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.
The FEBS Journal
Timely, authoritative reviews and cutting-edge primary research articles bring new insight into Plasmodium physiology, the latest advances in antimalarial therapies and vaccine development, and much more. We are grateful to the authors for their contributions and hope you find these articles engaging and informative!
Lopez, Guirouilh-Barbat and colleagues, The FEBS Journal
DNA double-strand breaks (DSBs) occur spontaneously in genomes following endogenous or exogenous stress. They are efficiently repaired by a tightly controlled DSB repair machinery, that could, in some instances, generate accidental genome rearrangements. In this State-of-the-Art Review, Lopez, Guirouilh-Barbat and colleagues explain the different mechanisms that drive these DSB repair-generated, non-programmed genome rearrangements and their consequences in somatic cells.
Meng W. and colleagues, FEBS Letters
Calmodulin-regulated spectrin-associated proteins (CAMSAPs) are noncentrosomal microtubule (MT)-regulating proteins, which recognize the growing minus ends of noncentrosomal MTs and protect them from depolymerization. Here, the authors show that CAMSAP2 controls retrograde transport of autophagosomes. Specifically, CAMSAP2 sequesters MT plus end tracking protein EB1, restraining its plus end localization and regulating autophagosome transport. The data suggest an unprecedented role of noncentrosomal MTs in autophagy.
An inhibitory epitope of human Toll-like receptor 4 resides on leucine-rich repeat 13 and is recognized by a monoclonal antibody
Tomioka Y. and colleagues, FEBS Letters
Excessive Toll-like receptor 4 (TLR4) signalling following lipopolysaccharide (LPS) binding is associated with inflammatory disorders and sepsis. Tomioka and colleagues had previously generated a series of TLR4-inhibiting antibodies. Now they identify the epitope of one of those, HT4, on leucine-rich repeat 13 (LRR13). LRR13 recognition by HT4 does not affect LPS binding but may block TLR4 dimerization. HT4 can be used in combination with antibodies recognizing other TLR4 epitopes to improve TLR4 inhibition.
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.
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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