Results for 'cancer metabolism'

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  1.  22
    Long non‐coding RNAs in cancer metabolism.Zhen-Dong Xiao, Li Zhuang & Boyi Gan - 2016 - Bioessays 38 (10):991-996.
    Altered cellular metabolism is an emerging hallmark of cancer. Accumulating recent evidence links long non‐coding RNAs (lncRNAs), a still poorly understood class of non‐coding RNAs, to cancer metabolism. Here we review the emerging findings on the functions of lncRNAs in cancer metabolism, with particular emphasis on how lncRNAs regulate glucose and glutamine metabolism in cancer cells, discuss how lncRNAs regulate various aspects of cancer metabolism through their cross‐talk with other macromolecules, (...)
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  2.  25
    Long non‐coding RNAs in cancer metabolism.Zhen-Dong Xiao, Li Zhuang & Boyi Gan - 2016 - Bioessays 38 (10):991-996.
    Altered cellular metabolism is an emerging hallmark of cancer. Accumulating recent evidence links long non‐coding RNAs (lncRNAs), a still poorly understood class of non‐coding RNAs, to cancer metabolism. Here we review the emerging findings on the functions of lncRNAs in cancer metabolism, with particular emphasis on how lncRNAs regulate glucose and glutamine metabolism in cancer cells, discuss how lncRNAs regulate various aspects of cancer metabolism through their cross‐talk with other macromolecules, (...)
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  3.  30
    Everything in moderation or moderating everything? Nutrient balancing in the context of evolution and cancer metabolism.Jonathan Sholl - 2022 - Biology and Philosophy 37 (2):1-32.
    While philosophers of science have marginally discussed concepts such as ‘nutrient’, ‘naturalness’, ‘food’, or the ‘molecularization’ of nutrition, they have yet to seriously engage with the nutrition sciences. In this paper, I offer one way to begin this engagement by investigating conceptual challenges facing the burgeoning field of nutritional ecology and the question of how organisms construct a ‘balanced’ diet. To provide clarity, I propose the distinction between nutrient balance as a property of foods or dietary patterns and nutrient balancing (...)
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  4.  14
    A second Warburg‐like effect in cancer metabolism: The metabolic shift of glutamine‐derived nitrogen.Manabu Kodama & Keiichi I. Nakayama - 2020 - Bioessays 42 (12):2000169.
    Carbon and nitrogen are essential elements for life. Glucose as a carbon source and glutamine as a nitrogen source are important nutrients for cell proliferation. About 100 years ago, it was discovered that cancer cells that have acquired unlimited proliferative capacity and undergone malignant evolution in their host manifest a cancer‐specific remodeling of glucose metabolism (the Warburg effect). Only recently, however, was it shown that the metabolism of glutamine‐derived nitrogen is substantially shifted from glutaminolysis to nucleotide (...)
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  5.  18
    Gut microbial metabolism and colon cancer: Can manipulations of the microbiota be useful in the management of gastrointestinal health?Antoaneta Belcheva, Thergiory Irrazabal & Alberto Martin - 2015 - Bioessays 37 (4):403-412.
    The gut microbiota is an important component of the human body and its immune‐modulating and metabolic activities are critical to maintain good health. Gut microbes, however, are sensitive to changes in diet, exposure to antibiotics, or infections, all of which cause transient disruptions in the microbial composition, a phenomenon known as dysbiosis. It is now recognized that microbial dysbiosis is at the root of many gastrointestinal disorders. However, the mechanisms through which bacterial dysbiosis initiates disease are not fully understood. Microbially‐derived (...)
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  6.  46
    Cancer: A de‐repression of a default survival program common to all cells?Mark Vincent - 2012 - Bioessays 34 (1):72-82.
    Cancer viewed as a programmed, evolutionarily conserved life‐form, rather than just a random series of disease‐causing mutations, answers the rarely asked question of what the cancer cell is for, provides meaning for its otherwise mysterious suite of attributes, and encourages a different type of thinking about treatment. The broad but consistent spectrum of traits, well‐recognized in all aggressive cancers, group naturally into three categories: taxonomy (“phylogenation”), atavism (“re‐primitivization”) and robustness (“adaptive resilience”). The parsimonious explanation is not convergent evolution, (...)
