4,328 results match your criteria Nature Cell Biology [Journal]


U2AF1 mutations induce oncogenic IRAK4 isoforms and activate innate immune pathways in myeloid malignancies.

Nat Cell Biol 2019 Apr 22. Epub 2019 Apr 22.

Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.

Spliceosome mutations are common in myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML), but the oncogenic changes due to these mutations have not been identified. Here a global analysis of exon usage in AML samples revealed distinct molecular subsets containing alternative spliced isoforms of inflammatory and immune genes. Interleukin-1 receptor-associated kinase 4 (IRAK4) was the dominant alternatively spliced isoform in MDS and AML and is characterized by a longer isoform that retains exon 4, which encodes IRAK4-long (IRAK4-L), a protein that assembles with the myddosome, results in maximal activation of nuclear factor kappa-light-chain-enhancer of B cells (NF-κB) and is essential for leukaemic cell function. Read More

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http://dx.doi.org/10.1038/s41556-019-0314-5DOI Listing

Splicing the innate immune signalling in leukaemia.

Nat Cell Biol 2019 Apr 22. Epub 2019 Apr 22.

Department of Pathology and Laura & Isaac Perlmutter Cancer Center, NYU School of Medicine, New York, NY, USA.

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http://dx.doi.org/10.1038/s41556-019-0323-4DOI Listing

Ultrastructure and dynamics of the actin-myosin II cytoskeleton during mitochondrial fission.

Nat Cell Biol 2019 Apr 15. Epub 2019 Apr 15.

Department of Biology, University of Pennsylvania, Philadelphia, PA, USA.

Mitochondrial fission involves the preconstriction of an organelle followed by scission by dynamin-related protein Drp1. Preconstriction is facilitated by actin and non-muscle myosin II through a mechanism that remains unclear, largely due to the unknown cytoskeletal ultrastructure at mitochondrial constrictions. Here, using platinum replica electron microscopy, we show that mitochondria in cells are embedded in an interstitial cytoskeletal network that contains abundant unbranched actin filaments. Read More

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http://dx.doi.org/10.1038/s41556-019-0313-6DOI Listing

Bone vascular niche E-selectin induces mesenchymal-epithelial transition and Wnt activation in cancer cells to promote bone metastasis.

Nat Cell Biol 2019 Apr 15. Epub 2019 Apr 15.

Department of Molecular Biology, Princeton University, Princeton, NJ, USA.

How disseminated tumour cells engage specific stromal components in distant organs for survival and outgrowth is a critical but poorly understood step of the metastatic cascade. Previous studies have demonstrated the importance of the epithelial-mesenchymal transition in promoting the cancer stem cell properties needed for metastasis initiation, whereas the reverse process of mesenchymal-epithelial transition is required for metastatic outgrowth. Here we report that this paradoxical requirement for the simultaneous induction of both mesenchymal-epithelial transition and cancer stem cell traits in disseminated tumour cells is provided by bone vascular niche E-selectin, whose direct binding to cancer cells promotes bone metastasis by inducing mesenchymal-epithelial transition and activating Wnt signalling. Read More

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http://dx.doi.org/10.1038/s41556-019-0309-2DOI Listing

Engineering a haematopoietic stem cell niche by revitalizing mesenchymal stromal cells.

Nat Cell Biol 2019 Apr 15. Epub 2019 Apr 15.

Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Albert Einstein College of Medicine, Bronx, NY, USA.

Haematopoietic stem cells (HSCs) are maintained by bone marrow niches in vivo, but the ability of niche cells to maintain HSCs ex vivo is markedly diminished. Expression of niche factors by Nestin-GFP mesenchymal-derived stromal cells (MSCs) is downregulated upon culture, suggesting that transcriptional rewiring may contribute to this reduced HSC maintenance potential. Using an RNA sequencing screen, we identified five genes encoding transcription factors (Klf7, Ostf1, Xbp1, Irf3 and Irf7) that restored HSC niche function in cultured bone marrow-derived MSCs. Read More

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http://www.nature.com/articles/s41556-019-0308-3
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http://dx.doi.org/10.1038/s41556-019-0308-3DOI Listing
April 2019
4 Reads

Author Correction: A lipid-based partitioning mechanism for selective incorporation of proteins into membranes of HIV particles.

