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Molecular Regulation and Therapeutic Potential of Thermogenic Fat Cells

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889198696 Year: Pages: 127 DOI: 10.3389/978-2-88919-869-6 Language: English
Publisher: Frontiers Media SA
Subject: Internal medicine --- Medicine (General)
Added to DOAB on : 2016-01-19 14:05:46
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Obesity has emerged as a major threat to public health in both the western and developing world. Essentially a disorder of energy balance, obesity occurs when energy intake and storage exceeds expenditure. Much of energy homeostasis depends on the activity and function of adipose tissue. Adipocytes in mammals fall into two categories classified by their primary functions: white fat cells that mediate energy storage and thermogenic fat cells that counteract hypothermia and obesity through adaptive thermogenesis. Whereas white fat and its function as an energy reservoir and endocrine organ have been studied for decades and are relatively well understood, until recently many aspects of the thermogenic fat biology have remained elusive. Accumulating evidence supports the hypothesis that thermogenic fat cells arise from at least two different developmental origins: the ones of a skeletal muscle-like lineage are now called “classical” brown fat cells, and the rest of the thermogenic fat cells are normally referred to as the beige fat cells. The last decade has witnessed an explosion of interest and studies focusing on the regulation of thermogenic fat cells and potential therapeutics targeting these adipocytes. Here we summarize the recent advancements in our understanding of these metabolically active fat cells.

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.

The Metabolic-Inflammatory Axis in Brain Aging and Neurodegeneration

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889452538 Year: Pages: 161 DOI: 10.3389/978-2-88945-253-8 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2018-02-27 16:16:44
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Impairment of energy metabolism is a hallmark of brain aging and several neurodegenerative diseases, such as the Alzheimer’s disease (AD). Age- and disease-related hypometabolism is commonly associated with oxidative stress and they are both regarded as major contributors to the decline in synaptic plasticity and cognition. Neuroinflammatory changes, entailing microglial activation and elevated expression of inflammatory cytokines, also correlate with age-related cognitive decline. It is still under debate whether the mitochondrial dysfunction-induced metabolic deficits or the microglia activation-mediated neuroinflammation is the initiator of the cognitive changes in aging and AD. Nevertheless, multiple lines of evidence support the notion that mitochondrial dysfunction and chronic inflammation exacerbate each other, and these mechanistic diversities have cellular redox dysregulation as a common denominator. This research topic focuses on the role of a metabolic-inflammatory axis encompassing the bioenergetic activity, brain inflammatory responses and their redox regulation in healthy brain aging and neurodegenerative diseases. Dynamic interactions among these systems are reviewed in terms of their causative or in-tandem occurrence and how the systemic environment, –e.g., insulin resistance, diabetes, and systemic inflammation–, impacts on brain function.

Redox Homeostasis Managers in Plants under Environmental Stresses

Authors: --- --- --- --- et al.
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889198788 Year: Pages: 208 DOI: 10.3389/978-2-88919-878-8 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Environmental Sciences
Added to DOAB on : 2016-01-19 14:05:46
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The production of cellular oxidants such as reactive oxygen species (ROS) is an inevitable con-sequence of redox cascades of aerobic metabolism in plants. This milieu is further aggravated by a myriad of adverse environmental conditions that plants, owing to their sessile life-style, have to cope with during their life cycle. Adverse conditions prevent plants reaching their full genetic potential in terms of growth and productivity mainly as a result of accelerated ROS generation-accrued redox imbalances and halted cellular metabolism. In order to sustain ROS-accrued consequences, plants tend to manage a fine homeostasis between the generation and antioxidants-mediated metabolisms of ROS and its reaction products. Well-known for their involvement in the regulation of several non-stress-related processes, redox related components such as proteinaceous thiol members such as thioredoxin, glutaredoxin, and peroxiredoxin proteins, and key soluble redox-compounds namely ascorbate (AsA) and glutathione (GSH) are also listed as efficient managers of cellular redox homeostasis in plants. The management of the cellular redox homeostasis is also contributed by electron carriers and energy metabolism mediators such as non-phosphorylated (NAD+) and the phosphorylated (NADP+) coenzyme forms and their redox couples DHA/AsA, GSSG/GSH, NAD+/NADH and NADP+/NADPH. Moreover, intracellular concentrations of these cellular redox homeostasis managers in plant cells fluctuate with the external environments and mediate dynamic signaling in pant stress responses. This research topic aims to exemplify new information on how redox homeostasis managers are modulated by environmental cues and what potential strategies are useful for improving cellular concentrations of major redox homeostasis managers. Additionally, it also aims to pro-vide readers detailed updates on specific topics, and to highlight so far unexplored aspects in the current context.

