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.
Hydrophobic domains of mouse polyomavirus minor capsid proteins promote membrane association and virus exit from the ER
Forstová and colleagues, The FEBS Journal
Mouse polyomavirus is a non-enveloped DNA virus that is internalised into the host cell after binding its membrane receptor. Viral capsids must then penetrate intracellular membranes to reach the host nucleus for successful infection. The location at which capsids breach cellular membranes and the underlying mechanism are still poorly understood. Forstová and colleagues now report that the hydrophobic domains of the polyomavirus minor structural protein VP2 and its variant VP3 mediate virus-ER membrane association and facilitate exit from the ER.
Mantovani, Del Sal and colleagues, The FEBS Journal
Mutations in the TP53 tumour suppressor gene are the most frequent type of mutations found in human cancers. Active research has shown that p53 mutants can deregulate multiple cellular processes resulting in tumour-promoting outcomes. In this State-of-the-Art Review, Mantovani et al. discuss how large-scale analyses of the processes affected by mutant p53 proteins in their tumour context in vivo can be harnessed to identify targets for mutant p53-centered therapies.
Barbry, P. and colleagues, FEBS Letters
Here, the authors report that two members of the miR-34/449 miRNA family previously annotated as miRNAs are actually isomiRs. 5'- IsomiR-34b and 5'-isomiR-449c have an extra uridine at their 5' end, are less abundantly expressed and have additional mRNA targets and biological activities when compared to canonical miR-34b and miR-449c. The study suggests that miRNA sequences should be carefully analyzed and any results on the miR-34/449 family should be interpreted with caution.
Altered lysosome distribution is an early neuropathological event in neurological forms of Gaucher disease
Futerman, A.H. and colleagues, FEBS Letters
Gaucher disease is a genetic syndrome caused by glucosylceramide (GlcCer) accumulation and associated with neuronal loss and neuroinflammation. Here, the authors report altered lysosome distribution as an early event in Gaucher disease, preceding any signs of neuropathology. Intriguingly, a subset of LIMP2-expressing lysosomes was misplaced around the nucleus, and this phenotype correlated with cytoskeletal defects.
Multiple expression cassette exchange via TP901-1, R4 and Bxb1 integrase systems on a mouse artificial chromosome
Obayashi and colleagues, FEBS Open Bio
Here, Obayashi and colleagues created a reporter system to evaluate the precise target DNA excision for TP901-1, R4 and Bxb1 integrases, utilised in lineage tracing. In response to transient expression of specific integrases in hamster ovary cells, luciferase expression was exchanged for fluorescent protein expression – 3 distinct luciferases and 3 fluorescent proteins created up to 8 expression patterns. This reporter system was inserted into a mouse artificial chromosome vector. The multiple expression cassette exchange via site-speciﬁc recombinases (MEEVS) platform explicated here could lead to complex genomic manipulations, not solely in tissue culture cells but in animals, yeast and plants - using combinations of SSRs, artificial chromosomes and other genome editing tools.
Brat and colleagues, Molecular Oncology
Glioblastoma (GBM) is the most malignant form of primary brain tumour, with a median survival of 12–15 months following standard therapy. GBM stem-like cells (GSCs) contribute to the rapid growth, therapeutic resistance and clinical recurrence of these fatal tumours. Brat and colleagues report that tri-partite motif-containing protein 8 (TRIM8) activates STAT3 signalling via the suppression of protein inhibitor of STAT3 (PIAS3) expression to perpetuate stemness and the self-renewing capabilities of GSCs. Targeting TRIM8 reduced GSC stem cell marker expression and self-renewal capacity, suggesting that TRIM8 and STAT3 signalling pathways are potential therapeutic targets for GBM.
About FEBS Press
News about FEBS Press
Cancer biology, Microbiology, Plant Biology, and Computational and Systems Biology
- We congratulate FEBS Letters author Prof. Yoshinori Ohsumi on winning the 2016 Nobel Prize in Physiology or Medicine
News about FEBS
FEBS bursaries to assist FEBS 2017 participation
Check out the FEBS bursary scheme for early-career scientists presenting work at the FEBS Congress...
Second call for 2018 FEBS Advanced Courses proposals: apply by 1 July
Expert scientists: advance your research field by organizing a FEBS-funded event!...
FEBS Summer Fellowships 2017
Support for pre-doctoral students for research in a different country: apply by April 1st...
FEBS Letters Cover Contest
Got a research-related picture worth a thousand words? Send it to FEBS Letters...
The February 2017 issue of FEBS News is out
A focus on the upcoming 42nd FEBS Congress, and lots more – enjoy browsing!..