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  7.  4
    Why do cancer cells break from host circadian rhythm? Insights from unicellular organisms.Aliaa A. Alamoudi - 2021 - Bioessays 43 (4):2000205.
    It is not clear why cancer cells choose to disrupt their circadian clock rhythms, and whether such disruption governs a selective fitness and a survival advantage. In this review, I focus on understanding the impacts of clock gene disruption on a simpler model, such as the unicellular cyanobacterium, in order to explain how cancer cells may alter the circadian rhythm to reprogram their metabolism based on their needs and status. It appears to be that the activation of (...)
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  8.  11
    Metabolic Reprogramming is a Hallmark of Metabolism Itself.Miguel Ángel Medina - 2020 - Bioessays 42 (10):2000058.
    The reprogramming of metabolism has been identified as one of the hallmarks of cancer. It is becoming more and more frequent to connect other diseases with metabolic reprogramming. This article aims to argue that metabolic reprogramming is not driven by disease but instead is the main hallmark of metabolism, based on its dynamic behavior that allows it to continuously adapt to changes in the internal and external conditions.
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  9.  24
    Citrate transport and metabolism in mammalian cells.Maria E. Mycielska, Ameet Patel, Nahit Rizaner, Maciej P. Mazurek, Hector Keun, Anup Patel, Vadivel Ganapathy & Mustafa B. A. Djamgoz - 2009 - Bioessays 31 (1):10-20.
    Citrate, an organic trivalent anion, is a major substrate for generation of energy in most cells. It is produced in mitochondria and used either in the Krebs' cycle or released into cytoplasm through a specific mitochondrial carriers. Citrate can also be taken up from blood through different plasma membrane transporters. In the cytoplasm, citrate can be used ultimately for fatty acid synthesis, which is increased in cancer cells. Here, we review the ways in which citrate can be transported and (...)
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  10.  23
    Targeting MYC in cancer therapy: RNA processing offers new opportunities.Cheryl M. Koh, Arianna Sabò & Ernesto Guccione - 2016 - Bioessays 38 (3):266-275.
    MYC is a transcription factor, which not only directly modulates multiple aspects of transcription and co‐transcriptional processing (e.g. RNA‐Polymerase II initiation, elongation, and mRNA capping), but also indirectly influences several steps of RNA metabolism, including both constitutive and alternative splicing, mRNA stability, and translation efficiency. As MYC is an oncoprotein whose expression is deregulated in multiple human cancers, identifying its critical downstream activities in tumors is of key importance for designing effective therapeutic strategies. With this knowledge and recent technological (...)
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  11. The Origins of “Dynamic Reciprocity”: Mina Bissell’s Expansive Picture of Cancer Causation.Anya Plutynski - 2018 - In Oren Harman & Michael R. Dietrich (eds.), Dreamers, Visionaries, and Revolutionaries in the Life Sciences. University of Chicago Press. pp. 96-.
    This chapter discusses Mina Bissell's pathbreaking research on cancer. Along with her colleagues and students, Bissell focused her attention on how the causal pathways regulating cell behavior were a two way street. Healthy cells’ and cancer cells’ behavior are both highly context-dependent. The pathway to this insight was not direct. Bissell’s work began with research into cellular metabolism. As a result of this early research, she found that cells can “change their fate” – revert to, or activate, (...)
     
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  12.  9
    Metabolomics meets lipidomics: Assessing the small molecule component of metabolism.Hector Gallart-Ayala, Tony Teav & Julijana Ivanisevic - 2020 - Bioessays 42 (12):2000052.
    Metabolomics, including lipidomics, is emerging as a quantitative biology approach for the assessment of energy flow through metabolism and information flow through metabolic signaling; thus, providing novel insights into metabolism and its regulation, in health, healthy ageing and disease. In this forward‐looking review we provide an overview on the origins of metabolomics, on its role in this postgenomic era of biochemistry and its application to investigate metabolite role and (bio)activity, from model systems to human population studies. We present (...)
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  13.  13
    Genetic polymorphism and cancer susceptibility: Evidence concerning acetyltransferases and cancer of the urinary bladder.David W. Hein - 1988 - Bioessays 9 (6):200-204.
