

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http://dx.doi.org/10.1038/s41556-018-0258-1DOI Listing
February 2019

The lysosome as a cellular centre for signalling, metabolism and quality control.

Nat Cell Biol 2019 Feb 2;21(2):133-142. Epub 2019 Jan 2.

Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley, CA, USA.

Long known as terminal degradation stations, lysosomes have emerged as sophisticated signalling centres that govern cell growth, division and differentiation. Lysosomes interface physically and functionally with other organelles, and the master regulator mechanistic target of rapamycin complex 1 kinase is activated on lysosomes in response to nutrient and growth factor inputs. Lysosomes also enable autophagy, a 'self-eating' process essential for quality control and stress adaptation. Read More

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http://dx.doi.org/10.1038/s41556-018-0244-7DOI Listing
February 2019
1 Read

Intergenerational and transgenerational epigenetic inheritance in animals.

Nat Cell Biol 2019 Feb 2;21(2):143-151. Epub 2019 Jan 2.

Systems Biology Program, Centre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.

Animals transmit not only DNA but also other molecules, such as RNA, proteins and metabolites, to their progeny via gametes. It is currently unclear to what extent these molecules convey information between generations and whether this information changes according to their physiological state and environment. Here, we review recent work on the molecular mechanisms by which 'epigenetic' information is transmitted between generations over different timescales, and the importance of this information for development and physiology. Read More

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http://dx.doi.org/10.1038/s41556-018-0242-9DOI Listing
February 2019
2 Reads

Integrin trafficking in cells and tissues.

Nat Cell Biol 2019 Feb 2;21(2):122-132. Epub 2019 Jan 2.

Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland.

Cell adhesion to the extracellular matrix is fundamental to metazoan multicellularity and is accomplished primarily through the integrin family of cell-surface receptors. Integrins are internalized and enter the endocytic-exocytic pathway before being recycled back to the plasma membrane. The trafficking of this extensive protein family is regulated in multiple context-dependent ways to modulate integrin function in the cell. Read More

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http://dx.doi.org/10.1038/s41556-018-0223-zDOI Listing
February 2019

Chemotherapy elicits pro-metastatic extracellular vesicles in breast cancer models.

Nat Cell Biol 2019 Feb 31;21(2):190-202. Epub 2018 Dec 31.

Swiss Institute for Experimental Cancer Research (ISREC), School of Life Sciences, École Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.

Cytotoxic chemotherapy is an effective treatment for invasive breast cancer. However, experimental studies in mice also suggest that chemotherapy has pro-metastatic effects. Primary tumours release extracellular vesicles (EVs), including exosomes, that can facilitate the seeding and growth of metastatic cancer cells in distant organs, but the effects of chemotherapy on tumour-derived EVs remain unclear. Read More

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http://dx.doi.org/10.1038/s41556-018-0256-3DOI Listing
February 2019

Direct generation of human naive induced pluripotent stem cells from somatic cells in microfluidics.

Nat Cell Biol 2019 Feb 31;21(2):275-286. Epub 2018 Dec 31.

Department of Molecular Medicine, Medical School, University of Padova, Padua, Italy.

Induced pluripotent stem cells (iPSCs) are generated via the expression of the transcription factors OCT4 (also known as POU5F1), SOX2, KLF4 and cMYC (OSKM) in somatic cells. In contrast to murine naive iPSCs, conventional human iPSCs are in a more developmentally advanced state called primed pluripotency. Here, we report that human naive iPSCs (niPSCs) can be generated directly from fewer than 1,000 primary human somatic cells, without requiring stable genetic manipulation, via the delivery of modified messenger RNAs using microfluidics. Read More

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http://dx.doi.org/10.1038/s41556-018-0254-5DOI Listing
February 2019

Retraction Note: NF-κB activation impairs somatic cell reprogramming in ageing.

Nat Cell Biol 2018 Dec 17. Epub 2018 Dec 17.

Departamento de Bioquímica y Biología Molecular, Facultad de Medicina, Instituto Universitario de Oncología, Universidad de Oviedo, 33006, Oviedo, Spain.

We, the authors, are retracting this Article due to issues that have come to our attention regarding data availability, data description and figure assembly. Specifically, original numerical data are not available for the majority of the graphs presented in the paper. Although original data were available for most EMSA and immunoblot experiments, those corresponding to the published EMSA data of Supplementary Fig. Read More

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http://www.nature.com/articles/s41556-018-0259-0
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December 2018
9 Reads

Memory of ancestral mitochondrial stress.

Nat Cell Biol 2018 Dec 17. Epub 2018 Dec 17.

Centre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.

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http://dx.doi.org/10.1038/s41556-018-0255-4DOI Listing
December 2018
19.679 Impact Factor

Fluidization-mediated tissue spreading by mitotic cell rounding and non-canonical Wnt signalling.

Nat Cell Biol 2019 Feb 17;21(2):169-178. Epub 2018 Dec 17.

Institute of Science and Technology Austria, Klosterneuburg, Austria.

Tissue morphogenesis is driven by mechanical forces that elicit changes in cell size, shape and motion. The extent by which forces deform tissues critically depends on the rheological properties of the recipient tissue. Yet, whether and how dynamic changes in tissue rheology affect tissue morphogenesis and how they are regulated within the developing organism remain unclear. Read More

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http://dx.doi.org/10.1038/s41556-018-0247-4DOI Listing
February 2019

Author Correction: Pericyte-like spreading by disseminated cancer cells activates YAP and MRTF for metastatic colonization.

