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Molecular Biology (molecular + biology)
Kinds of Molecular Biology Terms modified by Molecular Biology Selected AbstractsBook Review: Microbial Biodegradation: Genomics and Molecular Biology.ENGINEERING IN LIFE SCIENCES (ELECTRONIC), Issue 1 2008By E. Díaz (Ed.). No abstract is available for this article. [source] Molecular Biology in the Context of British, French, and American CulturesINTERNATIONAL SOCIAL SCIENCE JOURNAL, Issue 168 2001Pnina Geraldine Abir-Am First page of article [source] ASBMB and FAOBMB Inc.: Present status and future opportunitiesIUBMB LIFE, Issue 7 2010John de Jersey Past and present relationships of three biochemistry and molecular biology organizations: the Australian Society for Biochemistry and Molecular Biology; the Federation of Asian and Oceanian Biochemists and Molecular Biologists (FAOBMB); and the International Union for Biochemistry and Molecular Biology are discussed. The future of these organizations, particularly FAOBMB, is then considered in the light of factors behind their current status and likely future effects of globalization, growth in Asia, changes in disciplinary focus and contribution to global issues. © 2010 IUBMB IUBMB Life 62(7): 483,485, 2010 [source] The history of the Australian Society for Biochemistry and Molecular BiologyIUBMB LIFE, Issue 7 2010Liana Friedman Abstract The Australian Biochemical Society was established in 1955 and has played a crucial role in nurturing science in Australia. In 1990, the Society underwent a name change to become the Australian Society for Biochemistry and Molecular Biology (ASBMB). Today, the majority of ASBMB's members (1,000) work in universities and research institutes, although many also come from industry, hospitals, and government agencies. The Society is also strongly supported by its Sustaining Members, which are science-related companies and other commercial entities. © 2010 IUBMB IUBMB Life 62(7): 486,491, 2010 [source] The Korean Society for Biochemistry and Molecular BiologyIUBMB LIFE, Issue 5-6 2006Doo-Sik Kim No abstract is available for this article. [source] Welcome to the 19th International Congress of Biochemistry and Molecular BiologyIUBMB LIFE, Issue 4-5 2003Joel Weiner No abstract is available for this article. [source] Welcome to the 19th International Congress of Biochemistry and Molecular BiologyIUBMB LIFE, Issue 4-5 2003Brian Clark No abstract is available for this article. [source] The Xth International Meeting on Ciliate Molecular BiologyTHE JOURNAL OF EUKARYOTIC MICROBIOLOGY, Issue 2 20032003 at Saxtons River, To be held as a FASEB Summer Research Conference July 1, Vermont No abstract is available for this article. [source] Fundamentals of Molecular BiologyBIOCHEMISTRY AND MOLECULAR BIOLOGY EDUCATION, Issue 2 2010Akif Uzman No abstract is available for this article. [source] PCR as a specific, sensitive and simple method suitable for diagnosticsBIOCHEMISTRY AND MOLECULAR BIOLOGY EDUCATION, Issue 4 2000M. Gonzalo Claros PCR technology is a widespread method that has not reached students laboratory in anything else than a typical amplification reaction. We describe a simple application of PCR in pathogen diagnostics that enables students to identify which ampicillin-resistant organism is present in a cell culture. This experiment has been performed for one year in two "Experimental Biochemistry and Molecular Biology" courses with Biological and Chemical undergraduates. Using specific primers from the Escherichia coli ,-lactamase gene, they have been able to selectively amplify a ,-lactamase DNA fragment in E. coli but not in Staphylococcus aureus and, using different annealing temperatures, test the reaction specificity. By solving the "Study Questions", students understood the specificity and sensitivity of the method, as well as the rationale that should be applied when a molecular weight pattern is used for calculating unknown DNA sizes. © 2000 IUBMB. Published by Elsevier Science Ltd. All rights reserved. [source] Recommendations of the Committee on Education of the International Union of Biochemistry and Molecular BiologyBIOCHEMISTRY AND MOLECULAR BIOLOGY EDUCATION, Issue 1 2000Standards for the Ph.D. Degree in the Molecular Biosciences First page of article [source] Book review: Designs for Life : Molecular Biology after World War IIBIOESSAYS, Issue 8 2004Jennifer Rohn No abstract is available for this article. [source] Factors controlling the activity of the SERCA2a pump in the normal and failing