Cellular and Molecular Life Sciences

Journal Information
ISSN / EISSN : 1420-682X / 1420-9071
Current Publisher: Springer Science and Business Media LLC (10.1007)
Former Publisher: , Springer Science and Business Media LLC (10.1007) , Springer Science and Business Media LLC (10.1007) , Springer Singapore (10.1007) Springer Science and Business Media LLC (10.1007)
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Cellular and Molecular Life Sciences pp 1-14; doi:10.1007/s00018-021-03830-w

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Thai Q Tran,
Cellular and Molecular Life Sciences pp 1-18; doi:10.1007/s00018-021-03833-7

The publisher has not yet granted permission to display this abstract.
Cellular and Molecular Life Sciences pp 1-16; doi:10.1007/s00018-021-03834-6

Abstract:
Flaviviruses are positive-sense single-stranded RNA viruses that pose a considerable threat to human health. Flaviviruses replicate in compartmentalized replication organelles derived from the host endoplasmic reticulum (ER). The characteristic architecture of flavivirus replication organelles includes invaginated vesicle packets and convoluted membrane structures. Multiple factors, including both viral proteins and host factors, contribute to the biogenesis of the flavivirus replication organelle. Several viral nonstructural (NS) proteins with membrane activity induce ER rearrangement to build replication compartments, and other NS proteins constitute the replication complexes (RC) in the compartments. Host protein and lipid factors facilitate the formation of replication organelles. The lipid membrane, proteins and viral RNA together form the functional compartmentalized replication organelle, in which the flaviviruses efficiently synthesize viral RNA. Here, we reviewed recent advances in understanding the structure and biogenesis of flavivirus replication organelles, and we further discuss the function of virus NS proteins and related host factors as well as their roles in building the replication organelle.
Cellular and Molecular Life Sciences pp 1-15; doi:10.1007/s00018-021-03820-y

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, Jonatan Halvardson, Hanna Davies, Edyta Rychlicka-Buniowska, Jonas Mattisson, Behrooz Torabi Moghadam, Noemi Nagy, Kazimierz Węglarczyk, Karolina Bukowska-Strakova, Marcus Danielsson, et al.
Cellular and Molecular Life Sciences pp 1-15; doi:10.1007/s00018-021-03822-w

Abstract:
Epidemiological investigations show that mosaic loss of chromosome Y (LOY) in leukocytes is associated with earlier mortality and morbidity from many diseases in men. LOY is the most common acquired mutation and is associated with aberrant clonal expansion of cells, yet it remains unclear whether this mosaicism exerts a direct physiological effect. We studied DNA and RNA from leukocytes in sorted- and single-cells in vivo and in vitro. DNA analyses of sorted cells showed that men diagnosed with Alzheimer’s disease was primarily affected with LOY in NK cells whereas prostate cancer patients more frequently displayed LOY in CD4 + T cells and granulocytes. Moreover, bulk and single-cell RNA sequencing in leukocytes allowed scoring of LOY from mRNA data and confirmed considerable variation in the rate of LOY across individuals and cell types. LOY-associated transcriptional effect (LATE) was observed in ~ 500 autosomal genes showing dysregulation in leukocytes with LOY. The fraction of LATE genes within specific cell types was substantially larger than the fraction of LATE genes shared between different subsets of leukocytes, suggesting that LOY might have pleiotropic effects. LATE genes are involved in immune functions but also encode proteins with roles in other diverse biological processes. Our findings highlight a surprisingly broad role for chromosome Y, challenging the view of it as a “genetic wasteland”, and support the hypothesis that altered immune function in leukocytes could be a mechanism linking LOY to increased risk for disease.
Yiqian Gui,
Cellular and Molecular Life Sciences pp 1-13; doi:10.1007/s00018-021-03823-9

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Jianling Xie, Stuart P. De Poi, Sean J. Humphrey, Leanne K. Hein, John B. Bruning, Wenru Pan, Luke A. Selth, Timothy J. Sargeant,
Cellular and Molecular Life Sciences pp 1-18; doi:10.1007/s00018-021-03825-7

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Cellular and Molecular Life Sciences pp 1-13; doi:10.1007/s00018-021-03826-6

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Alicja Starosta,
Cellular and Molecular Life Sciences pp 1-25; doi:10.1007/s00018-021-03821-x

Abstract:
Duchenne muscular dystrophy (DMD) is a devastating chromosome X-linked disease that manifests predominantly in progressive skeletal muscle wasting and dysfunctions in the heart and diaphragm. Approximately 1/5000 boys and 1/50,000,000 girls suffer from DMD, and to date, the disease is incurable and leads to premature death. This phenotypic severity is due to mutations in the DMD gene, which result in the absence of functional dystrophin protein. Initially, dystrophin was thought to be a force transducer; however, it is now considered an essential component of the dystrophin-associated protein complex (DAPC), viewed as a multicomponent mechanical scaffold and a signal transduction hub. Modulating signal pathway activation or gene expression through epigenetic modifications has emerged at the forefront of therapeutic approaches as either an adjunct or stand-alone strategy. In this review, we propose a broader perspective by considering DMD to be a disease that affects myofibers and muscle stem (satellite) cells, as well as a disorder in which abrogated communication between different cell types occurs. We believe that by taking this systemic view, we can achieve safe and holistic treatments that can restore correct signal transmission and gene expression in diseased DMD tissues.
Cellular and Molecular Life Sciences pp 1-19; doi:10.1007/s00018-021-03816-8

Abstract:
Infection with H. pylori induces a strong host cellular response represented by induction of a set of molecular signaling pathways, expression of proinflammatory cytokines and changes in proliferation. Chronic infection and inflammation accompanied by secretory dysfunction can result in the development of gastric metaplasia and gastric cancer. Currently, it has been determined that the regulation of many cellular processes involves ubiquitinylation of molecular effectors. The binding of ubiquitin allows the substrate to undergo a change in function, to interact within multimolecular signaling complexes and/or to be degraded. Dysregulation of the ubiquitinylation machinery contributes to several pathologies, including cancer. It is not understood in detail how H. pylori impacts the ubiquitinylation of host substrate proteins. The aim of this review is to summarize the existing literature in this field, with an emphasis on the role of E3 ubiquitin ligases in host cell homeodynamics, gastric pathophysiology and gastric cancer.
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