Nat Cell Biol 2019 Apr 10. Epub 2019 Apr 10.

Howard Hughes Medical Institute, Janelia Research Campus, Ashburn, VA, USA.

In the version of this article originally published, the name of co-author Marc C. Johnson was missing the middle initial. The middle initial 'C. Read More

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http://dx.doi.org/10.1038/s41556-019-0327-0DOI Listing

A complex containing lysine-acetylated actin inhibits the formin INF2.

Nat Cell Biol 2019 Apr 8. Epub 2019 Apr 8.

Department of Biochemistry and Cell Biology, Geisel School of Medicine at Dartmouth, Hanover, NH, USA.

Inverted formin 2 (INF2) is a member of the formin family of actin assembly factors. Dominant missense mutations in INF2 are linked to two diseases: focal segmental glomerulosclerosis, a kidney disease, and Charcot-Marie-Tooth disease, a neuropathy. All of the disease mutations map to the autoinhibitory diaphanous inhibitory domain. Read More

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http://dx.doi.org/10.1038/s41556-019-0307-4DOI Listing
April 2019
1 Read

ALOX12 is required for p53-mediated tumour suppression through a distinct ferroptosis pathway.

Nat Cell Biol 2019 Apr 8. Epub 2019 Apr 8.

Institute for Cancer Genetics, and Department of Pathology and Cell Biology, and Herbert Irving Comprehensive Cancer Center, College of Physicians and Surgeons, Columbia University, New York, NY, USA.

It is well established that ferroptosis is primarily controlled by glutathione peroxidase 4 (GPX4). Surprisingly, we observed that p53 activation modulates ferroptotic responses without apparent effects on GPX4 function. Instead, ALOX12 inactivation diminishes p53-mediated ferroptosis induced by reactive oxygen species stress and abrogates p53-dependent inhibition of tumour growth in xenograft models, suggesting that ALOX12 is critical for p53-mediated ferroptosis. Read More

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http://www.nature.com/articles/s41556-019-0305-6
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http://dx.doi.org/10.1038/s41556-019-0305-6DOI Listing
April 2019
7 Reads

How membrane physics rules the HIV envelope.

Nat Cell Biol 2019 Apr;21(4):413-415

Laboratoire Physico Chimie Curie, Institut Curie, PSL Research University, CNRS UMR168, Paris, France.

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http://www.nature.com/articles/s41556-019-0312-7
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http://dx.doi.org/10.1038/s41556-019-0312-7DOI Listing
April 2019
3 Reads

Endothelial proteolytic activity and interaction with non-resorbing osteoclasts mediate bone elongation.

Nat Cell Biol 2019 04 1;21(4):430-441. Epub 2019 Apr 1.

Institute of Clinical Sciences, Imperial College London, London, UK.

Growth plate cartilage contributes to the generation of a large variety of shapes and sizes of skeletal elements in the mammalian system. The removal of cartilage and how this process regulates bone shape are not well understood. Here we identify a non-bone-resorbing osteoclast subtype termed vessel-associated osteoclast (VAO). Read More

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http://www.nature.com/articles/s41556-019-0304-7
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http://dx.doi.org/10.1038/s41556-019-0304-7DOI Listing
April 2019
4 Reads

Extracellular vesicle-packaged HIF-1α-stabilizing lncRNA from tumour-associated macrophages regulates aerobic glycolysis of breast cancer cells.

Nat Cell Biol 2019 04 1;21(4):498-510. Epub 2019 Apr 1.

Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.

Metabolic reprogramming is a hallmark of cancer. Here, we demonstrate that tumour-associated macrophages (TAMs) enhance the aerobic glycolysis and apoptotic resistance of breast cancer cells via the extracellular vesicle (EV) transmission of a myeloid-specific lncRNA, HIF-1α-stabilizing long noncoding RNA (HISLA). Mechanistically, HISLA blocks the interaction of PHD2 and HIF-1α to inhibit the hydroxylation and degradation of HIF-1α. Read More

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http://dx.doi.org/10.1038/s41556-019-0299-0DOI Listing

An opsin 5-dopamine pathway mediates light-dependent vascular development in the eye.

Nat Cell Biol 2019 04 1;21(4):420-429. Epub 2019 Apr 1.

The Visual Systems Group, Abrahamson Pediatric Eye Institute, Division of Pediatric Ophthalmology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.