    Acetyltransferase enzymes expressed in hepatic and extrahepatic tissues are products of an acetyltransferase gene locus. Acetylation capacity is regulated by simple autosomal Mendelian inheritance of two codominant alleles at this locus. Human slow acetylators are predisposed to bladder cancer from arylamine chemicals. The role of the bladder in arylamine metabolism and of bladder acetyltransferases in the etiology of bladder cancer is not fully understood, but the acetylator genotype‐dependent expression of arylamine N‐acetyltransferase and N‐hydroxyarylamine O‐acetyltransferase in bladder cytosol (...)
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  14.  6
    WRN rescues replication forks compromised by a BRCA2 deficiency: Predictions for how inhibition of a helicase that suppresses premature aging tilts the balance to fork demise and chromosomal instability in cancer.Arindam Datta & Robert M. Brosh - 2022 - Bioessays 44 (8):2200057.
    Hereditary breast and ovarian cancers are frequently attributed to germline mutations in the tumor suppressor genes BRCA1 and BRCA2. BRCA1/2 act to repair double‐strand breaks (DSBs) and suppress the demise of unstable replication forks. Our work elucidated a dynamic interplay between BRCA2 and the WRN DNA helicase/exonuclease defective in the premature aging disorder Werner syndrome. WRN and BRCA2 participate in complementary pathways to stabilize replication forks in cancer cells, allowing them to proliferate. Whether the functional overlap of WRN and (...)
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  15.  19
    mTORC2 activity in brain cancer: Extracellular nutrients are required to maintain oncogenic signaling.Kenta Masui, Noriyuki Shibata, Webster K. Cavenee & Paul S. Mischel - 2016 - Bioessays 38 (9):839-844.
    Mutations in growth factor receptor signaling pathways are common in cancer cells, including the highly lethal brain tumor glioblastoma (GBM) where they drive tumor growth through mechanisms including altering the uptake and utilization of nutrients. However, the impact of changes in micro‐environmental nutrient levels on oncogenic signaling, tumor growth, and drug resistance is not well understood. We recently tested the hypothesis that external nutrients promote GBM growth and treatment resistance by maintaining the activity of mechanistic target of rapamycin complex (...)
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  16.  8
    Linking the unfolded protein response to bioactive lipid metabolism and signalling in the cell non‐autonomous extracellular communication of ER stress.Nicole T. Watt, Anna McGrane & Lee D. Roberts - 2023 - Bioessays 45 (8):2300029.
    The endoplasmic reticulum (ER) organelle is the key intracellular site of both protein and lipid biosynthesis. ER dysfunction, termed ER stress, can result in protein accretion within the ER and cell death; a pathophysiological process contributing to a range of metabolic diseases and cancers. ER stress leads to the activation of a protective signalling cascade termed the Unfolded Protein Response (UPR). However, chronic UPR activation can ultimately result in cellular apoptosis. Emerging evidence suggests that cells undergoing ER stress and UPR (...)
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  17.  36
    The two faces of FBW7 in cancer drug resistance.Zhiwei Wang, Hidefumi Fukushima, Daming Gao, Hiroyuki Inuzuka, Lixin Wan, Alan W. Lau, Pengda Liu & Wenyi Wei - 2011 - Bioessays 33 (11):851-859.
    Chemotherapy is an important therapeutic approach for cancer treatment. However, drug resistance is an obstacle that often impairs the successful use of chemotherapies. Therefore, overcoming drug resistance would lead to better therapeutic outcomes for cancer patients. Recently, studies by our own and other groups have demonstrated that there is an intimate correlation between the loss of the F‐box and WD repeat domain‐containing 7 (FBW7) tumor suppressor and the incurring drug resistance. While loss of FBW7 sensitizes cancer cells (...)
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  18.  3
    Can natural selection and druggable targets synergize? Of nutrient scarcity, cancer, and the evolution of cooperation.Neil W. Blackstone & Jordan U. Gutterman - 2021 - Bioessays 43 (2):2000160.
    Since the dawn of molecular biology, cancer therapy has focused on druggable targets. Despite some remarkable successes, cell‐level evolution remains a potent antagonist to this approach. We suggest that a deeper understanding of the breakdown of cooperation can synergize the evolutionary and druggable‐targets approaches. Complexity requires cooperation, whether between cells of different species (symbiosis) or between cells of the same organism (multicellularity). Both forms of cooperation may be associated with nutrient scarcity, which in turn may be associated with a (...)
