The Experts below are selected from a list of 230556 Experts worldwide ranked by ideXlab platform
S. R. Mackey - One of the best experts on this subject based on the ideXlab platform.
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Biological rhythms workshop IA: Molecular Basis of rhythms generation
Cold Spring Harbor Symposia on Quantitative Biology, 2007Co-Authors: S. R. MackeyAbstract:Current circadian models are based on genetic, biochemical, and structural data that, when combined, provide a comprehensive picture of the Molecular Basis for rhythms generation. These models describe three basic elements-input pathways, oscillator, and output pathways-to which each Molecular component is assigned. The lines between these elements are often blurred because some proteins function in more than one element of the circadian system. The end result of these Molecular oscillations is the same in each system (near 24-hour timing), yet the proteins involved, the interactions among those proteins, and the regulatory feedback loops differ. Here, the currentmodels for the Molecular Basis for rhythms generation are described for the prokaryotic cyanobacterium Synechococcus elongatus as well as the eukaryotic systems Neurospora crassa, Drosophila melanogaster, Arabidopsis thaliana, and mammals (particularly rodents).
Andrew Arnold - One of the best experts on this subject based on the ideXlab platform.
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Molecular Basis of PTH Overexpression
Principles of Bone Biology, 2007Co-Authors: Geoffrey N. Hendy, Andrew ArnoldAbstract:Publisher Summary This chapter focuses on the Molecular Basis of parathyroid hormone (PTH) overexpression. Parathyroid hyperfunction is found in several disease states including sporadic primary and secondary hyperparathyroidism and familial disorders such as the multiple endocrine neoplasia (MEN) syndromes. Primary hyperparathyroidism is a common disorder characterized by hypercalcemia, caused by an excessive secretion of parathyroid hormone (PTH). This is due to both an increased parathyroid gland mass and a resetting of the control of PTH secretion from the parathyroid cell by the ambient calcium concentration. Patients with primary hyperparathyroidism have one or more enlarged parathyroid glands with a single, benign adenoma occurring in almost 85% of cases, while multiple hypercellular glands are present in about 15% of patients. Hyperparathyroidism may also occur as part of familial syndromes, such as multiple endocrine neoplasia types 1 and 2 (MEN 1 and 2), the hereditary hyperparathyroidism and jaw tumor (HPT-JT) syndrome, and familial hypocalciuric hypercalcemia (FHH) and neonatal severe hyperparathyroidism (NSHPT). Several advances have been achieved toward the goal of understanding the Molecular Basis of sporadic parathyroid tumorigenesis. The cyclin D1/PRAD1 oncogene has been identified as a parathyroid oncogene, is overexpressed in 20%–40% of parathyroid adenomas, and is also involved in the development of many additional tumor types. The gene responsible for MEN 1 has been identified, and mutations in menin contribute to 12%–17% of sporadic parathyroid adenomas. Mutations in the RET gene, the causal agent in MEN2, plus CASR and VDR, appear to contribute rarely if ever to the development of sporadic parathyroid tumors.
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Molecular Basis of hyperparathyroidism
Journal of Bone and Mineral Metabolism, 1997Co-Authors: Hideki Tahara, Andrew ArnoldAbstract:Several advances have been achieved toward an improved understanding of the Molecular Basis of human parathyroid tumorigenesis. One oncogene involved in the development of parathyroid tumors, PRAD1/cyclin D1 , has been discovered and is having a broad impact in oncology and cell-cycle biology. The general genomic locations of several novel putative parathyroid tumor suppressor genes have been identified, providing guideposts toward their specific identification. An already recognized tumor suppressor gene, RB , or a close neighbor on 13q, has been linked to the pathogenesis of parathyroid carcinomas. RET has been centrally implicated in MEN-2A, and investigators are on the verge of isolating the MEN1 gene, both of which are sure to have important basic and clinical implications relevant to parathyroid and other endocrine diseases. Although mutations in the CASR gene itself play a critical role in familial disease, they do not appear to be involved in sporadic parathyroid tumorigenesis, and investigation of genes important for its regulation is warranted. Finally, new Molecular genetic approaches will eventually permit the identification of additional parathyroid tumor-provoking genes and will begin to shed light upon other problems in parathyroid biology, such as the relationship between abnormal parathyroid cell proliferation and an altered setpoint in the mechanism linking extracellular calcium concentration to PTH secretion.