Role of Natural Compounds in Inflammation and Inflammatory-Related Diseases

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ISBN: 9783039215522 / 9783039215539 Year: Pages: 174 DOI: 10.3390/books978-3-03921-553-9 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Science (General) --- Chemistry (General)
Added to DOAB on : 2019-12-09 11:49:15
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The papers reported here will contribute to proposing new insights into the mechanisms of several conditions, as well as suggesting new diagnostic alternatives and therapeutic targets in widespread pathologies such inflammation and inflammatory-based diseases. The discovery of the new is, as always, anchored in recourse to the old.

Benefits of Resveratrol Supplementation

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ISBN: 9783039212750 / 9783039212767 Year: Pages: 260 DOI: 10.3390/books978-3-03921-276-7 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Science (General) --- Biology --- Nutrition and Food Sciences
Added to DOAB on : 2019-08-28 11:21:27
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In recent years, great attention has been paid to polyphenols due to their positive effects on health. One of the most widely-studied phenolic compounds is resveratrol. This molecule, which is naturally present in some foods, shows beneficial effects on various physiological and biochemical processes, thus representing a potential tool for the prevention or the treatment of diseases highly prevalent in our society. Several of these beneficial effects have been observed in human beings, but others only in pre-clinical studies so far, and therefore, it is mandatory to continue with the scientific research in this field. Indeed, new knowledge concerning these issues could enable the development of novel functional foods or nutraceuticals, incorporating resveratrol, suitable for preventing or treating diseases such as cancer, cardiovascular diseases, obesity, dislipemia, insulin resistance and diabetes, liver diseases, etc.

Biomedical Insights that Inform the Diagnosis of ME/CFS

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ISBN: 9783039283903 / 9783039283910 Year: Pages: 202 DOI: 10.3390/books978-3-03928-391-0 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Therapeutics --- Medicine (General)
Added to DOAB on : 2020-04-07 23:07:09
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Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a severe chronic health condition that is often misunderstood or ignored by health establishments. The lack of definitive diagnostic markers to separate ME/CFS patients from the healthy population as well as from other chronic disorders is problematic for both health professionals and researchers. A consortium of Australian researchers gathered to systematically understand ME/CFS, ranging from a deep analysis of clinical and pathology data to metabolomic profiles and the investigation of mitochondrial function. From this broad collaboration, a number of compelling insights have arisen that may form the basis of specific serum, blood, and/or urinary biomarkers of ME/CFS. This Special Edition reports on a conference centred on these biomedical discoveries, with other contributions, with a translation focus for predictive markers for ME/CFS diagnosis. By supporting health professionals with developments in diagnostics for this condition, the patients and their families will hopefully benefit from an improved recognition of the biomedical underpinnings of the condition and will be better able to access the care that is urgently required. This Special Edition contains a mix of speaker submissions and other accepted manuscripts that contributed to our objective of advancing biomedical insights to enable the accurate diagnosis of ME/CFS.

Keywords

myalgic encephalomyelitis --- chronic fatigue syndrome --- diagnosis --- symptoms --- muscles --- neurology --- myalgic encephalomyelitis --- chronic fatigue syndrome --- post-exertional malaise --- assessment --- patient-driven questionnaire --- participatory research --- myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) --- energy metabolism --- potential biomarkers --- fatigue syndrome --- chronic --- exercise --- hypoacetylation --- methylhistidine --- histone deacetylation --- myalgic encephalomyelitis --- chronic fatigue syndrome --- diagnostic biomarker --- inflammation and immunity --- metabolism --- mitochondria --- circadian rhythm --- neuro-inflammation --- myalgic encephalomyelitis --- chronic fatigue syndrome --- activin --- pathology --- biomarker --- cytokine --- machine learning --- reference intervals --- myalgic encephalomyelitis --- chronic fatigue syndrome --- ME/CFS --- diagnosis --- metabolism --- mitochondria --- inflammation --- immune system --- signaling --- gut microbiota --- tryptophan metabolism --- indoleamine-2,3-dioxygenase --- bistability --- kynurenine pathway --- substrate inhibition --- myalgic encephalomyelitis --- chronic fatigue syndrome --- mathematical model --- critical point --- immunological --- chronic fatigue syndrome --- myalgic encephalomyelitis --- biomarker --- neuroimmune --- Epstein Barr virus --- hypothalamic–pituitary–adrenal axis --- CFS (Chronic Fatigue Syndrome) --- ME (Myalgic Encephalomyelitis) --- medical retirement --- prognosis --- work rehabilitation --- n/a

