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.

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The FEBS Journal For high-quality full-length papers and reviews, with particular focus on biochemistry, molecular biology, structural biology and cell biology.
FEBS Letters For highly significant research letters that merit urgent publication, as well as timely reviews of wide interest in the molecular biosciences.
Molecular OncologyFor high-impact discoveries, approaches and technical advances in basic, clinical and discovery-driven translational cancer research.
FEBS Open Bio For rapid open access publication of scientifically sound research articles in the molecular and cellular life sciences.

Highlighted Articles

Montminy and colleagues

14-3-3 proteins mediate inhibitory effects of cAMP on salt-inducible kinases (SIKs)

Montminy and colleagues (2018), The FEBS Journal

Salt-inducible kinases (SIKs) regulate the expression of their targets such as cAMP-regulated transcriptional co-activators (CRTCs) and histone deacetylases (HDACs) via phosphorylation-dependent interaction with 14-3-3 proteins and cytoplasmic sequestration. Increased c-AMP signalling is known to inhibit SIK activity, but the underlying mechanism was unclear. Montminy and colleagues now show that protein kinase A (PKA)-mediated phosphorylation of SIKs induces their binding to 14-3-3 proteins and subsequent inhibition, revealing a dual role for 14-3-3 proteins on SIKs and their substrates.

Peña-Blanco and García-Sáez

Bax, Bak and beyond — mitochondrial performance in apoptosis

Peña-Blanco and García-Sáez (2018), The FEBS Journal

Following activation by apoptotic signals, the Bcl2-family members Bax and Bak oligomerise at the mitochondrial outer membrane and promote its permeabilization. In this State-of-the-Art Review, Peña-Blanco and García-Sáez discuss recent studies highlighting the structure of the Bax/Bak pores, their regulation by apoptotic signalling and the emerging role of the mitochondria on their function.

Peck and colleagues

Identification of a novel botulinum neurotoxin gene cluster in Enterococcus

M. W. Peck and colleagues, FEBS Letters

Clostridium botulinum neurotoxins (BoNTs) cause fatal neuroparalysis (botulism) by targeting the SNARE docking proteins of cholinergic neurons, thereby preventing exocytosis of the neurotransmitter acetylcholine. Here, using bioinformatics, the authors report the first complete boNT gene cluster in a non-clostridial genome. Identified in a species of Enterococcus, the putative BoNT contains all the functional domains of a typical BoNT and a novel cell attachment domain that has implications for pharmaceutical applications.

Michaelis and colleagues

Single-molecule nucleosome remodeling by INO80 and effects of histone tails

J. Michaelis and colleagues, FEBS Letters

INO80 is a multi-subunit ATP-dependent chromatin remodeling complex that functions in DNA replication, transcription, and damage repair. Here, the authors develop a single-molecule Foerster Resonance Energy Transfer (FRET) assay to investigate nucleosome sliding and positioning by INO80 and the influence of histone tails on this process. The findings indicate that histone tails pose a major regulatory barrier for the initiation of nucleosome remodeling by INO80.

Indoxyl sulfate

A uremic toxin (indoxyl sulfate) found in chronic kidney disease supresses bone formation and resorption

Inada and colleagues, FEBS Open Bio

Patients with chronic kidney disease (CKD) often present with bone turnover abnormalities, which has been associated with low serum levels of parathyroid hormone (PTH). Here, Inada and colleagues report that Indoxyl sulphate (IS), a uremic toxin known to accumulate in the blood of CKD patients, directly supresses osteoblast/osteoclast coupling and bone formation in vitro. This, combined with their previous findings that showed IS exacerbated low bone turnover induced by parathyroidectomy suggests that IS directly induces low bone turnover via the inhibition of bone formation using mechanisms separate from skeletal resistance to parathyroid hormone (PTH). This suggests IS initiates low-turnover bone disease in patients with CKD via a direct action upon both osteoclast precursors and osteoblasts to supress bone formation and resorption.


Dovitinib enhances temozolomide efficacy in glioblastoma cells

Hombach-Klonisch and colleagues, Molecular Oncology

Dovitinib (Dov), an FDA- approved oral drug, is able to cross the blood-brain barrier and has recently demonstrated promising efficacy in clinical trials for glioblastoma (GB) patients with recurrent disease. The Dov-mediated molecular mechanisms in GB cells remained unknown. Here, Hombach-Klonisch and colleagues show that Dov treatment attenuated the STAT3/LIN28/Let-7/HMGA2 regulatory axis in GB cells, and downregulated key base excision repair factors known to repair temozolomide (TMZ) induced DNA damage. Dual or sequential treatment with Dov and TMZ enhanced the efficacy of TMZ, reduced GB cell survival, growth, and self-renewal capacity and severely compromised the recovery of GB cells. Alternate administration of Dov and TMZ may improve therapeutic efficacy, especially in patients expected to exhibit increased TMZ resistance. These findings suggest ‘Dov priming’ is an encouraging novel therapeutic strategy to improve the efficacy of TMZ in patients with GB.

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