During mouse postnatal eye development, the embryonic hyaloid vascular network regresses from the vitreous as an adaption for high-acuity vision. This process occurs with precisely controlled timing. Here, we show that opsin 5 (OPN5; also known as neuropsin)-dependent retinal light responses regulate vascular development in the postnatal eye. Read More

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http://dx.doi.org/10.1038/s41556-019-0301-xDOI Listing
April 2019
2 Reads

A lipid-based partitioning mechanism for selective incorporation of proteins into membranes of HIV particles.

Nat Cell Biol 2019 04 1;21(4):452-461. Epub 2019 Apr 1.

Howard Hughes Medical Institute, Janelia Research Campus, Ashburn, VA, USA.

Particles that bud off from the cell surface, including viruses and microvesicles, typically have a unique membrane protein composition distinct from that of the originating plasma membrane. This selective protein composition enables viruses to evade the immune response and infect other cells. But how membrane proteins sort into budding viruses such as human immunodeficiency virus (HIV) remains unclear. Read More

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http://dx.doi.org/10.1038/s41556-019-0300-yDOI Listing
April 2019
1 Read

MicroRNAs tame CRISPR-Cas9.

Nat Cell Biol 2019 Apr;21(4):416-417

RNA Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA, USA.

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http://www.nature.com/articles/s41556-019-0302-9
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http://dx.doi.org/10.1038/s41556-019-0302-9DOI Listing
April 2019
4 Reads

Endothelial cells revealed as chondroclasts.

Nat Cell Biol 2019 Apr;21(4):417-419

Mount Sinai Bone Program, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

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http://dx.doi.org/10.1038/s41556-019-0306-5DOI Listing
April 2019
1 Read

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

Nat Cell Biol 2019 Mar 26. Epub 2019 Mar 26.

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

In the version of this article originally published, the Gene Expression Omnibus (GEO) accession number listed in the data availability section was incorrectly given as GSE10979 instead of GSE109795. The sentence should read "RNA-seq data that support the findings of this study have been deposited in the Gene Expression Omnibus (GEO) under accession code GSE109795," and the code should link to https://www.ncbi. Read More

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http://dx.doi.org/10.1038/s41556-019-0316-3DOI Listing

A nuclear phosphoinositide kinase complex regulates p53.

Nat Cell Biol 2019 04 18;21(4):462-475. Epub 2019 Mar 18.

University of Wisconsin-Madison, School of Medicine and Public Health, Madison, WI, USA.

The tumour suppressor p53 (encoded by TP53) protects the genome against cellular stress and is frequently mutated in cancer. Mutant p53 acquires gain-of-function oncogenic activities that are dependent on its enhanced stability. However, the mechanisms by which nuclear p53 is stabilized are poorly understood. Read More

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http://dx.doi.org/10.1038/s41556-019-0297-2DOI Listing
April 2019
1 Read
19.679 Impact Factor

Mitochondrial protein-induced stress triggers a global adaptive transcriptional programme.

Nat Cell Biol 2019 04 18;21(4):442-451. Epub 2019 Mar 18.

Cell Biology, University of Kaiserslautern, Kaiserslautern, Germany.

The cytosolic accumulation of mitochondrial precursors is hazardous to cellular fitness and is associated with a number of diseases. However, it is not observed under physiological conditions. Individual mechanisms that allow cells to avoid cytosolic accumulation of mitochondrial precursors have recently been discovered, but their interplay and regulation remain elusive. Read More

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http://dx.doi.org/10.1038/s41556-019-0294-5DOI Listing

Therapeutic targeting of macrophages enhances chemotherapy efficacy by unleashing type I interferon response.

Nat Cell Biol 2019 04 18;21(4):511-521. Epub 2019 Mar 18.

Division of Tumor Biology & Immunology, Oncode Institute, Netherlands Cancer Institute, Amsterdam, The Netherlands.