Pheochromocytoma (PHEO) and Paraganglioma (PGL)

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ISBN: 9783039216543 / 9783039216550 Year: Pages: 380 DOI: 10.3390/books978-3-03921-655-0 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General)
Added to DOAB on : 2019-12-09 11:49:16
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This book outlines some new advances in genetics, clinical evaluation, localization, therapy (newly including immunotherapy) of pheochromocytoma and paraganglioma including their metastatic counterparts. Well-known and experienced clinicians and scientists contributed to this book to include some novel approaches to these tumors. This book will serve to various health care professionals from different subspecialties, but mainly oncologists, endocrinologists, endocrine surgeons, pediatricians, and radiologists. This book shows that the field of pheochromocytoma/paraganglioma is evolving and a significant progress has been made in last 5 years requiring that health care professionals and scientists will learns new information and implement it in their clinical practice or scientific work, respectively. This book should not be missed by anybody who is focusing on neuroendocrine tumors, their newest evaluation and treatment.

Keywords

pheochromocytoma --- paraganglioma --- adrenocortical carcinoma --- adrenal tumor --- pan-cancer analysis --- neural crest --- neuroendocrine --- paraganglioma --- head and neck --- radiotherapy --- 18F-FDOPA --- PET --- GTV --- SDHB --- SDHD --- mortality --- paraganglioma --- pheochromocytoma --- radiofrequency ablation --- cryoablation --- percutaneous ethanol injection --- neuroendocrine tumor --- minimally invasive procedure --- percutaneous ablation --- PASS --- GAPP --- histology --- meta-analysis --- paraganglioma --- pheochromocytoma --- carotid body --- angiogenesis --- mitochondria --- neural crest --- neurogenesis --- paraganglioma --- stem-like tumor cells --- vasculogenesis --- xenograft --- pheochromocytoma --- catecholamine --- global longitudinal strain --- speckle-tracking echocardiography --- subclinical systolic dysfunction --- pheochromocytoma --- paraganglioma --- neuroendocrine tumor --- targeted therapy --- therapy resistance --- FGF21 --- pheochromocytoma --- paraganglioma --- diabetes mellitus --- obesity --- energy metabolism --- calorimetry --- chromogranin A --- metanephrines --- pheochromocytoma --- paraganglioma --- hypoxia --- pseudohypoxia --- spheroids --- HIF --- EPAS1 --- catecholamine --- pheochromocytoma and paraganglioma --- phosphorylation tyrosine hydroxylase --- dog --- pheochromocytoma --- paraganglioma --- SDHB --- SDHD --- mutation --- chromosomal alteration --- comparative genomics --- pheochromocytoma --- paraganglioma --- metastatic --- immunotherapy --- innate immunity --- adaptive immunity --- toll-like receptor --- pathogen-associated molecular patterns --- neutrophil --- T cell --- pheochromocytoma --- paraganglioma --- hypertension --- blood pressure variability --- average real variability --- weighted standard deviation --- paraganglioma --- somatostatinoma --- polycythemia --- EPAS1 --- transgenic mice --- erythropoietin --- pheochromocytoma --- paraganglioma --- TCA cycle --- germline mutation --- metastatic OR malignant pheochromocytoma --- paraganglioma --- ectopic secretion --- lL-6 --- normetanephrines --- VHL --- NF1 --- EPAS1 --- hypoxia-inducible factor --- inflammation --- radiosensitization --- succinate dehydrogenase --- mouse pheochromocytoma cells --- immunohistochemistry --- fluorescence imaging --- pheochromocytoma --- paraganglioma --- next-generation sequencing --- sporadic --- hereditary --- CNV detection --- pheochromocytoma --- paraganglioma --- PET-CT --- 11C-hydroxy-ephedrine --- adrenal incidentaloma --- pheochromocytoma --- paraganglioma --- 177Lu-DOTATATE --- peptide receptor radiotherapy --- PRRT --- neuroendocrine tumor --- NET --- PCC --- PGL --- postoperative --- pheochromocytoma --- hypertension --- hypotension --- arrhythmia --- PPGL --- catecholamines --- adrenomedullary function --- n/a

