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Emerging roles of long noncoding RNAs in neurological diseases and metabolic disorders

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889195718 Year: Pages: 76 DOI: 10.3389/978-2-88919-571-8 Language: English
Publisher: Frontiers Media SA
Subject: Biology --- Science (General) --- Genetics
Added to DOAB on : 2016-02-05 17:24:33
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Long noncoding RNAs (lncRNAs) are a new class of transcripts that are in general longer than 200 nucleotides and that have no protein-coding potential. The vast majority of vertebrate genomes encode diverse and complex lncRNAs that play regulatory roles at almost every step of gene expression. Recently, increasing evidence has implicated lncRNAs in the pathogenesis of various human diseases. The purpose of the Research Topic, "Emerging roles of long noncoding RNAs in neurological diseases and metabolic disorders", is to bring together leading researchers in the field who, through contributing to an organized and comprehensive collection of peer-reviewed articles, provide a broad perspective on the latest advances in the field. A number of interesting and cutting-edge areas will be covered as below, but this list is not exclusive:- The methodologies and technologies of identifying and studying lncRNAs - LncRNAs in gene-specific transcription - LncRNAs in epigenetic regulation - LncRNAs in post-transcriptional regulation - LncRNAs in disease - Mapping of noncoding single nucleotide polymorphisms associated with disease.

Host-adapted metabolism and its regulation in Bacterial Pathogens

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889195381 Year: Pages: 176 DOI: 10.3389/978-2-88919-538-1 Language: English
Publisher: Frontiers Media SA
Subject: Internal medicine --- Science (General)
Added to DOAB on : 2016-01-19 14:05:46
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Pathogens adapt their metabolism rapidly to the host. Our topic covers these phenomenon regarding extracellular and intracellular pathogens as well as general methods to elucidate different metabolic adaptation processes - an essential guide for any scientist wanting to keep abreast of recent developments in infection biology.

Endoplasmic Reticulum Stress Response and Transcriptional Reprogramming

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889194360 Year: Pages: 97 DOI: 10.3389/978-2-88919-436-0 Language: English
Publisher: Frontiers Media SA
Subject: Genetics --- Science (General)
Added to DOAB on : 2016-01-19 14:05:46
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Endoplasmic reticulum (ER) is an intracellular organelle responsible for protein folding and assembly, lipid and sterol biosynthesis, and calcium storage. A number of biochemical, physiological, or pathological stimuli can interrupt protein folding process, causing accumulation of unfolded or misfolded proteins in the ER lumen, a condition called “ER stress”. To cope with accumulation of unfolded or misfolded proteins, the ER has evolved a group of signaling pathways termed “Unfolded Protein Response (UPR)” or “ER stress response” to align cellular physiology. To maintain ER homeostasis, transcriptional regulation mediated through multiple UPR branches is orchestrated to increase ER folding capacity, reduce ER workload, and promote degradation of misfolded proteins. In recent years, accumulating evidence suggests that ER stress-triggered transcriptional reprogramming exists in many pathophysiological processes and plays fundamental roles in the initiation and progression of a variety of diseases, such as metabolic disease, cardiovascular disease, neurodegenerative disease, and cancer. Understanding effects and mechanisms of ER stressassociated transcriptional reprogramming has high impact on many areas of molecular genetics and will be particularly informative to the development of pharmacologic avenues towards the prevention and treatment of modern common human diseases by targeting the UPR signaling. For these reasons, ER stress response and transcriptional reprogramming are a timely and necessary topic of discussion for Frontiers in Genetics.The important topics in this area include but not limited to:(1) ER-resident transcription factors and their involvements in ER stress response and cell physiology; (2) Physiologic roles and molecular mechanisms of ER stress-associated transcriptional regulation in lipid and glucose metabolism; (3) In vitro and in vivo models for ER stress-associated transcriptional reprogramming; (4) ER stress-associated transcriptional regulation in human disease; (5) Therapeutic potentials by targeting ER stress response pathways.

T Cell Regulation by the Environment

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197330 Year: Pages: 115 DOI: 10.3389/978-2-88919-733-0 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2016-04-07 11:22:02
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Naïve T cells get activated upon encounter with their cognate antigen and differentiate into a specific subset of effector cells. These T cells are themselves plastic and are able to re-differentiate into another subset, changing both phenotype and function. Differentiation into a specific subset depends on the nature of the antigen and of the environmental milieu. Notably, certain nutrients, such as vitamins A and D, sodium chloride, have been shown to modulate T cell responses and influence T cell differentiation. Parasite infection can also skew Th differentiation. Similarly, the gut microbiota regulates the development of immune responses. Lastly, the key role of metabolism on T cells has also been demonstrated. This series of articles highlights some of the multiple links existing between environmental factors and T cell responses.

