EMBO Reports (EMBO Rep )

Publisher: European Molecular Biology Organization; Oxford University Press; HighWire Press, Nature Publishing Group

Description

EMBO Reports aims to provide high-quality scientific information in the very broadly defined area of molecular biology. EMBO Reports will have in three major sections: scientific reports reviews and science & society. The scientific reports shall be short high-quality papers of a maximum print-length of 5 pages. Papers of all areas of molecular biology will be welcome and the data presented will represent a major new insight into some aspect of molecular biology. Novelty will be a primary criterion as will the quality of the research that is reported. These papers will be reviewed and published rapidly as is in keeping with important primary scientific results. The review section will provide high-quality reviews of selected topics written by leading experts in the field. It will also report on papers of importance which are published in other scientific journals and in doing so will attempt to ensure that the material presented in EMBO Reports is appropriate for a broad readership. A particular emphasis will also be put on incisive reports of meetings at which the latest data are presented. The science & society section will be a mixture of information which is relevant to scientists working in the area of molecular biology discussion on topics which fall into the general category of the environment in which our research is performed and more in-depth articles in which specific scientific topics are dealt with in detail. By the combination of these sections EMBO Reports aims to be a leading widely read interesting journal which is synonymous with high-quality primary reports of research readable stimulating timely reviews and a forum for discussions which are of direct relevance to molecular biologists. In this way it complements the coverage to science which is provided by The EMBO Journal which has already shown the ability of EMBO to develop a journal of high quality in the area of molecular biology.

  • Impact factor
    7.19
  • 5-year impact
    7.40
  • Cited half-life
    6.10
  • Immediacy index
    1.69
  • Eigenfactor
    0.05
  • Article influence
    3.89
  • Website
    EMBO Reports website
  • Other titles
    EMBO reports (Online), European Molecular Biology Organization reports
  • ISSN
    1469-3178
  • OCLC
    46360308
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Nature Publishing Group

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 6 months embargo
  • Conditions
    • Authors retain copyright
    • Published source must be acknowledged and DOI cited
    • Must link to publisher version
    • Publisher's version/PDF cannot be used
    • On author's personal website and institutional repository
    • If funding agency rules apply, authors may post authors version to their relevant funding body's archive, 6 months after publication
  • Classification
    ​ yellow