AMP-Activated Protein Kinase Signalling

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ISBN: 9783038976622 Year: Pages: 452 DOI: 10.3390/books978-3-03897-663-9 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Science (General) --- Biology
Added to DOAB on : 2019-03-21 14:08:22
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Starting from a kinase of interest, AMP-activated protein kinase (AMPK) has gone far beyond an average biomolecule. Being expressed in all mammalian cell types and probably having a counterpart in every eukaryotic cell, AMPK has attracted interest in virtually all areas of biological research. Structural and biophysical insights have greatly contributed to a molecular understanding of this kinase. From good old protein biochemistry to modern approaches, such as systems biology and advanced microscopy, all disciplines have provided important information. Thus, multiple links to cellular events and subcellular localizations have been established. Moreover, the crucial involvement of AMPK in human health and disease has been evidenced. AMPK accordingly has moved from an interesting enzyme to a pharmacological target. However, despite our extensive current knowledge about AMPK, the growing community is busier than ever. This book provides a snapshot of recent and current AMPK research with an emphasis on work providing molecular insight, including but not limited to novel physiological and pathological functions, or regulatory mechanisms. Up-to-date reviews and research articles are included.

Keywords

exercise --- glucose uptake --- AMP-activated protein kinase --- TBC1D4 --- AS160 --- AMP-activated protein kinase --- developmental origins of health and disease (DOHaD) --- hypertension --- kidney disease --- nutrient-sensing signals --- oxidative stress --- renin-angiotensin system --- AMPK --- autophagy --- co-expression --- microarrays --- 3T3-L1 --- adipocyte --- differentiation --- AMPK --- tight junctions --- epithelial cells --- ZO-1 --- par complex --- MDCK --- nectin-afadin --- adherent junctions --- TAK1 --- AMPK --- phosphorylation --- AMPK kinase --- endothelial nitric-oxide synthase --- vasodilation --- phenylephrine --- vasoconstriction --- endothelial cells --- ionomycin --- AMPK --- liver --- lipid metabolism --- fatty acid oxidation --- indirect calorimetry --- atrophy --- regrowth --- sirtuin 1 (SIRT1) --- peroxisome proliferator-activated receptor gamma coactivator 1-? (PGC1?) --- heat shock protein --- fiber-type --- AMPK --- monocytes --- macrophages --- differentiation --- autophagy --- AML --- MDS --- CML --- CMML --- pregnancy --- catechol-O-methyltransferase --- 2-methoxyestradiol --- preeclampsia --- gestational diabetes mellitus --- AMPK --- IL-1? --- NLRP3 --- nutrition --- dietary fatty acids --- metabolic-inflammation --- nutrigenomics --- AMPK --- LKB1 --- autophagy --- proteasome --- hypertrophy --- atrophy --- skeletal muscle --- AICAR --- mTOR --- protein synthesis --- AMPK --- epigenetics --- chromatin remodeling --- histone modification --- DNA methylation --- medulloblastoma --- sonic hedgehog --- AMPK --- AMP-activated protein kinase (AMPK) --- spermatozoa --- motility --- mitochondria --- membranes --- signaling --- stress --- assisted reproduction techniques --- AMP-activated protein kinase --- epigenetics --- protein acetylation --- KATs --- HDACs --- acetyl-CoA --- NAD+ --- AMP-activated protein kinase --- glycogen --- exercise --- metabolism --- cellular energy sensing --- energy utilization --- liver --- skeletal muscle --- metabolic disease --- glycogen storage disease --- resveratrol --- AMPK --- hepatocyte --- liver --- steatosis --- transporter --- carrier --- pump --- membrane --- energy deficiency --- AMPK --- infection --- mycobacteria --- host defense --- energy metabolism --- AMPK --- activation loop --- AID --- ?-linker --- ?-linker --- CBS --- LKB1 --- CaMKK2 --- ?RIM --- hypothalamus --- adenosine monophosphate-activated protein kinase --- adipose tissue --- food intake --- adaptive thermogenesis --- beiging --- AMPK --- HDAC4/5 --- p70S6K --- MyHC I(?), motor endplate remodeling --- soleus muscle --- mechanical unloading --- hindlimb suspension --- AMPK --- synaptic activation --- PKA --- CREB --- soluble Adenylyl cyclase --- Immediate early genes --- transcription --- AMPK --- autophagy --- metabolism --- mTOR --- ULK --- AMP-activated protein kinase --- protein kinase B --- Akt --- insulin signalling --- A769662 --- endothelial function --- n/a