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  19.  6
    Paneth cells: Maintaining dynamic microbiome‐host homeostasis, protecting against inflammation and cancer.Vladimir N. Nikolenko, Marine V. Oganesyan, Maria V. Sankova, Kirill V. Bulygin, Andzhela D. Vovkogon, Negoriya A. Rizaeva & Mikhail Y. Sinelnikov - 2021 - Bioessays 43 (3):2000180.
    The human intestines are constantly under the influence of numerous pathological factors: enteropathogenic microorganisms, food antigens, physico‐chemical stress associated with digestion and bacterial metabolism, therefore it must be provided with a system of protection against adverse impact. Recent studies have shown that Paneth cells play a crucial role in maintaining homeostasis of the small intestines. Paneth cells perform many vital functions aimed at maintaining a homeostatic balance between normal microbiota, infectious pathogens and the human body, regulate the qualitative composition (...)
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  20.  25
    The Warburg effect then and now: From cancer to inflammatory diseases.Eva M. Palsson‐McDermott & Luke Aj O'neill - 2013 - Bioessays 35 (11):965-973.
    Inflammatory immune cells, when activated, display much the same metabolic profile as a glycolytic tumor cell. This involves a shift in metabolism away from oxidative phosphorylation towards aerobic glycolysis, a phenomenon known as the Warburg effect. The result of this change in macrophages is to rapidly provide ATP and metabolic intermediates for the biosynthesis of immune and inflammatory proteins. In addition, a rise in certain tricarboxylic acid cycle intermediates occurs notably in citrate for lipid biosynthesis, and succinate, which activates (...)
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  21.  19
    The Effectiveness of Interventions for Developmental Dyslexia: Rhythmic Reading Training Compared With Hemisphere-Specific Stimulation and Action Video Games.Alice Cancer, Silvia Bonacina, Alessandro Antonietti, Antonio Salandi, Massimo Molteni & Maria Luisa Lorusso - 2020 - Frontiers in Psychology 11.
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  22.  20
    Improving reading skills in students with dyslexia: the efficacy of a sublexical training with rhythmic background.Silvia Bonacina, Alice Cancer, Pier Luca Lanzi, Maria Luisa Lorusso & Alessandro Antonietti - 2015 - Frontiers in Psychology 6.
  23.  3
    Editorial: Creativity in Pathological Brain Conditions Across the Lifespan.Barbara Colombo, Alice Cancer, Lindsey Carruthers & Alessandro Antonietti - 2022 - Frontiers in Psychology 13.
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  24.  5
    Creative Thinking and Dyscalculia: Conjectures About a Still Unexplored Link.Sara Magenes, Alessandro Antonietti & Alice Cancer - 2021 - Frontiers in Psychology 12.
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  25.  18
    The Double-Edged Helix: Social Implications of Genetics in a Diverse Society.Joseph S. Alper, Catherine Ard, Adrienne Asch, Peter Conrad, Jon Beckwith, American Cancer Society Research Professor of Microbiology and Molecular Genetics Jon Beckwith, Harry Coplan Professor of Social Sciences Peter Conrad & Lisa N. Geller - 2002
    The rapidly changing field of genetics affects society through advances in health-care and through implications of genetic research. This study addresses the impacts of new genetic discoveries and technologies on different segments of today's society. The book begins with a chapter on genetic complexity, and subsequent chapters discuss moral and ethical questions arising from today's genetics from the perspectives of health care professionals, the media, the general public, special interest groups and commercial interests.
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  26.  14
    Creative Thinking in Tourette's Syndrome: An Uncharted Topic.Laura Colautti, Sara Magenes, Sabrina Rago, Carlotta Zanaboni Dina, Alice Cancer & Alessandro Antonietti - 2021 - Frontiers in Psychology 12.
  27.  45
    Van Rensselaer Potter: An Intellectual Memoir.Peter J. Whitehouse - 2002 - Cambridge Quarterly of Healthcare Ethics 11 (4):331-334.
