FEBS Press is pleased to welcome its fourth journal, Molecular Oncology, to this platform. Molecular Oncology is now fully Open Access and all content from the past 10 years is now available for all to read. The publication of high-quality journals by scientists for scientists is one the core objectives of The Federation of European Biochemical Societies (FEBS), with the revenue raised supporting fellowships, courses, congresses and other activities.
di Masi and colleagues, The FEBS Journal
The heat shock protein 90 (Hsp90α) modulates the stability of several DNA damage response (DDR) proteins including MRE11/RAD50/NBN (MRN trimer). di Masi and colleagues now reveal that NBN and the ataxia-telangiectasia-mutated (ATM) kinase are Hsp90α clients and that Hsp90α facilitates NBN–ATM crosstalk in response to DNA damage. Upon IR-induced DNA double-strand breaks (DSBs), ATM phosphorylates NBN and Hsp90α. NBN then dissociates from Hsp90α and relocalises to the DSBs together with MRE11 and RAD50 to promote the DDR.
Kanneganti and colleagues, The FEBS Journal
The inflammasome is a protein complex that forms in the cytoplasm in response to cellular damage or the presence of pathogen-associated molecules resulting from infection. Undegraded self-DNA and histones can also induce inflammasome formation and drive ‘sterile inflammation’. In this Viewpoint, Kanneganti and colleagues discuss the roles of the inflammasome during nucleic-acid- and histone-driven ‘sterile inflammation’ and highlight emerging roles of pathogens and commensal microbes in the development of ‘sterile inflammation’.
Crystallographic and solution structure of the N-terminal domain of the Rel protein from Mycobacterium tuberculosis
Grüber, G. and colleagues, FEBS Letters
Hyperphosphorylated guanine nucleotides [(p)ppGpp] have a central role in the stringent response, which enables bacteria to survive under stressful conditions. In Mycobacterium tuberculosis, the synthesis and hydrolysis of (p)ppGpp is catalyzed by MtRel. Here, the authors present structural analyses of the MtRel N-terminus harboring the synthetase and hydrolase domains. The study paves the way for the development of antibacterials targeting MtRel.
Amino acids suppress the expression of PAT1 on lysosomes via inducing the cleavage of a targeting signal
W. Liu, Y. Jin and colleagues, FEBS Letters
The amino acid (AA) transporter PAT1 shows a dynamic localization pattern. AA deprivation promotes lysosomal localization of PAT1 and subsequent AA transport from the lysosome to the cytosol. Here, the authors identify a tyrosine-based lysosomal localization signal on PAT1 that is cleaved in the presence of AAs but not under conditions of AA deprivation. Interestingly, direct interaction of this signal with amino acids was sufficient to induce cleavage and prevent lysosomal localization of PAT1.
The neuronal and astrocytic protein SLC38A10 transports glutamine, glutamate, and aspartate, suggesting a role in neurotransmission
Hellsten and colleagues, FEBS Open Bio
Within brain cells, glutamine transporters are essential for the monitoring and control of glutamate and GABA levels. Here, Hellsten and colleagues report the first histological and functional characterisation of SLC38A10, a previous orphan member of the SLC38 family of amino acid transporters. SLC38A10 immunostaining was abundant in the mouse brain, showing colocalised staining with markers for neurons and astrocytes. Transport assays suggest the transporter is bidirectional and can mediate uptake and efflux of multiple neurotransmitters. Together, these studies suggest that SLC38A10 may potentially play a role in excitatory and inhibitory neurotransmission.
Epithelial/mesenchymal plasticity: how have quantitative mathematical models helped improve our understanding?
Levine and colleagues, Molecular Oncology
Epithelial-to-mesenchymal transition (EMT) and mesenchymal-to-epithelial transition (MET) are thought to be fundamental in the metastatic dissemination of carcinomas. EMT and MET are not discrete states, with carcinoma cells frequently exhibiting a spectrum of epithelial/mesenchymal phenotypes. Currently, whether epithelial/mesenchymal plasticity is requisite for metastatic dissemination remains unknown. Here, Levine et al. focus on epithelial/mesenchymal plasticity and its role in metastatic outgrowth, suggesting alternative mechanisms that may underpin successful dissemination beyond the classic EMT/MET view. The authors highlight several hypotheses that may attune conflicting observations, and put forward a framework of key questions that may offer valuable insight into the metastatic mechanisms in multiple tumour models.
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