DNA Replication Stress

Author:
ISBN: 9783039213894 / 9783039213900 Year: Pages: 368 DOI: 10.3390/books978-3-03921-390-0 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Science (General) --- Biology
Added to DOAB on : 2019-12-09 16:10:12
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This Special Issue of International Journal of Molecular Sciences (IJMS) is dedicated to the mechanisms mediated at the molecular and cellular levels in response to adverse genomic perturbations and DNA replication stress. The relevant proteins and processes play paramount roles in nucleic acid transactions to maintain genomic stability and cellular homeostasis. A total of 18 articles are presented which encompass a broad range of highly relevant topics in genome biology. These include replication fork dynamics, DNA repair processes, DNA damage signaling and cell cycle control, cancer biology, epigenetics, cellular senescence, neurodegeneration, and aging. As Guest Editor for this IJMS Special Issue, I am very pleased to offer this collection of riveting articles centered on the theme of DNA replication stress. The blend of articles builds upon a theme that DNA damage has profound consequences for genomic stability and cellular homeostasis that affect tissue function, disease, cancer, and aging at multiple levels and through unique mechanisms. I thank the authors for their excellent contributions, which provide new insight into this fascinating and highly relevant area of genome biology.

Keywords

barley --- chromosome --- DNA replication pattern --- EdU --- mutagens --- DNA replication --- DNA damage --- DNA repair --- genome integrity --- A549 cells --- H1299 cells --- heterogeneity --- DNA damage response --- 8-chloro-adenosine --- DNA replication --- S phase --- origin firing --- TopBP1 --- ATR --- DNA fiber assay --- APE2 --- ATR-Chk1 DDR pathway --- Genome integrity --- SSB end resection --- SSB repair --- SSB signaling --- DNA replication stress --- genome stability --- ubiquitin --- replication fork restart --- translesion synthesis --- template-switching --- homologous recombination --- Fanconi Anemia --- G protein-coupled receptor (GPCR) --- aging --- DNA damage --- ?-arrestin --- G protein-coupled receptor kinase (GRK) --- interactome --- G protein-coupled receptor kinase interacting protein 2 (GIT2) --- ataxia telangiectasia mutated (ATM) --- clock proteins --- energy metabolism --- neurodegeneration --- cellular senescence --- ageing --- Alzheimer’s disease --- multiple sclerosis --- Parkinson’s disease --- lipofuscin --- SenTraGorTM (GL13) --- senolytics --- DNA replication --- DNA repair --- DNA damage response --- DNA translocation --- DNA helicase --- superfamily 2 ATPase --- replication restart --- fork reversal --- fork regression --- chromatin remodeler --- C9orf72 --- ALS --- motor neuron disease --- R loops, nucleolar stress --- neurodegeneration --- Difficult-to-Replicate Sequences --- replication stress --- non-B DNA --- Polymerase eta --- Polymerase kappa --- genome instability --- common fragile sites --- Microsatellites --- cancer --- DNA double-strand repair --- premature aging --- post-translational modification --- protein stability --- replication stress --- Werner Syndrome --- Werner Syndrome Protein --- dormant origins --- replicative stress --- replication timing --- DNA damage --- genome instability --- cancer --- Thermococcus eurythermalis --- endonuclease IV --- AP site analogue --- spacer --- DNA repair --- DNA repair --- double strand break repair --- exonuclease 1 --- EXO1 --- mismatch repair --- MMR --- NER --- nucleotide excision repair --- strand displacements --- TLS --- translesion DNA synthesis --- POL? --- mutation frequency --- mutations spectra --- SupF --- mutagenicity --- oxidative stress --- DNA damage --- DNA repair --- replication --- 8-oxoG --- epigenetic --- gene expression --- helicase --- cell cycle checkpoints --- genomic instability --- G2-arrest --- cell death --- repair of DNA damage --- adaptation --- n/a

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