Nat Cell Biol 2018 Dec 12. Epub 2018 Dec 12.

Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

In the version of this Article originally published, the authors inadvertently included the term 'pericytic mimicry' in relation to ref. 54. This has now been corrected by inserting an additional reference at position 51 and amending the text in the Discussion relating to 'pericytic mimicry', ref. Read More

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http://www.nature.com/articles/s41556-018-0257-2
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http://dx.doi.org/10.1038/s41556-018-0257-2DOI Listing
December 2018
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A chromatin integration labelling method enables epigenomic profiling with lower input.

Nat Cell Biol 2019 Feb 10;21(2):287-296. Epub 2018 Dec 10.

Division of Transcriptomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.

Chromatin plays a crucial role in gene regulation, and chromatin immunoprecipitation followed by sequencing (ChIP-seq) has been the standard technique for examining protein-DNA interactions across the whole genome. However, it is difficult to obtain epigenomic information from limited numbers of cells by ChIP-seq because of sample loss during chromatin preparation and inefficient immunoprecipitation. In this study, we established an immunoprecipitation-free epigenomic profiling method named chromatin integration labelling (ChIL), which enables the amplification of genomic sequences closely associated with the target molecules before cell lysis. Read More

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http://dx.doi.org/10.1038/s41556-018-0248-3DOI Listing
February 2019

N6-methyldeoxyadenine is a transgenerational epigenetic signal for mitochondrial stress adaptation.

Nat Cell Biol 2018 Dec 3. Epub 2018 Dec 3.

State Key Laboratory of Membrane Biology, Institute of Molecular Medicine, Beijing Key Laboratory of Cardiometabolic Molecular Medicine and Peking-Tsinghua Center for Life Sciences, Peking University, Beijing, China.

N6-methyldeoxyadenine (6mA), a major type of DNA methylation in bacteria, represents a part of restriction-modification systems to discriminate host genome from invader DNA. With the recent advent of more sensitive detection techniques, 6mA has also been detected in some eukaryotes. However, the physiological function of this epigenetic mark in eukaryotes remains elusive. Read More

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http://dx.doi.org/10.1038/s41556-018-0238-5DOI Listing
December 2018
3 Reads

Tumour heterogeneity and metastasis at single-cell resolution.

Nat Cell Biol 2018 Dec 26;20(12):1349-1360. Epub 2018 Nov 26.

Department of Anatomy, and Helen Diller Comprehensive Cancer Center, University of California, San Francisco, CA, USA.

Tumours comprise a heterogeneous collection of cells with distinct genetic and phenotypic properties that can differentially promote progression, metastasis and drug resistance. Emerging single-cell technologies provide a new opportunity to profile individual cells within tumours and investigate what roles they play in these processes. This Review discusses key technological considerations for single-cell studies in cancer, new findings using single-cell technologies and critical open questions for future applications. Read More

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http://www.nature.com/articles/s41556-018-0236-7
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http://dx.doi.org/10.1038/s41556-018-0236-7DOI Listing
December 2018
8 Reads

Social media for scientists.

Authors:

Nat Cell Biol 2018 Dec;20(12):1329

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http://dx.doi.org/10.1038/s41556-018-0253-6DOI Listing
December 2018
1 Read

Autophagy and the cell biology of age-related disease.

Nat Cell Biol 2018 Dec 26;20(12):1338-1348. Epub 2018 Nov 26.

Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, USA.

Macroautophagy (autophagy) is a conserved lysosomal degradation process essential for cellular homeostasis and adaption to stress. Accumulating evidence indicates that autophagy declines with age and that impaired autophagy predisposes individuals to age-related diseases, whereas interventions that stimulate autophagy often promote longevity. In this Review, we examine how the autophagy pathway restricts cellular damage and degeneration, and the impact of these functions towards tissue health and organismal lifespan. Read More

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http://dx.doi.org/10.1038/s41556-018-0235-8DOI Listing
December 2018
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Targeting BAF-perturbed cancers.

Nat Cell Biol 2018 Dec;20(12):1332-1333

Stowers Institute for Medical Research, Kansas City, MO, USA.

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http://dx.doi.org/10.1038/s41556-018-0246-5DOI Listing
December 2018
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TBK1 and IKKε restrain cell death.

Nat Cell Biol 2018 Dec;20(12):1330-1331

Department of Physiological Chemistry, Genentech, South San Francisco, CA, USA.

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http://dx.doi.org/10.1038/s41556-018-0239-4DOI Listing
December 2018
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Loss of G9a preserves mutation patterns but increases chromatin accessibility, genomic instability and aggressiveness in skin tumours.

Nat Cell Biol 2018 Dec 19;20(12):1400-1409. Epub 2018 Nov 19.

Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.

Mutations in, and the altered expression of, epigenetic modifiers are pervasive in human tumours, making epigenetic factors attractive antitumour targets. The open-versus-closed chromatin state within the cells-of-origin of cancer correlates with the uneven distribution of mutations. However, the long-term effect of targeting epigenetic modifiers on mutability in patients with cancer is unclear. Read More

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http://www.nature.com/articles/s41556-018-0233-x
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http://dx.doi.org/10.1038/s41556-018-0233-xDOI Listing
December 2018
12 Reads