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Recombinant DNA Strategies for Determining the Molecular Basis of Endocrine Disorders
The Journal of Clinical Endocrinology and Metabolism, 1990Co-Authors: J. Larry Jameson, Andrew ArnoldAbstract:Advances in recombinant DNA technology have revolutionized experimental approaches for understanding the Molecular Basis for diseases. In endocrinology, a field that is solidly based upon the foundations of cell biology and physiology, there is now great potential for describing disease processes at both a Molecular and a clinical level. The goal of this review is to describe some of the recombinant DNA strategies that have been used to define the Molecular Basis for endocrine disorders
A. K. Daly - One of the best experts on this subject based on the ideXlab platform.
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Molecular Basis of polymorphic drug metabolism
Journal of Molecular Medicine, 1995Co-Authors: A. K. DalyAbstract:Genetic polymorphisms with functional effects occur in many of the genes encoding drug metabolizing enzymes and are an important cause of adverse drug reations. Recent advances in the understanding of the Molecular genetics of drug-metabolizing enzymes, particularly the cytochromes P450, has enabled the Molecular Basis of several polymorphisms to be elucidated and genotyping assays using the polymerase chain reaction to be developed. Polymorphisms in this category include those in the cytochrome P450 genes CYP2D6 , CYP2C19 , CYP2A6 , CYP2C9 and CYP2E1 , the glutathione S -transferase genes GSTM1 and GSTT1 and the N -acetyltransferase gene NAT2 . The Molecular Basis and impotance to drug metabolism of the various polymorphisms as well as evidence for the existence of polymorphisms in other genes encoding drug-metabolizing enzymes such as the UDP-glucuronosyltransferases, the sulphotransferases and the methyltransferases are discussed.
Michael C Stein - One of the best experts on this subject based on the ideXlab platform.
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Molecular Basis of ethnic differences in drug disposition and response
Annual Review of Pharmacology and Toxicology, 2001Co-Authors: Alastair J J Wood, Michael C SteinAbstract:Ethnicity is an important demographic variable contributing to interindividual variability in drug metabolism and response. In this rapidly expanding research area many genetic factors that account for the effects of ethnicity on pharmacokinetics, pharmacodynamics, and drug safety have been identified. This review focuses on recent developments that have improved understanding of the Molecular mechanisms responsible for such interethnic differences. Genetic variations that may provide a Molecular Basis for ethnic differences in drug metabolizing enzymes (CYP 2C9, 2C19, 2D6, and 3A4), drug transporter (P-glycoprotein), drug receptors (adrenoceptors), and other functionally important proteins (eNOS and G proteins) are discussed. A better understanding of the Molecular Basis underlying ethnic differences in drug metabolism, transport, and response will contribute to improved individualization of drug therapy.
Seirian Sumner - One of the best experts on this subject based on the ideXlab platform.
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social parasitism and the Molecular Basis of phenotypic evolution
Frontiers in Genetics, 2015Co-Authors: Alessandro Cini, Anne Segondspichon, George B J Busby, Solenn Patalano, Rita Cervo, Seirian SumnerAbstract:Contrasting phenotypes arise from similar genomes through a combination of losses, gains, co-option and modifications of inherited genomic material. Understanding the Molecular Basis of this phenotypic diversity is a fundamental challenge in modern evolutionary biology. Comparisons of the genes and their expression patterns underlying traits in closely related species offer an unrivaled opportunity to evaluate the extent to which genomic material is reorganized to produce novel traits. Advances in Molecular methods now allow us to dissect the Molecular machinery underlying phenotypic diversity in almost any organism, from single-celled entities to the most complex vertebrates. Here we discuss how comparisons of social parasites and their free-living hosts may provide unique insights into the Molecular Basis of phenotypic evolution. Social parasites evolve from a eusocial ancestor and are specialized to exploit the socially acquired resources of their closely-related eusocial host. Molecular comparisons of such species pairs can reveal how genomic material is re-organized in the loss of ancestral traits (i.e., of free-living traits in the parasites) and the gain of new ones (i.e., specialist traits required for a parasitic lifestyle). We define hypotheses on the Molecular Basis of phenotypes in the evolution of social parasitism and discuss their wider application in our understanding of the Molecular Basis of phenotypic diversity within the theoretical framework of phenotypic plasticity and shifting reaction norms. Currently there are no data available to test these hypotheses, and so we also provide some proof of concept data using the paper wasp social parasite/host system (Polistes sulcifer—Polistes dominula). This conceptual framework and first empirical data provide a spring-board for directing future genomic analyses on exploiting social parasites as a route to understanding the evolution of phenotypic specialization.