    Van Rensselaer Potter was the first voice to utter the word “bioethics,” yet he is too little appreciated by the bioethics community. My expectations for my first visit with Professor Van Rensselaer Potter were primed by conversations with leaders and historians of the field of biomedical ethics, including Warren Reich, Al Jonsen, and David Thomasma. When mentioning my interest in environmental ethics and my concerns for the current state of biomedical ethics, I was told that I must meet Van. On (...)
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  28.  4
    Noncanonical functions of the serine‐arginine‐rich splicing factor (SR) family of proteins in development and disease.Rebecca E. Wagner & Michaela Frye - 2021 - Bioessays 43 (4):2000242.
    Members of the serine/arginine (SR)‐rich protein family of splicing factors play versatile roles in RNA processing steps and are often essential for normal development. Dynamic changes in RNA processing and turnover allow fast cellular adaptions to a changing microenvironment and thereby closely cooperate with transcription factor networks that establish cell identity within tissues. SR proteins play fundamental roles in the processing of pre‐mRNAs by regulating constitutive and alternative splicing. More recently, SR proteins have also been implicated in other aspects of (...)
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  29.  38
    Human Endogenous Formaldehyde as an Anticancer Metabolite: Its Oxidation Downregulation May Be a Means of Improving Therapy.Yuri L. Dorokhov, Ekaterina V. Sheshukova, Tatiana E. Bialik & Tatiana V. Komarova - 2018 - Bioessays 40 (12):1800136.
    Malignant cells are characterized by an increased content of endogenous formaldehyde formed as a by‐product of biosynthetic processes. Accumulation of formaldehyde in cancer cells is combined with activation of the processes of cellular formaldehyde clearance. These mechanisms include increased ALDH and suppressed ADH5/FDH activity, which oncologists consider poor and favorable prognostic markers, respectively. Here, the sources and regulation of formaldehyde metabolism in cancer cells are reviewed. The authors also analyze the participation of oncoproteins such as fibulins, FGFR1, (...)
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  30.  29
    Cellular lifespan and senescence: a complex balance between multiple cellular pathways.David Dolivo, Sarah Hernandez & Tanja Dominko - 2016 - Bioessays 38 (S1):33-44.
    The study of cellular senescence and proliferative lifespan is becoming increasingly important because of the promises of autologous cell therapy, the need for model systems for tissue disease and the implication of senescent cell phenotypes in organismal disease states such as sarcopenia, diabetes and various cancers, among others. Here, we explain the concepts of proliferative cellular lifespan and cellular senescence, and we present factors that have been shown to mediate cellular lifespan positively or negatively. We review much recent literature and (...)
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  31.  5
    The eukaryotic translation initiation factor eIF4E unexpectedly acts in splicing thereby coupling mRNA processing with translation.Katherine L. B. Borden - 2024 - Bioessays 46 (1):2300145.
    Recent findings position the eukaryotic translation initiation factor eIF4E as a novel modulator of mRNA splicing, a process that impacts the form and function of resultant proteins. eIF4E physically interacts with the spliceosome and with some intron‐containing transcripts implying a direct role in some splicing events. Moreover, eIF4E drives the production of key components of the splicing machinery underpinning larger scale impacts on splicing. These drive eIF4E‐dependent reprogramming of the splicing signature. This work completes a series of studies demonstrating eIF4E (...)
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  32.  18
    mTOR Senses Intracellular pH through Lysosome Dispersion from RHEB.Zandra E. Walton, Rebekah C. Brooks & Chi V. Dang - 2019 - Bioessays 41 (7):1800265.
    Acidity, generated in hypoxia or hypermetabolic states, perturbs homeostasis and is a feature of solid tumors. That acid peripherally disperses lysosomes is a three‐decade‐old observation, yet one little understood or appreciated. However, recent work has recognized the inhibitory impact this spatial redistribution has on mechanistic target of rapamycin complex 1 (mTORC1), a key regulator of metabolism. This finding argues for a paradigm shift in localization of mTORC1 activator Ras homolog enriched in brain (RHEB), a conclusion several others have now (...)
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  33.  10
    mTORC1 and ferroptosis: Regulatory mechanisms and therapeutic potential.Guang Lei, Li Zhuang & Boyi Gan - 2021 - Bioessays 43 (8):2100093.