Recent studies have revealed a role for macrophages and neutrophils in limiting chemotherapy efficacy; however, the mechanisms underlying the therapeutic benefit of myeloid-targeting agents in combination with chemotherapy are incompletely understood. Here, we show that targeting tumour-associated macrophages by colony-stimulating factor-1 receptor (CSF-1R) blockade in the K14cre;Cdh1;Trp53 transgenic mouse model for breast cancer stimulates intratumoural type I interferon (IFN) signalling, which enhances the anticancer efficacy of platinum-based chemotherapeutics. Notably, anti-CSF-1R treatment also increased intratumoural expression of type I IFN-stimulated genes in patients with cancer, confirming that CSF-1R blockade is a powerful strategy to trigger an intratumoural type I IFN response. Read More

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http://www.nature.com/articles/s41556-019-0298-1
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http://dx.doi.org/10.1038/s41556-019-0298-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6451630PMC
April 2019
10 Reads

Macrophage interference on chemotherapy.

Nat Cell Biol 2019 Apr;21(4):411-412

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

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http://dx.doi.org/10.1038/s41556-019-0303-8DOI Listing
April 2019
2 Reads

AMPK-mediated activation of MCU stimulates mitochondrial Ca entry to promote mitotic progression.

Nat Cell Biol 2019 04 11;21(4):476-486. Epub 2019 Mar 11.

State Key Laboratory of Toxicology and Medical Countermeasures, Institute of Pharmacology and Toxicology, National Center of Biomedical Analysis, Beijing, China.

The capacity of cells to alter bioenergetics in response to the demands of various biological processes is essential for normal physiology. The coordination of energy sensing and production with highly energy-demanding cellular processes, such as cell division, is poorly understood. Here, we show that a cell cycle-dependent mitochondrial Ca transient connects energy sensing to mitochondrial activity for mitotic progression. Read More

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http://dx.doi.org/10.1038/s41556-019-0296-3DOI Listing
April 2019
4 Reads

Author Correction: The Rho GTPase Rnd1 suppresses mammary tumorigenesis and EMT by restraining Ras-MAPK signalling.

Nat Cell Biol 2019 04;21(4):534

Cell Biology Program, Sloan-Kettering Institute for Cancer Research, Memorial Sloan-Kettering Cancer Center, New York, New York, 10065, USA.

In the version of this Article originally published the same blot was inadvertently presented as both p-Rb and Cyclin A in Fig. 2a. This blot corresponds to the p-Rb panel, as can be seen in the unprocessed version of these blots in Supplementary Fig. Read More

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http://dx.doi.org/10.1038/s41556-019-0288-3DOI Listing
April 2019
4 Reads

Author Correction: Bmi1 is essential in Twist1-induced epithelial-mesenchymal transition.

Nat Cell Biol 2019 04;21(4):533

Genomic Research Center, Taipei Veterans General Hospital, Taipei, 112, Taiwan.

In the version of Supplementary Fig. 3c originally published with this Article, the authors mistakenly duplicated a blot from Supplementary Fig. 3b. Read More

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http://dx.doi.org/10.1038/s41556-019-0290-9DOI Listing
April 2019
4 Reads

Epithelial polarity limits EMT.

Nat Cell Biol 2019 Mar;21(3):299-300

Department of Dermatology, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Center for Molecular Medicine Cologne, University of Cologne, Cologne, Germany.

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http://dx.doi.org/10.1038/s41556-019-0284-7DOI Listing
March 2019
5 Reads

Author Correction: MicroRNA-146a directs the symmetric division of Snail-dominant colorectal cancer stem cells.

Nat Cell Biol 2019 Feb 28. Epub 2019 Feb 28.

Institute of Clinical Medicine, National Yang-Ming University, Taipei, 11221, Taiwan.

In the version of Supplementary Fig. 6c originally published with this Article, the immunoprecipitation (IP) and immunoblotting (IB) tags in the top panel were mislabelled. In addition, in Supplementary Fig. Read More

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http://dx.doi.org/10.1038/s41556-019-0286-5DOI Listing
February 2019
4 Reads

Author Correction: Per2 induction limits lymphoid-biased haematopoietic stem cells and lymphopoiesis in the context of DNA damage and ageing.

Nat Cell Biol 2019 Feb 26. Epub 2019 Feb 26.

Research Group on Stem Cell Aging, Leibniz Institute on Aging - Fritz Lipmann Institute (FLI), Beutenbergstr. 11, 07745, Jena, Germany.