Synthetic Biology: Engineering complexity and refactoring cell capabilities

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196852 Year: Pages: 123 DOI: 10.3389/978-2-88919-685-2 Language: English
Publisher: Frontiers Media SA
Subject: Biotechnology --- General and Civil Engineering
Added to DOAB on : 2015-10-30 16:33:44
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One of the key features of biological systems is complexity, where the behavior of high level structures is more than the sum of the direct interactions between single components. Synthetic Biologists aim to use rational design to build new systems that do not already exist in nature and that exhibit useful biological functions with different levels of complexity. One such case is metabolic engineering, where, with the advent of genetic and protein engineering, by supplying cells with chemically synthesized non-natural amino acids and sugars as new building blocks, it is now becoming feasible to introduce novel physical and chemical functions and properties into biological entities. The rules of how complex behaviors arise, however, are not yet well understood. For instance, instead of considering cells as inert chassis in which synthetic devices could be easily operated to impart new functions, the presence of these systems may impact cell physiology with reported effects on transcription, translation, metabolic fitness and optimal resource allocation. The result of these changes in the chassis may be failure of the synthetic device, unexpected or reduced device behavior, or perhaps a more permissive environment in which the synthetic device is allowed to function. While new efforts have already been made to increase standardization and characterization of biological components in order to have well known parts as building blocks for the construction of more complex devices, also new strategies are emerging to better understand the biological dynamics underlying the phenomena we observe. For example, it has been shown that the features of single biological components [i.e. promoter strength, ribosome binding affinity, etc] change depending on the context where the sequences are allocated. Thus, new technical approaches have been adopted to preserve single components activity, as genomic insulation or the utilization of prediction algorithms able to take biological context into account. There have been noteworthy advances for synthetic biology in clinical technologies, biofuel production, and pharmaceuticals production; also, metabolic engineering combined with microbial selection/adaptation and fermentation processes allowed to make remarkable progress towards bio-products formation such as bioethanol, succinate, malate and, more interestingly, heterologous products or even non-natural metabolites. However, despite the many progresses, it is still clear that ad hoc trial and error predominates over purely bottom-up, rational design approaches in the synthetic biology community. In this scenario, modelling approaches are often used as a descriptive tool rather than for the prediction of complex behaviors. The initial confidence on a pure reductionist approach to the biological world has left space to a new and deeper investigation of the complexity of biological processes to gain new insights and broaden the categories of synthetic biology. In this Research Topic we host contributions that explore and address two areas of Synthetic Biology at the intersection between rational design and natural complexity: (1) the impact of synthetic devices on the host cell, or "chassis" and (2) the impact of context on the synthetic devices. Particular attention will be given to the application of these principles to the rewiring of cell metabolism in a bottom-up fashion to produce non-natural metabolites or chemicals that should eventually serve as a substitute for petrol-derived chemicals, and, on a long-term view, to provide economical, ecological and ethical solutions to today’s energetic and societal challenges.

CD4+ T cell differentiation in infection: amendments to the Th1/Th2 axiom

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889195657 Year: Pages: 111 DOI: 10.3389/978-2-88919-565-7 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2016-01-19 14:05:46
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CD4+ T lymphocytes play an essential role in host defense against bacterial, parasitic and viral infections. During infection, under the influence of intrinsic signals received through peptide-MHC/TCR interactions and extrinsic signals provided by pathogen-conditioned dendritic and other accessory cells, CD4+ T cells proliferate and differentiate into specialized T helper (Th) effectors, which produce distinct sets of cytokines tailored to combat a specific class of microbes. The concept of CD4+ T cell multi-functionality was developed after the seminal discovery of Th1 and Th2 cells nearly 30 years ago. Although the Th1/Th2 paradigm has successfully withstood the test of time, in the past decade additional Th subsets (Th17, Tfh, Th22, Th9) have been identified. Similarly, single cell analyses of cytokines and master transcriptional factors have revealed that, at the population level, CD4+ T cell responses are far more heterogeneous than initially anticipated. While some of the checkpoints in Th cell specification have been identified, recent studies of transcriptional and epigenetic regulation have uncovered a significant flexibility during the course CD4+ T lymphocyte polarization. In addition, Th cells expressing cytokines with counteracting functions, as a measure of self-regulation, display yet another level of diversity. Understanding the mechanisms that control the balance between stability vs. plasticity of Th effectors both at the time of initiation of immune response and during development of CD4 T cell memory is critical for the rational design of better vaccines and new immunotherapeutic strategies. This research topic will cover current views on Th cell development, with a focus on the mechanisms that govern differentiation, function and regulation of effector Th cells in the context of microbial infections.

