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Molecular Pathways of Estrogen Receptor Action

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ISBN: 9783038972969 9783038972976 Year: Pages: 304 DOI: 10.3390/books978-3-03897-297-6 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Biology
Added to DOAB on : 2018-10-22 10:23:01
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ca. 200 words; this text will present the book in all promotional forms (e.g. flyers). Please describe the book in straightforward and consumer-friendly terms.[Estrogen receptors (ERs) are typical members of the superfamily of nuclear receptors that mainly function as ligand-inducible transcription factors that bind chromatin, as homodimers, at specific response elements. A tight reciprocal coupling between rapid ‘non-genomic’ and ‘genomic’ ER actions may also occur in many physiological processes. ERs have long been evaluated for their roles in controlling the expression of genes involved in vital cellular processes such as proliferation, apoptosis, and differentiation. Therefore, given the various and pleiotropic functions of ERs, the dysregulation of their pathways contributes to several diseases such as the hormone-dependent breast; endometrial and ovarian cancers; and neurodegenerative diseases, cardiovascular diseases, and osteoporosis. In this printed edition of the Special Issue, “Molecular Pathways of Estrogen Receptor Action”, promising results on understanding the mechanisms underlying ER-mediated effects in various pathophysiological processes are represented, covering different roles of ER pathways in the tumorigenesis, the resistance to endocrine therapy, the dynamics of 3D genome organization, and cross-talk with other signaling pathways. This Special Issue also provides insight into the emerging roles of estrogen-signaling pathways in lung cancer, the tumor microenvironment, and the immune system.]

Essential Pathways and Circuits of Autism Pathogenesis

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199051 Year: Pages: 181 DOI: 10.3389/978-2-88919-905-1 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology --- Genetics
Added to DOAB on : 2016-01-19 14:05:46
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The Centers for Disease Control and Prevention estimate that 1 in 68 children in the United states is afflicted with autism spectrum disorders (ASD), yet at this time, there is no cure for the disease. Autism is characterized by delays in the development of many basic skills, most notably the ability to socialize and adapt to novelty. The condition is typically identified in children around 3 years of age, however the high heritability of autism suggests that the disease process begins at conception. The identification of over 500 ASD risk genes, has enabled the molecular genetic dissection of the pathogenesis of the disease in model organisms such as mice. Despite the genetic heterogeneity of ASD etiology, converging evidence suggests that these disparate genetic lesions may result in the disruption of a limited number of key biochemical pathways or circuits. Classification of patients into groups by pathogenic rather than etiological categories, will likely aid future therapeutic development and clinical trials. In this set of papers, we explore the existing evidence supporting this view. Specifically, we focus on biochemical cascades such as mTOR and ERK signaling, the mRNA network bound by FMRP and UBE3A, dorsal and ventral striatal circuits, cerebellar circuits, hypothalamic projections, as well as prefrontal and anterior cingulate cortical circuits. Special attention will be given to studies that demonstrate the necessity and/or sufficiency of genetic disruptions (e.g. by molecular deletion and/or replacement) in these pathways and circuits for producing characteristic behavioral features of autism. Necessarily these papers will be heavily weighted towards basic mechanisms elucidated in animal models, but may also include investigations in patients.

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.

Cell Signaling in Host-Pathogen Interactions: The Host Point of View

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889454556 Year: Pages: 414 DOI: 10.3389/978-2-88945-455-6 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology --- Science (General) --- Microbiology
Added to DOAB on : 2018-11-16 17:17:57
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The ability of pathogens, such as parasites, bacteria, fungi and viruses to invade, persist and adapt in both invertebrate and vertebrate hosts is multifactorial and depends on both pathogen and host fitness. Communication between a pathogen and its host relies on a wide and dynamic array of molecular interactions. Through this constant communication most pathogens evolved to be relatively benign, whereas killing of its host by a pathogen represents a failure to adapt. Pathogens are lethal to their host when their interaction has not been long enough for adaptation. Evolution has selected conserved immune receptors that recognize signature patterns of pathogens as non-self elements and initiate host innate responses aimed at eradicating infection. Conversely, pathogens evolved mechanisms to evade immune recognition and subvert cytokine secretion in order to survive, replicate and cause disease. The cell signaling machinery is a critical component of the immune system that relays information from the receptors to the nucleus where transcription of key immune genes is activated. Host cells have developed signal transduction systems to maintain homeostasis with pathogens. Most cellular processes and cell signaling pathways are tightly regulated by protein phosphorylation in which protein kinases are key protagonists. Pathogens have developed multiple mechanisms to subvert important signal transduction pathways such as the mitogen activated protein kinase (MAPK) and the nuclear factor kB (NF-kB) pathways. Pathogens also secrete effectors that manipulate actin cytoskeleton and its regulators, hijack cell cycle machinery and alter vesicular trafficking. This research topic focuses on the cellular signaling mechanisms that are essential for host immunity and their subversion by pathogens.