    Ferroptosis, a form of regulated cell death triggered by lipid hydroperoxide accumulation, has an important role in a variety of diseases and pathological conditions, such as cancer. Targeting ferroptosis is emerging as a promising means of therapeutic intervention in cancer treatment. Polyunsaturated fatty acids, reactive oxygen species, and labile iron constitute the major underlying triggers for ferroptosis. Other regulators of ferroptosis have also been discovered recently, among them the mechanistic target of rapamycin complex 1 (mTORC1), a central controller (...)
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  34.  13
    Improved network performance via antagonism: From synthetic rescues to multi‐drug combinations.Adilson E. Motter - 2010 - Bioessays 32 (3):236-245.
    Recent research shows that a faulty or sub‐optimally operating metabolic network can often be rescued by the targeted removal of enzyme‐coding genes – the exact opposite of what traditional gene therapy would suggest. Predictions go as far as to assert that certain gene knockouts can restore the growth of otherwise nonviable gene‐deficient cells. Many questions follow from this discovery: What are the underlying mechanisms? How generalizable is this effect? What are the potential applications? Here, I approach these questions from the (...)
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  35.  74
    Accumulation of potentially toxic elements in fourfinger threadfin (Eleutheronema tetradactylum) and black pomfret (Parastromateus niger) from Selangor, Malaysia.Chuck Chuan Ng - 2024 - Environmental Monitoring and Assessment 196 (382).
    The accumulation of potentially toxic elements (PTEs) has raised public awareness due to harmful contamination to both human and marine creatures. This study was designed to determine the concentration of copper (Cu), zinc (Zn), cadmium (Cd), and nickel (Ni) in the intestine, kidney, muscle, gill, and liver tissues of local commercial edible fish, fourfinger threadfin (Eleutheronema tetradactylum), and black pomfret (Parastromateus niger) collected from Morib (M) and Kuala Selangor (KS). Among the studied PTEs, Cu and Zn were essential elements to (...)
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  36.  39
    Phosphatidylinositol‐4‐phosphate: The Golgi and beyond.Maria A. De Matteis, Cathal Wilson & Giovanni D'Angelo - 2013 - Bioessays 35 (7):612-622.
    Initially identified as a key phosphoinositide that controls membrane trafficking at the Golgi complex, phosphatidylinositol‐4‐phosphate (PI4P) has emerged as a key molecule in the regulation of a diverse array of cellular functions. In this review we will discuss selected examples of the findings that in the last few years have significantly increased our awareness of the regulation and roles of PI4P in the Golgi complex and beyond. We will also highlight the role of PI4P in infection and cancer. We (...)
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  37.  4
    Food Consumption From Islamic Perspective: Evidence From Qur’an and Sunnah.Rawda Abdel Moneim Al-Amin - 2023 - European Journal for Philosophy of Religion 15 (3):257-280.
    The Holy Quran and the Sunnah provide the Islamic approach to a complete food system, regulating the consumption of food and drinks, clarifying permissibility and prohibition, to protect human health. This analytical study aimed to explore various categories and benefits of food in Islam derived from plants and animals, focusing specifically on how Islamic Shariah advocates halal food consumption, and what permissions or prohibitions are granted, highlighting the underlying religious evidence and reasoning. The data was collected through both inductive and (...)
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  38.  20
    Anoxia, wound healing, VL30 elements, and the molecular basis of malignant conversion.Garth R. Anderson & Daniel L. Stoler - 1993 - Bioessays 15 (4):265-272.
    Although VL30 retrotransposable elements have been associated with certain cancers for nearly twenty years, because of their expression in rodent malignancies and recombination into murine sarcoma viruses, their causative role, if any, in cancer has been uncertain and enigmatic. Recent findings suggest loss of normal transcriptional control of specific VL30 element expression may make a critical contribution to tumor progression at a step associated with malignant conversion, by bringing into play a cellular program normally involved in wound healing. This (...)
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  39.  8
    Nutrient Sensing by Histone Marks: Reading the Metabolic Histone Code Using Tracing, Omics, and Modeling.Scott E. Campit, Alia Meliki, Neil A. Youngson & Sriram Chandrasekaran - 2020 - Bioessays 42 (9):2000083.
