Journal Cover Nature Communications
  [SJR: 6.539]   [H-I: 114]   [216 followers]  Follow
    
  This is an Open Access Journal Open Access journal
   ISSN (Online) 2041-1723
   Published by NPG Homepage  [135 journals]
  • Loss of microRNA-128 promotes cardiomyocyte proliferation and heart
           regeneration
    • Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration

      Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration, Published online: 16 February 2018; doi:10.1038/s41467-018-03019-z

      During early postnatal development in mammals, cardiomyocytes exit the cell cycle, losing their regenerative capacity. Here the authors show that, following myocardial infarction, loss of microRNA-128 promotes cardiomyocyte proliferation and cardiac regeneration in adult mice partly via enhancing the expression of the chromatin modifier SUZ12.Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration, Published online: 2018-02-16; doi:10.1038/s41467-018-03019-z2018-02-16
      DOI: 10.1038/s41467-018-03019-z
       
  • Author Correction: Uplift of the central transantarctic mountains
    • Author Correction: Uplift of the central transantarctic mountains

      Author Correction: Uplift of the central transantarctic mountains, Published online: 16 February 2018; doi:10.1038/s41467-018-03349-y

      Author Correction: Uplift of the central transantarctic mountainsAuthor Correction: Uplift of the central transantarctic mountains, Published online: 2018-02-16; doi:10.1038/s41467-018-03349-y2018-02-16
      DOI: 10.1038/s41467-018-03349-y
       
  • Chemisorption of polysulfides through redox reactions with organic
           molecules for lithium–sulfur batteries
    • Chemisorption of polysulfides through redox reactions with organic molecules for lithium–sulfur batteries

      Chemisorption of polysulfides through redox reactions with organic molecules for lithium–sulfur batteries, Published online: 16 February 2018; doi:10.1038/s41467-018-03116-z

      Novel cathode design holds the key to enabling high performance lithium-sulfur batteries. Here the authors utilize anthraquinone to chemically stabilize polysulfides, revealing that the keto groups of anthraquinone play a critical role in forming strong Lewis acid-based chemical bonding.Chemisorption of polysulfides through redox reactions with organic molecules for lithium–sulfur batteries, Published online: 2018-02-16; doi:10.1038/s41467-018-03116-z2018-02-16
      DOI: 10.1038/s41467-018-03116-z
       
  • Host defense against oral microbiota by bone-damaging T cells
    • Host defense against oral microbiota by bone-damaging T cells

      Host defense against oral microbiota by bone-damaging T cells, Published online: 16 February 2018; doi:10.1038/s41467-018-03147-6

      IL-17-producing T cells are protective against infection, but the authors of this article previously showed that these cells also contribute to inflammatory bone destruction. Here they show in the context of periodontitis that microbiota-driven Th17-mediated bone destruction may actually be a physiological rather than a pathological process, as associated tooth loss prevents dissemination of oral bacteria.Host defense against oral microbiota by bone-damaging T cells, Published online: 2018-02-16; doi:10.1038/s41467-018-03147-62018-02-16
      DOI: 10.1038/s41467-018-03147-6
       
  • Identifying noncoding risk variants using disease-relevant gene regulatory
           networks
    • Identifying noncoding risk variants using disease-relevant gene regulatory networks

      Identifying noncoding risk variants using disease-relevant gene regulatory networks, Published online: 16 February 2018; doi:10.1038/s41467-018-03133-y

      Current methods for prioritization of non-coding genetic risk variants are based on sequence and chromatin features. Here, Gao et al. develop ARVIN, which predicts causal regulatory variants using disease-relevant gene-regulatory networks, and validate this approach in reporter gene assays.Identifying noncoding risk variants using disease-relevant gene regulatory networks, Published online: 2018-02-16; doi:10.1038/s41467-018-03133-y2018-02-16
      DOI: 10.1038/s41467-018-03133-y
       
  • Delayed gut microbiota development in high-risk for asthma infants is
           temporarily modifiable by Lactobacillus supplementation
    • Delayed gut microbiota development in high-risk for asthma infants is temporarily modifiable by Lactobacillus supplementation

      Delayed gut microbiota development in high-risk for asthma infants is temporarily modifiable by Lactobacillus supplementation, Published online: 16 February 2018; doi:10.1038/s41467-018-03157-4

      Gut microbial dysbiosis in infancy is associated with childhood atopy and the development of asthma. Here, the authors show that gut microbiota perturbation is evident in the very earliest stages of postnatal life, continues throughout infancy, and can be partially rescued by Lactobacillus supplementation in high-risk for asthma infants.Delayed gut microbiota development in high-risk for asthma infants is temporarily modifiable by Lactobacillus supplementation, Published online: 2018-02-16; doi:10.1038/s41467-018-03157-42018-02-16
      DOI: 10.1038/s41467-018-03157-4
       
  • Bone marrow lympho-myeloid malfunction in obesity requires precursor
           cell-autonomous TLR4
    • Bone marrow lympho-myeloid malfunction in obesity requires precursor cell-autonomous TLR4

      Bone marrow lympho-myeloid malfunction in obesity requires precursor cell-autonomous TLR4, Published online: 16 February 2018; doi:10.1038/s41467-018-03145-8

      Obesity can affect bone marrow cell differentiation and the generation of myeloid and lymphoid cells. Here, the authors show that diet and obesity, as well as low-dose lipopolysaccharide, can alter Toll-like receptor 4 signaling bone marrow cells to skew the myeloid-lymphoid homeostasis in mice.Bone marrow lympho-myeloid malfunction in obesity requires precursor cell-autonomous TLR4, Published online: 2018-02-16; doi:10.1038/s41467-018-03145-82018-02-16
      DOI: 10.1038/s41467-018-03145-8
       
  • Physical basis of amyloid fibril polymorphism
    • Physical basis of amyloid fibril polymorphism

      Physical basis of amyloid fibril polymorphism, Published online: 16 February 2018; doi:10.1038/s41467-018-03164-5

      Amyloid fibril structures can display polymorphism. Here the authors reveal the cryo-EM structures of several different fibril morphologies of a peptide derived from an amyloidogenic immunoglobulin light chain and present a mathematical analysis of physical factors that influence fibril polymorphism.Physical basis of amyloid fibril polymorphism, Published online: 2018-02-16; doi:10.1038/s41467-018-03164-52018-02-16
      DOI: 10.1038/s41467-018-03164-5
       
 
 
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