The Coming of Age of Insulin-Signalling in Insects

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193141 Year: Pages: 138 DOI: 10.3389/978-2-88919-314-1 Language: English
Publisher: Frontiers Media SA
Subject: Physiology --- Science (General)
Added to DOAB on : 2016-02-05 17:24:33
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The new millennium has seen a major paradigm shift in insect endocrinology. Great advancements are being made which establish that nutrition and growth play a central role in diverse cellular and physiological phenomena during insect development and reproduction. Nutrition affects rates of growth and is mainly regulated by the function of the pathway of insulin/insulin-like growth factor signalling. This pathway is highly conserved across species and ultimately regulates rates of cell growth and proliferation in growing organs. Insulin and insulin-like peptides (ILPs) are some of the best studied hormones in the animal kingdom and all share a common structural motif and initiate a wide range of closely similar physiological processes in higher organisms. In insects, nutrition, via circulating sugar, promotes release of ILPs from brain neurosecretory cells into the haemolymph, which act on peripheral tissues and stimulate protein synthesis and cell growth. Therefore, insect ILPs are common mediators between nutrition and growth in insects and are functionally analogous to mammalian insulin. The 1980s and 1990s witnessed great progress in elucidation of the physiological and molecular mechanism of action of numerous insect hormones involved in regulation of growth, development, reproduction and metabolism. But the signals for the initiation or termination of controlled events remained largely unknown. ILPs were first identified from the silkmoth Bombyx mori and were named bombyxins, but related peptides were soon found in numerous species and their functions elucidated. The insulin signalling pathway is now recognized as a central factor in the timing of cell proliferation, growth, longevity, reproduction, and reproductive diapause, as well as social behaviour. Recent work has revealed that the insulin signalling pathway is closely integrated with that of various other hormones, including ecdysteroids, the juvenile hormones and neuropeptide(s) such a prothoracicotropic hormone. In addition, the pathway is also linked with both circadian (daily) and photoperiodic (seasonal) clocks potentially providing a basis for its timing function. This Research Topic aims to provide the only current collection of recent advances on insect ILPs. We encouraged submissions on all areas related to identification, characterization, regulation and physiological functions of insect ILPs. We welcomed both full and short reviews and original research articles.

Glycolysis at 75: Is it time to tweak the first elucidated metabolic pathway in history?

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889195862 Year: Pages: 126 DOI: 10.3389/978-2-88919-586-2 Language: English
Publisher: Frontiers Media SA
Subject: Nutrition and Food Sciences --- Medicine (General) --- Neurology --- Science (General)
Added to DOAB on : 2016-03-10 08:14:32
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Glycolysis, the pathway of enzymatic reactions responsible for the breakdown of glucose into two trioses and further into pyruvate or lactate, was elucidated in 1940. For more than seven decades, it has been taught precisely the way its sequence was proposed by Embden, Meyerhof and Parnas. Accordingly, two outcomes of this pathway were proposed, an aerobic glycolysis, with pyruvate as its final product, and an anaerobic glycolysis, identical to the aerobic one, except for an additional reaction, where pyruvate is reduced to lactate. Several studies in the 1980s have shown that both muscle and brain tissues can oxidize and utilize lactate as an energy substrate, challenging this monocarboxylate’s reputation as a useless end-product of anaerobic glycolysis. These findings were met with great skepticism about the idea that lactate could be playing a role in bioenergetics. In the past quarter of a century monocarboxylate transporters (MCTs) were identified and localized in both cellular and mitochondrial membranes. A lactate receptor has been identified. Direct and indirect evidence now indicate that the enzyme lactate dehydrogenase (LDH) resides not only in the cytosol, as part of the glycolytic pathway machinery, but also in the mitochondrial outer membrane. The mitochondrial form of the enzyme oxidizes lactate to pyruvate and concomitantly produces the reducing agent NADH. These findings have shed light on a major drawback of the originally proposed aerobic version of the glycolytic pathway i.e., its inability to regenerate NAD+, as opposed to anaerobic glycolysis that features the cyclical ability of regenerating NAD+ upon pyruvate reduction to lactate by the cytosolic form of LDH. The malate-aspartate shuttle (MAS), a major redox shuttle in the brain, was proposed as an alternative pathway for NAD+ generation for aerobic glycolysis. Nonetheless, would MAS really be necessary for that function if glycolysis always proceeds to the end-products, lactate and NAD+? An additional dilemma the originally proposed aerobic glycolysis presents has to do with the glycolytic pathway of erythrocytes, which despite its highly aerobic environment, always produces lactate as its end-product. It is time to reexamine the original, dogmatic separation of glycolysis into two distinct pathways and put to test the hypothesis of a unified, singular pathway, the end-product of which is lactate, the real substrate of the mitochondrial TCA cycle.