heartBIOFACTORS, Issue 6 2009Ilse Vandecaetsbeek Abstract Heart failure is the leading cause of death in western countries and is often associated with impaired Ca2+ handling in the cardiomyocyte. In fact, cardiomyocyte relaxation and contraction are tightly controlled by the activity of the cardiac sarco(endo)plasmic reticulum (ER/SR) Ca2+ pump SERCA2a, pumping Ca2+ from the cytosol into the lumen of the ER/SR. This review addresses three important facets that control the SERCA2 activity in the heart. First, we focus on the alternative splicing of the SERCA2 messenger, which is strictly regulated in the developing heart. This splicing controls the formation of three SERCA2 splice variants with different enzymatic properties. Second, we will discuss the role and regulation of SERCA2a activity in the normal and failing heart. The two well-studied Ca2+ affinity modulators phospholamban and sarcolipin control the activity of SERCA2a within a narrow window. An aberrantly high or low Ca2+ affinity is often observed in and may even trigger cardiac failure. Correcting SERCA2a activity might therefore constitute a therapeutic approach to improve the contractility of the failing heart. Finally, we address the controversies and unanswered questions of other putative regulators of the cardiac Ca2+ pump, such as sarcalumenin, HRC, S100A1, Bcl-2, HAX-1, calreticulin, calnexin, ERp57, IRS-1, and ,2. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Renal glutathione transport: Identification of carriers, physiological functions, and controversiesBIOFACTORS, Issue 6 2009Lawrence H. Lash Abstract Glutathione (GSH) is an endogenous tripeptide composed of the amino acids L -glutamate, L -cysteine, and glycine. It is found in virtually all aerobic cells and plays critical roles in maintenance of cellular redox homeostasis and drug metabolism. An important component of its regulation is transport across biological membranes. Because GSH is a charged, hydrophilic molecule, transport occurs via catalysis by specific carrier proteins rather than by simple diffusion. Although it has been clearly understood that efflux of GSH across membranes such as the canalicular and sinusoidal plasma membranes in hepatocytes and the brush-border plasma membrane in renal proximal tubules is a key step in GSH turnover and interorgan metabolism, the existence and physiological functions of uptake of GSH across various epithelial plasma membranes has been subject to some debate. Besides transport across plasma membranes, GSH transport across intracellular membranes, most notably the mitochondrial inner membrane, has received some attention in recent years because of the importance of mitochondrial redox status and the mitochondrial GSH pool in cellular physiology and pathology. This commentary will focus on renal transport processes for GSH and will discuss some of the controversies that have existed and still seem to exist in the literature, specifically regarding uptake of intact GSH by basolateral membranes of renal proximal tubular cells and uptake of intact GSH by the mitochondrial inner membrane. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Uncoupling proteins: A complex journey to function discoveryBIOFACTORS, Issue 5 2009Federica Cioffi Abstract Since their discovery, uncoupling proteins have aroused great interest due to the crucial importance of energy-dissipating system for cellular physiology. The uncoupling effect and the physiological role of UCP1 (the first-described uncoupling protein) are well established. However, the reactions catalyzed by UCP1 homologues (UCPs), and their physiological roles are still under debate, with the literature containing contrasting results. Current hypothesis propose several physiological functions for novel UCPs, such as: (i) attenuation of reactive oxygen species production and protection against oxidative damage, (ii) thermogenic function, although UCPs do not generally seem to affect thermogenesis, UCP3 can be thermogenic under certain conditions, (iii) involvement in fatty acid handling and/or transport, although recent experimental evidence argues against the previously hypothesized role for UCPs in the export of fatty acid anions, (iv) fatty acid hydroperoxide export, although this function, due to the paucity of the experimental evidence, remains hypothetical, (v) Ca2+ uptake, although results for and against a role in Ca2+ uptake are still emerging, (vi) a signaling role in pancreatic beta cells, where it attenuates glucose-induced insulin secretion. From the above, it is evident that more research will be needed to establish universally accepted functions for UCPs. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Cell biology of molybdenumBIOFACTORS, Issue 5 2009Ralf R. Mendel Abstract The transition element molybdenum (Mo) is an essential micronutrient that is needed as catalytically active metal during enzyme catalysis. In humans four enzymes depend on Mo: sulfite oxidase, xanthine oxidoreductase, aldehyde oxidase, and mitochondrial amidoxime reductase. In addition to these enzymes, plants harbor a fifth Mo-enzyme namely nitrate reductase. To gain biological activity and fulfill its function in enzymes, Mo has to be complexed by a pterin compound thus forming the molybdenum cofactor. This article will review the way that Mo takes from uptake into the cell, via formation of the molybdenum cofactor and its storage, up to the final insertion of the molybdenum cofactor into apometalloenzymes. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] The function of vascular endothelial growth factorBIOFACTORS, Issue 4 2009Bonnie J. Nieves Abstract Vascular endothelial growth factor (VEGF) is considered the master regulator of angiogenesis during growth and development, as well as in disease states such as cancer, diabetes, and macular degeneration. This review details our current understanding of VEGF signaling and discusses the benefits and unexpected side effects of promising anti-angiogenic therapeutics that are currently being used to inhibit neovacularization in tumors. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Mammalian NDR/LATS protein kinases in hippo tumor suppressor signalingBIOFACTORS, Issue 4 2009Alexander Hergovich Abstract The NDR/LATS family of kinases is a subgroup of the AGC group of protein kinases and is conserved from lower eukaryotes to humans. Like other AGC kinases, NDR/LATS kinases require phosphorylation of conserved Ser/Thr residues for activation. On the one hand, binding of the coactivator MOB to NDR/LATS allows autophosphorylation. On the other hand, MST kinases directly phosphorylate NDR/LATS kinases. In addition to our understanding of the molecular activation mechanisms, recent studies have shown that LATS kinases play a central role in Hippo/SWH (Salvador/Warts/Hippo) tumor suppressor pathways, which coordinate cell proliferation and apoptosis by regulating proto-oncogenes, such as YAP and TAZ. In this review, we summarize current knowledge of Merlin/MST/SAV/MOB/LATS/NDR/YAP/TAZ networks (also termed mammalian Hippo signaling) and their roles in mammalian cellular transformation. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Greasing the wheels of A, clearance in Alzheimer's Disease: The role of lipids and apolipoprotein EBIOFACTORS, Issue 3 2009Jianjia Fan Abstract Although apolipoprotein E (apoE) is the most common genetic risk factor for Alzheimer's Disease (AD), how apoE participates in AD pathogenesis remains incompletely understood. ApoE is also the major carrier of lipids in the brain. Here, we review studies showing that the lipidation status of apoE influences the metabolism of A, peptides, which accumulate as amyloid deposits in the neural parenchyma and cerebrovasculature. One effect of apoE is to inhibit the transport of A, across the blood-brain-barrier (BBB), particularly when apoE is lipidated. A second effect is to facilitate the proteolytic degradation of A, by neprilysin and insulin degrading enzyme (IDE), which is enhanced when apoE is lipidated. We also describe how apoE becomes lipidated and how this impacts A, metabolism. Specifically, genetic loss of the cholesterol transporter ABCA1 impairs apoE lipidation and promotes amyloid deposition in AD mouse models. ABCA1 catalyses the ATP-dependent transport of cholesterol and phospholipids from the plasma membrane to lipid-free apolipoproteins including apoE. Conversely, selective overexpression of ABCA1 increases apoE lipidation in the central nervous system (CNS) and eliminates the formation of amyloid plaques in vivo. Deficiency of Liver-X-Receptors (LXRs), transcription factors that stimulate ABCA1 and apoE expression, exacerbates AD pathogenesis in vivo, whereas treatment of AD mice with synthetic LXR agonists reduces amyloid load and improves cognitive performance. These studies provide new insights into the mechanisms by which apoE affects A, metabolism, and offer opportunities to develop novel therapeutic approaches to reduce the leading cause of dementia in the elderly. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Amino acids as regulators of gene expression in mammals: Molecular mechanismsBIOFACTORS, Issue 3 2009Alain Bruhat Abstract In mammals, the impact of nutrients on gene expression has become an important area of research. Because amino acids have multiple and important functions, their homeostasis has to be finely maintained. However, amino acidemia can be affected in some nutritional conditions and by various forms of stress. Consequently, mammals have to adjust physiological functions involved in the adaptation to amino acid availability. Part of this regulation involves the modulation of numerous gene expression. It has been shown that amino acids by themselves can modify the expression of target genes. This review focuses on the recent advances in the understanding of the mechanisms involved in the control of mammalian gene expression in response to amino acid limitation. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Mitochondrial complementation preventing respiratory dysfunction caused by mutant mtDNABIOFACTORS, Issue 2 2009Akitsugu Sato Abstract The mitochondrial theory of aging is the idea that age-associated mitochondrial dysfunction is caused by accumulation of somatic mutations in mitochondrial DNA (mtDNA). However, mitochondria are considered to be a dynamic organelle that repeats fusion and fission. Through fusion and fission, there is an extensive and continuous exchange of mtDNA and its products between mitochondria. This mitochondrial complementation prevents individuals from expression of respiratory dysfunction caused by pathogenic mutant mtDNAs. Thus, the presence of mitochondrial complementation does not support the mitochondrial theory of aging. Moreover, the presence of mitochondrial complementation enables gene therapy for mitochondrial diseases using nuclear transplantation of zygotes. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Pentraxins: Multifunctional proteins at the interface of innate immunity and inflammationBIOFACTORS, Issue 2 2009Livija Deban Abstract Pentraxins are a family of multimeric pattern recognition proteins highly conserved in evolution. On the basis of the primary structure of the protomer, pentraxins are divided into two groups: short pentraxins and long pentraxins. C reactive protein, the first pattern recognition receptor identified, and serum amyloid P component are classic short pentraxins produced in the liver in response to IL-6. Long pentraxins, including the prototype PTX3, are expressed in a variety of tissues. PTX3 is produced by a variety of cells and tissues, most notably dendritic cells and macrophages, in response to Toll-like receptor (TLR) engagement and inflammatory cytokines. Through interaction with several ligands, including selected pathogens and apoptotic cells, pentraxins play a role in complement activation, pathogen recognition and apoptotic cell clearance. In addition, PTX3 is involved in the deposition of extracellular matrix and female fertility. Unlike the classic short pentraxins CRP and SAP, PTX3 primary sequence and regulation are highly conserved in man and mouse. Thus, gene targeting identified PTX3 (and presumably other members of the family) as multifunctional soluble pattern recognition receptors acting as a nonredundant component of the humoral arm of innate immunity and involved in tuning inflammation, matrix deposition, and female fertility. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Mechanism of action of vitamin C in sepsis: Ascorbate modulates redox signaling in endotheliumBIOFACTORS, Issue 1 2009John X. Wilson Abstract Circulating levels of vitamin C (ascorbate) are low in patients with sepsis. Parenteral administration of ascorbate raises plasma and tissue concentrations of the vitamin and may decrease morbidity. In animal models of sepsis, intravenous ascorbate injection increases survival and protects several microvascular functions, namely, capillary blood flow, microvascular permeability barrier, and arteriolar responsiveness to vasoconstrictors and vasodilators. The effects of parenteral ascorbate on microvascular function are both rapid and persistent. Ascorbate quickly accumulates in microvascular endothelial cells, scavenges reactive oxygen species, and acts through tetrahydrobiopterin to stimulate nitric oxide production by endothelial nitric oxide synthase. A major reason for the long duration of the improvement in microvascular function is that cells retain high levels of ascorbate, which alter redox-sensitive signaling pathways to diminish septic induction of NADPH oxidase and inducible nitric oxide synthase. These observations are consistent with the hypothesis that microvascular function in sepsis may be improved by parenteral administration of ascorbate as an adjuvant therapy. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Interferons and viral infectionsBIOFACTORS, Issue 1 2009Volker Fensterl Abstract Interferons represent a family of cytokines, which is of central importance in the innate immune response to virus infections. All interferons act as secreted ligands of specific cell surface receptors, eliciting the transcription of hundreds of interferon-stimulated genes whose protein products have antiviral activity, as well as antimicrobial, antiproliferative/antitumor, and immunomodulatory effects. Expression of type I and III interferons is induced in virtually all cell types upon recognition of viral molecular patterns, especially nucleic acids, by cytoplasmic and endosomal receptors, whereas type II interferon is induced by cytokines such as IL-12, and its expression is restricted to immune cells such as T cells and NK cells. The effectiveness of the interferon system in counteracting viral infections is reflected by the multitude of inhibitors of interferon induction or interferon action that are encoded by many viruses, preventing their eradication and resulting in the continued coexistence of viruses and vertebrates. The unique biological functions of interferons have led to their therapeutic use in the treatment of diseases such as hepatitis, multiple sclerosis, and certain leukemias. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Nitric oxide and vascular insulin resistanceBIOFACTORS, Issue 1 2009Guoyao Wu Abstract Obesity and type-II diabetes are growing major health issues worldwide. They are the leading risk factors for vascular insulin resistance, which plays an important role in the pathogenesis of cardiovascular disease, the leading cause of death in developed nations. Recent studies have shown that reduced synthesis of nitric oxide (NO; a major vasodilator) from L -arginine in endothelial cells is a major factor contributing to the impaired action of insulin in the vasculature of obese and diabetic subjects. The decreased NO generation results from a deficiency of (6R)-5,6,7,8-tetrahydrobiopterin [BH4; an essential cofactor for NO synthase (NOS)], as well as increased generation of glucosamine (an inhibitor of the pentose cycle for the production of NADPH, another cofactor for NOS) from glucose and L -glutamine. Accordingly, endothelial dysfunction can be prevented by (1) enhancement of BH4 synthesis through supplementation of its precursor (sepiapterin) via the salvage pathway; (2) transfer of the gene for GTP cyclohydrolase-I (the first and key regulatory enzyme for de novo synthesis of BH4); or (3) dietary supplementation of L -arginine (which stimulates GTP cyclohydrolase-I expression and inhibits hexosamine production). Modulation of the arginine,NO pathway by BH4 and arginine is beneficial for ameliorating vascular insulin resistance in obesity and diabetes. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Sarcopenia of aging: Underlying cellular mechanisms and protection by calorie restrictionBIOFACTORS, Issue 1 2009Emanuele Marzetti Abstract Sarcopenia, the loss of muscle mass and function, is a common feature of aging and impacts on individual health and quality of life. Several cellular mechanisms have been involved in the pathogenesis of this syndrome, including mitochondrial dysfunction, altered apoptotic and autophagic signaling, and, more recently, trace metal dyshomeostasis. Calorie restriction (CR) without malnutrition has been shown to ameliorate the age-related loss of muscle mass in a variety a species. Mechanisms of protection span from preservation of mitochondrial functional and structural integrity to mitochondrial biogenesis, reduction of oxidative stress, and favorable modulation of apoptotic and autophagic signaling pathways. Importantly, preliminary evidence indicates that moderate CR may promote muscle mitochondrial biogenesis in middle-aged human subjects. Further research is warranted to investigate whether CR may represent a safe and efficient strategy to delay the onset and mitigate the progression of sarcopenia in older adults. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Evidence for the role of Th17 cell inhibition in the prevention of autoimmune diseases by anti-interluekin-6 receptor antibodyBIOFACTORS, Issue 1 2009Masahiko Mihara Abstract Deregulated production of interleukin-6 (IL-6) has been found in several chronic inflammatory autoimmune disorders, including rheumatoid arthritis (RA) and inflammatory bowel diseases. Treatment with tocilizumab, a humanized anti-human IL-6 receptor (IL-6R) antibody, significantly improved disease activity and inhibited the progression of joint destruction in RA patients, but the reason why IL-6 blockade causes improvement of RA is still unclear. In this review, we discuss the influence of anti-IL-6R antibody treatment on the differentiation of Th17 cells, which are thought to be involved in the pathogenesis of autoimmune diseases in animal models, present new results for the effect of anti-IL-6R antibody on the induction of Th17 cells in a mouse collagen-induced arthritis model, and come to the conclusion that anti-IL-6R antibody inhibited the differentiation of Th17 cells in mouse models. It is thought that this inhibitory action may contribute to the therapeutic effects of anti-IL-6R antibody in human autoimmune diseases. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Endocrine fibroblast growth factors as regulators of metabolic homeostasisBIOFACTORS, Issue 1 2009Hiroshi Kurosu Abstract Endocrine fibroblast growth factors (FGFs) function as hormones that maintain specific metabolic states by controlling homeostasis of bile acid, glucose, fatty acid, phosphate, and vitamin D. Endocrine FGFs exert their biological activity through a common design of coreceptor system consisting of the Klotho gene family of transmembrane proteins and cognate FGF receptors. Moreover, expression of endocrine FGFs is regulated by nuclear receptors whose lipophilic ligands are generated under the control of these hormones in the target organs. Thus, novel endocrine axes have emerged that regulate diverse metabolic processes through feedback loops composed of the FGF, Klotho, FGF receptor, and nuclear receptor gene families. This review summarizes the role of Klotho family proteins in the regulation of metabolic activity and expression of the endocrine FGFs. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Serglycin proteoglycan: Regulating the storage and activities of hematopoietic proteasesBIOFACTORS, Issue 1 2009Gunnar Pejler Abstract Serglycin (SG), like all other proteoglycans, consists of a protein "core" to which sulfated and thereby negatively charged polysaccharide chains of glycosaminoglycan type are attached. The recent generation of mice lacking a functional SG gene has revealed a number of biological functions of SG. In particular, it has been shown that SG has a key role in promoting the storage and in regulating the activities of a number of proteases expressed in hematopoietic cell types, most notably various mast cell proteases. In this review, we summarize the recent development in our understanding of the biological function of SG, in particular by focusing on the novel insight provided through analysis of the SG-deficient mouse strain. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Gastrin-releasing peptide: Different forms, different functionsBIOFACTORS, Issue 1 2009Joseph Ischia Abstract All forms of the neuropeptide gastrin-releasing peptide (GRP) are derived from the precursor proGRP1-125. Amidated GRP18-27, which together with amidated GRP1-27 was long thought to be the only biologically relevant product of the GRP gene, is involved in a multitude of physiological functions and acts as a mitogen, morphogen, and proangiogenic factor in certain cancers. Recently, GRP has been implicated in several psychiatric conditions, in the maintenance of circadian rhythm, in spinal transmission of the itch sensation, and in inflammation and wound repair. The actions of GRP are mediated by the GRP receptor. Over the last decade, nonamidated peptides derived from proGRP, such as the glycine-extended form GRP18-28 and recombinant and synthetic fragments from proGRP31-125, have been shown to be biologically active in a range of tissues and in cancer cell lines. While GRP18-28 acts via the GRP receptor, the identity of the receptor for proGRP31-125 and its fragments has not yet been established. Nonamidated fragments are also present in normal tissues and in various cancers. In fact, proGRP31-98 is the most sensitive serum biomarker in patients with small cell lung cancer and is a significant predictor of poor survival in patients with advanced prostate cancer. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] | |||||||||||||||||||||||||||||||||||||||||||