Promiscuous functions of the prion protein gene family

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196050 Year: Pages: 113 DOI: 10.3389/978-2-88919-605-0 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Biology
Added to DOAB on : 2016-08-16 10:34:25
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The cellular prion protein PrPC is a ubiquitous GPI-anchored protein. While PrPC has been the focus of intense research for its involvement in a group of neurodegenerative disorders known as transmissible spongiform encephalopathies (TSE), much less attention has been devoted to its physiological function. This notably relates to the lack of obvious abnormalities of mice, goat or cattle lacking PrPC. This apparently normal phenotype in these PrPC-deficient animals however contrasts with the very high degree of conservation of the prion protein gene (Prnp) in mammalian species (over 80%), and the presence of genes with similarities to Prnp in birds, reptiles, amphibians and fish. This high conservation together with its ubiquitous expression, - albeit at highest levels in the brain-, suggest that PrPC has major physiological functions. Dissecting PrPC function is further complicated by the occurrence, in mammals, of two potentially partially redundant homologues, Doppel, and Shadoo. The biological overlaps between members of the prion protein family are still under investigation and much debated. Similarly, although in vitro analyses have suggested various functions for PrPC, notably in cell death and survival processes, some have yielded conflicting results and/or discrepancies with in vivo studies. This Research Topic brings together the accumulated knowledge regarding the biological roles of the prion protein family, from the animal to the molecular scale.

Second hand smoke and COPD: lessons from animal studies

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193165 Year: Pages: 91 DOI: 10.3389/978-2-88919-316-5 Language: English
Publisher: Frontiers Media SA
Subject: Physiology --- Science (General)
Added to DOAB on : 2016-02-05 17:24:33
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Cigarette smoke exposure is the key initiator of chronic inflammation, alveolar destruction, and the loss of alveolar blood vessels that lead to the development of chronic obstructive pulmonary disease (COPD) which is comprised of emphysema and chronic bronchitis. Exposure to secondhand smoke (SHS) is the major risk factor for non-smokers to develop emphysema. While the first-hand smoke is directly inhaled by smokers, passive smoking occurs when non-smokers are involuntary exposed to environmental tobacco smoke also known as second hand smoke (SHS). SHS is a mixture of 2 forms of smoke that come from burning tobacco: side stream smoke (smoke that comes from the end of a lit cigarette, pipe, or cigar) and mainstream smoke (smoke that is exhaled by a smoker). These two types of smoke have basically the same composition, however in SHS many toxic components are more concentrated than in first-hand smoke, therefore more hazardous for people’s health. Several pathological events have been implicated in the development of SHS-induced COPD, but many aspects of this pathology remain poorly understood halting the development of new advanced treatments for this detrimental disease. In this respect we have welcomed leading investigators in the field to share their research findings and provide their thoughts regarding the mechanisms of the SHS exposure-induced immune responses and inflammatory mechanisms of lung destruction in SHS-induced COPD and related comorbidities.