Publications in this journal

  • EMBO Reports 11/2014; 15(11).
  • EMBO Reports 11/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Recent studies have highlighted the importance of regulatory non-coding RNAs and epigenetics in controlling the differentiation of somatic stem cells. Two major pathways characterize these fields: micro-RNAs (miRNAs) and DNA methylation. In this issue of EMBO Reports, Lv et al show that during mammalian corticogenesis, miR-15b inhibits cytosine demethylation by targeting Tet3, a key methylcytosine dioxygenase. This leads to the epigenetic downregulation of cyclin D1. As a result, cell cycle and differentiation of neural progenitors are altered, promoting their switch to neurogenesis. Hence, Lv et al elegantly bring together miRNAs and DNA methylation in the cell cycle control of neural progenitors and neurogenesis.
    EMBO Reports 11/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: RNA ligation can regulate RNA function by altering RNA sequence, structure and coding potential. For example, the function of XBP1 in mediating the unfolded protein response requires RNA ligation, as does the maturation of some tRNAs. Here, we describe a novel in vivo model in Caenorhabditis elegans for the conserved RNA ligase RtcB and show that RtcB ligates the xbp-1 mRNA during the IRE-1 branch of the unfolded protein response. Without RtcB, protein stress results in the accumulation of unligated xbp-1 mRNA fragments, defects in the unfolded protein response, and decreased lifespan. RtcB also ligates endogenous pre-tRNA halves, and RtcB mutants have defects in growth and lifespan that can be bypassed by expression of pre-spliced tRNAs. In addition, animals that lack RtcB have defects that are independent of tRNA maturation and the unfolded protein response. Thus, RNA ligation by RtcB is required for the function of multiple endogenous target RNAs including both xbp-1 and tRNAs. RtcB is uniquely capable of performing these ligation functions, and RNA ligation by RtcB mediates multiple essential processes in vivo.
    EMBO Reports 11/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Pluripotency-associated transcription factor Foxd3 is required for maintaining pluripotent cells. However, molecular mechanisms underlying its function are largely unknown. Here, we report that Foxd3 suppresses differentiation induced by calcineurin–NFAT signaling to maintain the ESC identity. Mechanistically, Foxd3 interacts with NFAT proteins and recruits co-repressor Tle4, a member of the Tle repressor family highly expressed in undifferentiated ESCs, to suppress NFATc3's transcriptional activities. Furthermore, global transcriptome analysis shows that Foxd3 and NFATc3 co-regulate a set of differentiation-associated genes in ESCs. Collectively, our study establishes a molecular and functional link between a pluripotency-associated factor and an important ESC differentiation-inducing pathway.
    EMBO Reports 11/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: The transcription factor HIF-1α is essential for cells to rapidly adapt to low oxygen levels (hypoxia). HIF-1α is frequently deregulated in cancer and correlates with poor patient prognosis. Here, we demonstrate that the deubiquitinase Cezanne regulates HIF-1α homeostasis. Loss of Cezanne decreases HIF-1α target gene expression due to a reduction in HIF-1α protein levels. Surprisingly, although the Cezanne-regulated degradation of HIF-1α depends on the tumour suppressor pVHL, hydroxylase and proteasome activity are dispensable. Our data suggest that Cezanne is essential for HIF-1α protein stability and that loss of Cezanne stimulates HIF-1α degradation via proteasome-independent routes, possibly through chaperone-mediated autophagy.
    EMBO Reports 10/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Id proteins are dominant-negative regulators within the HLH family of proteins. In embryonic stem cells (ESCs), Id1 and Id3 maintain the pluripotent state by preventing neural differentiation. The Id1-interacting protein Zrf1 plays a crucial role as a chromatin-bound factor in specification of the neural fate from ESCs. Here, we show that Id1 blocks Zrf1 recruitment to chromatin, thus preventing the activation of neural genes in ESCs. Upon differentiation, Id1 expression decreases thus inducing Zrf1 binding to neural genes. Importantly, depletion of Zrf1 rescues the expression of Polycomb targets involved in neural specification which are up-regulated in Id1 knock-out ESCs. We therefore identified Zrf1 as transcriptional regulator of neural fate downstream of Id1 in ESCs.
    EMBO Reports 10/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Phosphoinositides are a class of phospholipids generated by the action of phosphoinositide kinases with key regulatory functions in eukaryotic cells. Here, we present the atomic structure of phosphatidylinositol 4-kinase type IIα (PI4K IIα), in complex with ATP solved by X-ray crystallography at 2.8 Å resolution. The structure revealed a non-typical kinase fold that could be divided into N- and C-lobes with the ATP binding groove located in between. Surprisingly, a second ATP was found in a lateral hydrophobic pocket of the C-lobe. Molecular simulations and mutagenesis analysis revealed the membrane binding mode and the putative function of the hydrophobic pocket. Taken together, our results suggest a mechanism of PI4K IIα recruitment, regulation, and function at the membrane.
    EMBO Reports 10/2014; 15(10):1085-1092.
  • EMBO Reports 10/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: MicroRNAs (miRNAs) are important regulators of mouse brain development. However, their precise roles in this context remain to be elucidated. Through screening of expression profiles from a miRNA microarray and experimental analysis, we show here that miR-15b controls several aspects of cortical neurogenesis. miR-15b inhibits cortical neural progenitor cell (NPC) proliferation and promotes cell-cycle exit and neuronal differentiation. Additionally, miR-15b expression decreases the number of apical progenitors and increases basal progenitors in the VZ/SVZ. We also show that miR-15b binds to the 3′ UTR of TET3, which plays crucial roles during embryonic development by enhancing DNA demethylation. TET3 promotes cyclin D1 expression, and miR-15b reduces TET3 expression and 5hmC levels. Notably, TET3 expression rescues miR-15b-induced impaired NPC proliferation and increased cell-cycle exit in vivo. Our results not only reveal a link between miRNAs, TET, and DNA demethylation but also demonstrate critical roles for miR-15b and TET3 in maintaining the NPC pool during early neocortical development.
    EMBO Reports 10/2014;
  • EMBO Reports 10/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: In response to a variety of stresses, mammalian cells undergo a persistent proliferative arrest known as cellular senescence. Many senescence-inducing stressors are potentially oncogenic, strengthening the notion that senescence evolved alongside apoptosis to suppress tumorigenesis. In contrast to apoptosis, senescent cells are stably viable and have the potential to influence neighboring cells through secreted soluble factors, which are collectively known as the senescence-associated secretory phenotype (SASP). However, the SASP has been associated with structural and functional tissue and organ deterioration and may even have tumor-promoting effects, raising the interesting evolutionary question of why apoptosis failed to outcompete senescence as a superior cell fate option. Here, we discuss the advantages that the senescence program may have over apoptosis as a tumor protective mechanism, as well as non-neoplastic functions that may have contributed to its evolution. We also review emerging evidence for the idea that senescent cells are present transiently early in life and are largely beneficial for development, regeneration and homeostasis, and only in advanced age do senescent cells accumulate to an organism's detriment.
    EMBO Reports 10/2014;
  • EMBO Reports 10/2014;
  • EMBO Reports 10/2014;
  • EMBO Reports 10/2014;
  • EMBO Reports 10/2014; 15(10).