    Several metabolites serve as substrates for histone modifications and communicate changes in the metabolic environment to the epigenome. Technologies such as metabolomics and proteomics have allowed us to reconstruct the interactions between metabolic pathways and histones. These technologies have shed light on how nutrient availability can have a dramatic effect on various histone modifications. This metabolism–epigenome cross talk plays a fundamental role in development, immune function, and diseases like cancer. Yet, major challenges remain in understanding the interactions between (...)
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  40.  14
    Nijmegen breakage syndrome: consequences of defective DNA double strand break repair.Martin Digweed, André Reis & Karl Sperling - 1999 - Bioessays 21 (8):649-656.
    The autosomal recessive genetic disorder, Nijmegen Breakage Syndrome, is characterised by an excessively high risk for the development of lymphatic tumours and an extreme sensitivity towards ionising radiation. The most likely explanation for these characteristics, a deficiency in the repair of DNA lesions, has been greatly substantiated by the recent cloning of the gene mutated in Nijmegen Breakage Syndrome patients and the analysis of its protein product, nibrin. The direct involvement of this protein in the processing of DNA double strand (...)
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  41.  6
    DNA topoisomerases: Advances in understanding of cellular roles and multi‐protein complexes via structure‐function analysis.Shannon J. McKie, Keir C. Neuman & Anthony Maxwell - 2021 - Bioessays 43 (4):2000286.
    DNA topoisomerases, capable of manipulating DNA topology, are ubiquitous and indispensable for cellular survival due to the numerous roles they play during DNA metabolism. As we review here, current structural approaches have revealed unprecedented insights into the complex DNA‐topoisomerase interaction and strand passage mechanism, helping to advance our understanding of their activities in vivo. This has been complemented by single‐molecule techniques, which have facilitated the detailed dissection of the various topoisomerase reactions. Recent work has also revealed the importance of (...)
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  42.  14
    Fanconi anaemia proteins: Major roles in cell protection against oxidative damage.Giovanni Pagano & Hagop Youssoufian - 2003 - Bioessays 25 (6):589-595.
    Fanconi anaemia (FA) is a cancer‐prone genetic disorder that is characterised by cytogenetic instability and redox abnormalities. Although rare subtypes of FA (B, D1 and D2) have been implicated in DNA repair through links with BRCA1 and BRCA2, such a role has yet to be demonstrated for gene products of the common subtypes. Instead, these products have been strongly implicated in xenobiotic metabolism and redox homeostasis through interactions of FANCC with cytochrome P‐450 reductase and with glutathione S‐transferase, and (...)
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  43.  21
    Reversible Ser/Thr SHIP phosphorylation: A new paradigm in phosphoinositide signalling?William'S. Elong Edimo, Veerle Janssens, Etienne Waelkens & Christophe Erneux - 2012 - Bioessays 34 (8):634-642.
    Phosphoinositide (PI) phosphatases such as the SH2 domain‐containing inositol 5‐phosphatases 1/2 (SHIP1 and 2) are important signalling enzymes in human physiopathology. SHIP1/2 interact with a large number of immune and growth factor receptors. Tyrosine phosphorylation of SHIP1/2 has been considered to be the determining regulatory modification. However, here we present a hypothesis, based on recent key publications, highlighting the determining role of Ser/Thr phosphorylation in regulating several key properties of SHIP1/2. Since a subunit of the Ser/Thr phosphatase PP2A has been (...)
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  44.  11
    The molecular biology of the polycyclic aromatic hydrocarbon inducible cytochrome P‐450; the past is prologue.P. L. Iversen, R. N. Hines & Edward Bresnick - 1986 - Bioessays 4 (1):15-19.
    The heme‐containing cytochromes P‐450 are a ubiquitous family of monooxygenase isozymes responsible for the oxidative metabolism of a wide variety of endogenous as well as exogenous compounds. Many of the compounds metabolized by this enzyme system are effectively detoxified and converted to derivatives more easily eliminated from the organism. However, some compounds can be activated to reactive species capable of eliciting a cascade of toxic lesions, including cancer. Since its discovery nearly 30 years ago, the cytochrome P‐450 enzyme (...)
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  45.  15
    How does oncogene transformation render tumor cells hypersensitive to nutrient deprivation?Gabriel Leprivier & Poul H. Sorensen - 2014 - Bioessays 36 (11):1082-1090.