Mechanisms of Adiponectin Action

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ISBN: 9783039212453 / 9783039212460 Year: Pages: 222 DOI: 10.3390/books978-3-03921-246-0 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Social Sciences --- Sociology
Added to DOAB on : 2019-08-28 11:21:27
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The adipokine adiponectin is very concentrated in plasma, and decreased levels of adiponectin are associated with pathological conditions such as obesity, diabetes, cardiovascular diseases, and metabolic syndrome. When produced in its full-length form, adiponectin self-associates to generate multimeric complexes. The full-length form of adiponectin can be cleaved by the globular form of elastase that is produced locally, and the resulting biological effects are exerted in a paracrine or autocrine manner. The different forms of adiponectin bind to specific receptors consisting of two G-protein-independent, seven-transmembrane-spanning receptors, called AdipoR1 and AdipoR2, while T-cadherin has been identified as a potential receptor for high molecular weight complexes of adiponectin. Adiponectin exerts a key role in cellular metabolism, regulating glucose levels as well as fatty acid breakdown. However, its biological effects are heterogeneous, involving multiple target tissues. The Special Issue “Mechanisms of Adiponectin Action” highlights the pleiotropic role of this hormone through 3 research articles and 7 reviews. These papers focus on the recent knowledge regarding adiponectin in different target tissues, both in healthy and in diseased conditions.

Research of Pathogenesis and Novel Therapeutics in Arthritis

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ISBN: 9783038970651 / 9783038970668 Year: Pages: 366 DOI: 10.3390/books978-3-03897-066-8 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Therapeutics
Added to DOAB on : 2019-06-26 08:44:06
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Arthritis has a high prevalence globally and includes over 100 different types, the most common of which are rheumatoid arthritis, osteoarthritis, psoriatic arthritis, and inflammatory arthritis. The exact etiology of arthritis remains unclear and no cure exists. Anti-inflammatory drugs are commonly used in the treatment of arthritis but are associated with significant side effects. Novel modes of therapy and additional prognostic biomarkers are urgently needed for arthritis patients. This book summarizes and discusses the global picture of the current understanding of arthritis.

Keywords

biosimilars --- Th9 lymphocytes --- rheumatoid arthritis --- infliximab --- rheumatoid arthritis --- bone erosion --- osteoblasts --- next-generation sequencing --- bioinformatics --- microRNA --- messenger RNA --- osteoarthritis --- cell signaling --- IL1? --- WNT --- antagonists --- computational modeling --- nitric oxide --- clodronate --- gene expression --- osteoarthritis --- progenitor cells --- SOX9 --- spondyloarthropathies --- inflammation --- mesenchymal stem cells --- visfatin --- IL-6 --- TNF-? --- osteoarthritis --- miR-199a-5p --- Epstein-Barr virus --- glycoprotein 42 --- rheumatoid arthritis --- shared epitope --- triptolide --- rheumatoid arthritis --- basic research --- clinical translation --- osteoarthritis (OA) --- articular cartilage --- molecular pathology --- therapeutics --- rheumatoid arthritis --- antibodies --- collagen --- glycosylation --- disease pathways --- therapy --- experimental arthritis --- TNF? --- etanercept --- infliximab --- adalimumab --- certolizumab pegol --- golimumab --- rheumatoid arthritis --- therapeutic antibody --- structure --- fraxinellone --- collagen-induced arthritis --- rheumatoid arthritis --- inflammatory arthritis --- osteoclastogenesis --- sclareol --- rheumatoid arthritis --- synovial cell --- collagen --- mice --- cytokines --- Th17 --- MAPK --- arthritis --- osteoarthritis --- rheumatoid arthritis --- small-molecule inhibitor --- chondrocytes --- tumor necrosis factor-alpha --- inflammation --- rheumatoid arthritis --- osteoarthritis --- angiogenesis --- cytokines --- chemokines --- early osteoarthritis --- articular cartilage --- proliferation --- fibroblast growth factor 2 --- mitogen activated protein kinase --- transforming growth factor ? --- SMA- and MAD-related protein --- interleukin --- nuclear factor kappa B --- miRNA --- adjuvant arthritis --- arthritis --- biomarkers --- celastrol --- inflammation --- microRNA --- miRNA --- rat --- rheumatoid arthritis --- Traditional Chinese medicine --- tripterine --- triterpenoid --- spinal fusion --- biological --- osteoblast --- osteoclast --- bisphosphonate --- parathyroid hormone --- bone morphogenetic protein --- receptor activator of nuclear factor ?B --- stem cell --- drug delivery system --- anticitrullinated peptide antibodies --- antirheumatic drug --- autoimmune --- disease-modifying --- immunology --- pathology --- rheumatoid factor --- rheumatoid arthritis --- osteoarthritis --- adipokines --- obesity --- rheumatoid arthritis --- osteoarthritis --- anti-arthritis --- biomarkers