30 years old: O-GlcNAc Reaches Age of Reason - Regulation of Cell Signaling and Metabolism by O-GlcNAcylation

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889195916 Year: Pages: 113 DOI: 10.3389/978-2-88919-591-6 Language: English
Publisher: Frontiers Media SA
Subject: Internal medicine --- Medicine (General)
Added to DOAB on : 2016-03-10 08:14:32
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Hundreds post-translational modifications (PTM) were characterized among which a large variety of glycosylations including O-GlcNAcylation. Since its discovery, O-GlcNAcylation has emerged as an unavoidable PTM widespread in the living beings including animal and plant cells, protists, bacteria and viruses. In opposition to N- and O-glycosylations, O-GlcNAcylation only consists in the transfer of a single N-acetylglucosamine moiety through a beta-linkage onto serine and threonine residues of proteins confined within the cytosol, the nucleus and the mitochondria. The O-GlcNAc group is provided by UDP-GlcNAc, the end-product of the hexosamine biosynthetic pathway located at the crossroad of cell metabolisms making O-GlcNAcylation a PTM which level tightly reflects nutritional status; therefore regulation of cell homeostasis should be intimately correlated to lifestyle and environment. Like phosphorylation, with which it can compete, O-GlcNAcylation is reversible. This versatility is managed by OGT (O-GlcNAc transferase) that transfers the GlcNAc group and OGA (O-GlcNAcase) that removes it. Also, like its unsweetened counterpart, O-GlcNAcylation controls fundamental processes, e.g. protein fate, chromatin topology, DNA demethylation and, as recently revealed, circadian clock. Deregulation of O-GlcNAc dynamism may be involved in the emergence of cancers, neuronal and metabolic disorders such as Alzheimer's or diabetes respectively. This Research Topic in Frontiers in Endocrinology is the opportunity to celebrate the thirtieth anniversary of the discovery of "O-GlcNAc" by Gerald W. Hart.

Origin and spatiotemporal dynamics of the peroxisomal endomembrane system

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889194643 Year: Pages: 148 DOI: 10.3389/978-2-88919-464-3 Language: English
Publisher: Frontiers Media SA
Subject: Physiology --- Science (General)
Added to DOAB on : 2016-03-10 08:14:32
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The peroxisome is an organelle with essential roles in lipid metabolism, maintenance of reactive oxygen species homeostasis, and anaplerotic replenishment of tricarboxylic acid cycle intermediates destined for mitochondria. Peroxisomes constitute a dynamic endomembrane system. The homeostatic state of this system is upheld via two pathways for assembling and maintaining the diverse peroxisomal compartments constituting it; the relative contribution of each pathway to preserving such system may vary in different organisms and under various physiological conditions. One pathway begins with the targeting of certain peroxisomal membrane proteins to an endoplasmic reticulum template and their exit from the template via pre-peroxisomal carriers; these carriers mature into metabolically active peroxisomes containing the entire complement of membrane and matrix proteins. Another pathway operates via growth and maturation of pre-existing peroxisomal precursors that do not originate from the endoplasmic reticulum; mature peroxisomes proliferate by undergoing fission. Recent studies have uncovered new roles for the peroxisomal endomembrane system in orchestrating important developmental decisions and defining organismal longevity. This Frontiers Special Topic Issue is focused on the advances in our understanding of how evolutionarily distant organisms coordinate the formation, maturation, proliferation, maintenance, inheritance and quality control of the peroxisomal endomembrane system and how peroxisomal endomembranes communicate with other cellular compartments to orchestrate complex biological processes and various developmental programs from inside the cell.

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