FEBS Letters最新文献

In inner ear hair cells, the stereocilia are inserted into a dense F-actin-enriched meshwork named the cuticular plate, which provides support to the stereocilia. Enah/Vasp-like (EVL) was shown to localize at the cuticular plate, and evl knockdown leads to disrupted cuticular plate and disorganized stereocilia in Xenopus hair cells. In the present work, we show that Evl transcripts are specifically expressed in mouse hair cells, and EVL is localized to the cuticular plate. However, the cuticular plate and stereocilia are unaffected by Evl knockout, and auditory function is largely normal in Evl knockout mice. In conclusion, our present data suggest that EVL is not essential for cuticular plate and stereocilia development in mouse auditory hair cells.

RETRACTION: R. Bakalova, H. Ohba, Z. Zhelev, T. Kubo, M. Fujii, M. Ishikawa, Y. Shinohara, and Y. Baba, ‘Antisense inhibition of Bcr-Abl/c-Abl synthesis promotes telomerase activity and upregulates tankyrase in human leukemia cells,' FEBS Letters 564, no. 1–2 (2004): 73–84, https://doi.org/10.1016/S0014-5793(04)00318-7.

The above article, published online on 9 April 2004 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Michael Brunner; FEBS Press; the National Institute of Advanced Industrial Science and Technology (AIST); and John Wiley and Sons Ltd.

Following publication, concerns were raised by a third-party regarding several figures in the article. The subsequent institutional investigation conducted by the AIST revealed:

Therefore, the conclusions of the paper are substantially compromised and the institute has recommended the paper to be retracted. The editors of the journal agree with the retraction based on the institutional investigation.

Although publication in scholarly peer-reviewed journals remains the gold standard for communication of findings in the life sciences, the gold has been debased in the digital age by various impurities, including (a) reviewer fatigue, (b) fraud, paper mills, and the perils of artificial intelligence, (c) predatory journals, (d) the ongoing use of journal impact factor as a proxy for individual article quality, and (e) salami-slicing and other unethical practices. In this article, I present a detailed overview of these problems, as well as solutions proposed and implemented to counter them. Finally, I suggest that these are all symptomatic of a wider problem, namely the culture of ‘publish or perish’ and ongoing issues with how researcher performance is evaluated for grant, hiring, and promotion decisions. Only by working towards a global shift in the way scientists view the purpose of publication can we finally remove the impurities and refine the gold.

Respiratory complex I is a central metabolic enzyme coupling NADH oxidation and quinone reduction with proton translocation. Despite the knowledge of the structure of the complex, the coupling of both processes is not entirely understood. Here, we use a combination of site-directed mutagenesis, biochemical assays, and redox-induced FTIR spectroscopy to demonstrate that the quinone chemistry includes the protonation and deprotonation of a specific, conserved aspartic acid residue in the quinone binding site (D325 on subunit NuoCD in Escherichia coli). Our experimental data support a proposal derived from theoretical considerations that deprotonation of this residue is involved in triggering proton translocation in respiratory complex I.

Hematopoietic system aging is characterized by both hematopoietic stem cell (HSC) and niche degeneration resulting in myeloid lineage-biased differentiation, reduced B cell and T cell lymphopoiesis, increased HSC mobilization, and fat deposition in the bone marrow.

Both alterations in RNA splicing and editing during HSC aging contribute to increased myeloid lineage skewing and inflammation-responsive transcription factors, underscoring the importance of epitranscriptomic mechanisms in the acquisition of an age-related phenotype.

Recent advances in single-cell (sc) transcriptomics have revolutionized our understanding of dendritic cells (DCs), pivotal players of the immune system. ScRNA-sequencing (scRNA-seq) has unraveled a previously unrecognized complexity and heterogeneity of DC subsets, shedding light on their ontogeny and specialized roles. However, navigating the rapid technological progress and computational methods can be daunting for researchers unfamiliar with the field. This review aims to provide immunologists with a comprehensive introduction to sc transcriptomic analysis, offering insights into recent developments in DC biology. Addressing common analytical queries, we guide readers through popular tools and methodologies, supplemented with references to benchmarks and tutorials for in-depth understanding. By examining findings from pioneering studies, we illustrate how computational techniques have expanded our knowledge of DC biology. Through this synthesis, we aim to equip researchers with the necessary tools and knowledge to navigate and leverage scRNA-seq for unraveling the intricacies of DC biology and advancing immunological research.