mTOR in Human Diseases

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ISBN: 9783039210602 / 9783039210619 Year: Pages: 480 DOI: 10.3390/books978-3-03921-061-9 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General)
Added to DOAB on : 2019-06-26 08:44:06
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The mechanistic target of rapamycin (mTOR) is a major signaling intermediary that coordinates favorable environmental conditions with cell growth. Indeed, as part of two functionally distinct protein complexes, named mTORC1 and mTORC2, mTOR regulates a variety of cellular processes, including protein, lipid, and nucleotide synthesis, as well as autophagy. Over the last two decades, major molecular advances have been made in mTOR signaling and have revealed the complexity of the events implicated in mTOR function and regulation. In parallel, the role of mTOR in diverse pathological conditions has also been identified, including in cancer, hamartoma, neurological, and metabolic diseases. Through a series of articles, this book focuses on the role played by mTOR in cellular processes, metabolism in particular, and highlights a panel of human diseases for which mTOR inhibition provides or might provide benefits. It also addresses future studies needed to further characterize the role of mTOR in selected disorders, which will help design novel therapeutic approaches. It is therefore intended for everyone who has an interest in mTOR biology and its application in human pathologies.

Keywords

acute myeloid leukemia --- metabolism --- mTOR --- PI3K --- phosphorylation --- epithelial to mesenchymal transition --- mTOR inhibitor --- pulmonary fibrosis --- transcriptomics --- miRNome --- everolimus --- mTOR --- thyroid cancer --- sodium iodide symporter (NIS)/SLC5A5 --- dopamine receptor --- autophagy --- AKT --- mTOR --- AMPK --- mTOR --- Medulloblastoma --- MBSCs --- mTOR --- T-cell acute lymphoblastic leukemia --- targeted therapy --- combination therapy --- mTOR --- metabolic diseases --- glucose and lipid metabolism --- anesthesia --- neurotoxicity --- synapse --- mTOR --- neurodevelopment --- mTOR --- rapamycin --- autophagy --- protein aggregation --- methamphetamine --- schizophrenia --- tumour cachexia --- mTOR --- signalling --- metabolism --- proteolysis --- lipolysis --- mTOR --- mTORC1 --- mTORC2 --- rapamycin --- rapalogues --- rapalogs --- mTOR inhibitors --- senescence --- ageing --- aging --- cancer --- neurodegeneration --- immunosenescence --- senolytics --- biomarkers --- leukemia --- cell signaling --- metabolism --- apoptosis --- miRNA --- mTOR inhibitors --- mTOR --- tumor microenvironment --- angiogenesis --- immunotherapy --- fluid shear stress --- melatonin --- chloral hydrate --- nocodazole --- MC3T3-E1 cells --- primary cilia --- mTOR complex --- metabolic reprogramming --- cancer --- microenvironment --- nutrient sensor --- oral cavity squamous cell carcinoma (OSCC) --- NVP-BEZ235 --- mTOR --- p70S6K --- mTOR --- advanced biliary tract cancers --- mTOR --- NGS --- illumina --- IonTorrent --- eIFs --- mTOR --- autophagy --- Parkinson’s disease --- mTOR --- PI3K --- cancer --- inhibitor --- therapy --- mTOR --- laminopathies --- lamin A/C --- Emery-Dreifuss muscular dystrophy (EDMD) --- Hutchinson-Gilford progeria syndrome (HGPS) --- autophagy --- cellular signaling --- metabolism --- bone remodeling --- ageing --- mTOR --- fructose --- glucose --- liver --- lipid metabolism --- gluconeogenesis --- Alzheimer’s disease --- autophagy --- mTOR signal pathway --- physical activity --- microRNA --- mTOR --- spermatogenesis --- male fertility --- Sertoli cells --- n/a

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