    Oncogene activation leads to cellular transformation by deregulation of biological processes such as proliferation and metabolism. Paradoxically, this can also sensitize cells to nutrient deprivation, potentially representing an Achilles' heel in early stage tumors. The mechanisms underlying this phenotype include loss of energetic and redox homeostasis as a result of metabolic reprogramming, favoring synthesis of macromolecules. Moreover, an emerging mechanism involving the deregulation of mRNA translation elongation through inhibition of eukaryotic elongation factor 2 kinase (eEF2K) is presented. The potential (...)
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  46.  4
    WT1: what has the last decade told us?Melissa Little, Greg Holmes & Patrick Walsh - 1999 - Bioessays 21 (3):191-202.
    When positionally cloned in late 1989, it was anticipated that mutations within the Wilms' tumour suppressor gene (WT1) would prove responsible for this common solid kidney cancer of childhood. Characterisation of the WT1 expression pattern and of the structure of the encoded protein isoforms and their mode of action has now spanned almost a decade. WT1 proteins act as nucleic acid-binding zinc finger-containing transcription factors involved in both transactivation and repression. These activities are facilitated and constrained by interactions with (...)
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  47.  17
    PuF, an antimetastatic and developmental signaling protein, interacts with the Alzheimer's amyloid-beta precursor protein via a tissue-specific proximal regulatory element.D. K. Lahiri, B. Maloney, J. T. Rogers & Y. W. Ge - 2013 - Bmc Genomics 14:68.
    BACKGROUND: Alzheimer's disease is intimately tied to amyloid-beta peptide. Extraneuronal brain plaques consisting primarily of Abeta aggregates are a hallmark of AD. Intraneuronal Abeta subunits are strongly implicated in disease progression. Protein sequence mutations of the Abeta precursor protein account for a small proportion of AD cases, suggesting that regulation of the associated gene may play a more important role in AD etiology. The APP promoter possesses a novel 30 nucleotide sequence, or "proximal regulatory element" , at -76/-47, from the (...)
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  48.  35
    Exploiting human and mouse transcriptomic data: Identification of circadian genes and pathways influencing health.Emma E. Laing, Jonathan D. Johnston, Carla S. Möller-Levet, Giselda Bucca, Colin P. Smith, Derk-Jan Dijk & Simon N. Archer - 2015 - Bioessays 37 (5):544-556.
    The power of the application of bioinformatics across multiple publicly available transcriptomic data sets was explored. Using 19 human and mouse circadian transcriptomic data sets, we found that NR1D1 and NR1D2 which encode heme‐responsive nuclear receptors are the most rhythmic transcripts across sleep conditions and tissues suggesting that they are at the core of circadian rhythm generation. Analyzes of human transcriptomic data show that a core set of transcripts related to processes including immune function, glucocorticoid signalling, and lipid metabolism (...)
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  49.  8
    NIPSNAP protein family emerges as a sensor of mitochondrial health.Esmat Fathi, Jay M. Yarbro & Ramin Homayouni - 2021 - Bioessays 43 (6):2100014.
    Since their discovery over two decades ago, the molecular and cellular functions of the NIPSNAP family of proteins (NIPSNAPs) have remained elusive until recently. NIPSNAPs interact with a variety of mitochondrial and cytoplasmic proteins. They have been implicated in multiple cellular processes and associated with different physiologic and pathologic conditions, including pain transmission, Parkinson's disease, and cancer. Recent evidence demonstrated a direct role for NIPSNAP1 and NIPSNAP2 proteins in regulation of mitophagy, a process that is critical for cellular health (...)
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  50.  25
    Endothelial Metabolic Control of Lymphangiogenesis.Pengchun Yu, Guosheng Wu, Heon-Woo Lee & Michael Simons - 2018 - Bioessays 40 (6):1700245.
    Lymphangiogenesis is an important developmental process that is critical to regulation of fluid homeostasis, immune surveillance and response as well as pathogenesis of a number of diseases, among them cancer, inflammation, and heart failure. Specification, formation, and maturation of lymphatic blood vessels involves an interplay between a series of events orchestrated by various transcription factors that determine expression of key genes involved in lymphangiogenesis. These are traditionally thought to be under control of several key growth factors including vascular growth (...)
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