In the version of this Article originally published, the authors mistakenly used the same images for the Fig. 2d Per upper Merge, DAPI and p-RPA2 (Ser33), and Fig. 3e upper 2 months, WT Per2 DAPI and Merge panels. Read More

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http://dx.doi.org/10.1038/s41556-019-0279-4DOI Listing
February 2019
3 Reads

53BP1 nuclear bodies enforce replication timing at under-replicated DNA to limit heritable DNA damage.

Nat Cell Biol 2019 04 25;21(4):487-497. Epub 2019 Feb 25.

Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.

Failure to complete DNA replication is a stochastic by-product of genome doubling in almost every cell cycle. During mitosis, under-replicated DNA (UR-DNA) is converted into DNA lesions, which are inherited by daughter cells and sequestered in 53BP1 nuclear bodies (53BP1-NBs). The fate of such cells remains unknown. Read More

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http://www.nature.com/articles/s41556-019-0293-6
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http://dx.doi.org/10.1038/s41556-019-0293-6DOI Listing
April 2019
3 Reads

Apical-basal polarity inhibits epithelial-mesenchymal transition and tumour metastasis by PAR-complex-mediated SNAI1 degradation.

Nat Cell Biol 2019 03 25;21(3):359-371. Epub 2019 Feb 25.

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

Loss of apical-basal polarity and activation of epithelial-mesenchymal transition (EMT) both contribute to carcinoma progression and metastasis. Here, we report that apical-basal polarity inhibits EMT to suppress metastatic dissemination. Using mouse and human epithelial three-dimensional organoid cultures, we show that the PAR-atypical protein kinase C (aPKC) polarity complex inhibits EMT and invasion by promoting degradation of the SNAIL family protein SNAI1. Read More

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http://dx.doi.org/10.1038/s41556-019-0291-8DOI Listing
March 2019
19.679 Impact Factor

Ubiquilins regulate autophagic flux through mTOR signalling and lysosomal acidification.

Nat Cell Biol 2019 03 25;21(3):384-396. Epub 2019 Feb 25.

Program in Developmental Biology, Baylor College of Medicine (BCM), Houston, TX, USA.

Although the aetiology of amyotrophic lateral sclerosis (ALS) remains poorly understood, impaired proteostasis is a common feature of different forms of ALS. Mutations in genes encoding ubiquilins, UBQLN2 and UBQLN4, cause familial ALS. The role of ubiquilins in proteasomal degradation is well established, but their role in autophagy-lysosomal clearance is poorly defined. Read More

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http://dx.doi.org/10.1038/s41556-019-0281-xDOI Listing
March 2019
2 Reads

A microRNA-inducible CRISPR-Cas9 platform serves as a microRNA sensor and cell-type-specific genome regulation tool.

Nat Cell Biol 2019 04 25;21(4):522-530. Epub 2019 Feb 25.

Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Institute of Molecular Medicine, Peking University, Beijing, China.

microRNAs (miRNAs) are small noncoding RNAs that play important regulatory roles in plants, animals and viruses. Measuring miRNA activity in vivo remains a big challenge. Here, using an miRNA-mediated single guide RNA (sgRNA)-releasing strategy and dCas9-VPR to drive a transgene red fluorescent protein, we create an miRNA sensor that can faithfully measure miRNA activity at cellular levels and use it to monitor differentiation status of stem cells. Read More

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http://dx.doi.org/10.1038/s41556-019-0292-7DOI Listing
April 2019
3 Reads

H4K20me0 recognition by BRCA1-BARD1 directs homologous recombination to sister chromatids.

Nat Cell Biol 2019 03 25;21(3):311-318. Epub 2019 Feb 25.

Biotech Research and Innovation Centre, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.

Genotoxic DNA double-strand breaks (DSBs) can be repaired by error-free homologous recombination (HR) or mutagenic non-homologous end-joining. HR supresses tumorigenesis, but is restricted to the S and G2 phases of the cell cycle when a sister chromatid is present. Breast cancer type 1 susceptibility protein (BRCA1) promotes HR by antagonizing the anti-resection factor TP53-binding protein 1(53BP1) (refs. Read More

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http://dx.doi.org/10.1038/s41556-019-0282-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6420097PMC
March 2019
1 Read

Author Correction: Sin1 phosphorylation impairs mTORC2 complex integrity and inhibits downstream Akt signalling to suppress tumorigenesis.

Nat Cell Biol 2019 Feb 19. Epub 2019 Feb 19.

Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, 02215, USA.

In the version of this Article originally published, the labels for Rictor and mTOR in the whole cell lysate (WCL) blots were swapped in Fig. 3b and the mTOR blot was placed upside down. Unprocessed blots of mTOR were also missing from Supplementary Fig. Read More

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http://dx.doi.org/10.1038/s41556-019-0280-yDOI Listing
February 2019
1 Read

Distinct functions of ATG16L1 isoforms in membrane binding and LC3B lipidation in autophagy-related processes.

Nat Cell Biol 2019 03 18;21(3):372-383. Epub 2019 Feb 18.

Department of Molecular Medicine, Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Oslo, Norway.

Covalent modification of LC3 and GABARAP proteins to phosphatidylethanolamine in the double-membrane phagophore is a key event in the early phase of macroautophagy, but can also occur on single-membrane structures. In both cases this involves transfer of LC3/GABARAP from ATG3 to phosphatidylethanolamine at the target membrane. Here we have purified the full-length human ATG12-5-ATG16L1 complex and show its essential role in LC3B/GABARAP lipidation in vitro. Read More

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http://dx.doi.org/10.1038/s41556-019-0274-9DOI Listing
March 2019
70 Reads
19.679 Impact Factor

IRE1α maintains HSC stemness under ER-stress.

Nat Cell Biol 2019 Mar;21(3):297-298

Department of Medicine V, Hematology, Oncology and Rheumatology, University Hospital Heidelberg, Heidelberg, Germany.

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http://dx.doi.org/10.1038/s41556-019-0295-4DOI Listing

Adaptive endoplasmic reticulum stress signalling via IRE1α-XBP1 preserves self-renewal of haematopoietic and pre-leukaemic stem cells.

Nat Cell Biol 2019 03 18;21(3):328-337. Epub 2019 Feb 18.

Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.

Over their lifetime, long-term haematopoietic stem cells (HSC) are exposed to a variety of stress conditions that they must endure. Many stresses, such as infection/inflammation, reactive oxygen species, nutritional deprivation and hypoxia, activate unfolded protein response signalling, which induces either adaptive changes to resolve the stress or apoptosis to clear the damaged cell. Whether unfolded-protein-response signalling plays any role in HSC regulation remains to be established. Read More

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http://dx.doi.org/10.1038/s41556-019-0285-6DOI Listing

NAD metabolism governs the proinflammatory senescence-associated secretome.

Nat Cell Biol 2019 03 18;21(3):397-407. Epub 2019 Feb 18.

Gene Expression and Regulation Program, The Wistar Institute, Philadelphia, PA, USA.

Cellular senescence is a stable growth arrest that is implicated in tissue ageing and cancer. Senescent cells are characterized by an upregulation of proinflammatory cytokines, which is termed the senescence-associated secretory phenotype (SASP). NAD metabolism influences both tissue ageing and cancer. Read More

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http://dx.doi.org/10.1038/s41556-019-0287-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6448588PMC
March 2019
2 Reads

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

Nat Cell Biol 2019 03 11;21(3):305-310. 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
March 2019
7 Reads
19.679 Impact Factor

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

Nat Cell Biol 2019 03 11;21(3):348-358. 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
March 2019
11 Reads

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 Mar;21(3):408-409

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
March 2019
6 Reads

Golgi mechanics controls lipid metabolism.

Nat Cell Biol 2019 Mar;21(3):301-302

Institut Necker-Enfants Malades, Paris, France.

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

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

Nat Cell Biol 2019 03 4;21(3):338-347. 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
March 2019
9 Reads

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

Nat Cell Biol 2019 02 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://www.nature.com/articles/s41556-018-0271-4
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http://dx.doi.org/10.1038/s41556-018-0271-4DOI Listing
February 2019
7 Reads

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 02 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
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6414065PMC
February 2019
3 Reads

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

Nat Cell Biol 2019 02 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 02 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 02 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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http://dx.doi.org/10.1038/s41556-018-0264-3DOI Listing
February 2019
13 Reads

Targeting the perivascular niche sensitizes disseminated tumour cells to chemotherapy.

Nat Cell Biol 2019 02 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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http://dx.doi.org/10.1038/s41556-018-0267-0DOI Listing
February 2019
22 Reads
19.679 Impact Factor