molecular cellular genetics (27 Ergebnisse)

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Sprache: Englisch Pappband. Noch eingeschweißtes Exemplar!

Zustand: Good. Volume 4. This is an ex-library book and may have the usual library/used-book markings inside.This book has hardback covers. In good all round condition. No dust jacket. Please note the Image in this listing is a stock photo and may not match the covers of the actual item,900grams, ISBN:9780521815253.

Hardcover. Zustand: Near Fine. 1st Edition. 1996 hardback in excellent clean condition, covers clean and unscuffed. Note that to send outside the Uk will incur extra shiping due to weight.

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Taschenbuch. Zustand: Neu. The Carbonic Anhydrases | Cellular Physiology and Molecular Genetics | N. D. Carter (u. a.) | Taschenbuch | xviii | Englisch | 2013 | Springer | EAN 9781489907523 | Verantwortliche Person für die EU: Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu.

Taschenbuch. Zustand: Neu. Alzheimer's Disease | Advances in Genetics, Molecular and Cellular Biology | Sangram S. Sisodia (u. a.) | Taschenbuch | x | Englisch | 2010 | Springer | EAN 9781441941954 | Verantwortliche Person für die EU: Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu.

Taschenbuch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - Alzheimer's Disease: Advances in Genetics, Cellular and Molecular Biology provides exciting, comprehensive and up-to-date summaries of the most important recent advances in the genetic, molecular, biochemical, and cell biological studies of AD. The studies and advances described in this volume will help to accelerate the process of rational drug discovery and soon serve to extend and enhance the mental health and lifespan of our burgeoning elderly population.In 1906, Dr. Alois Alzheimer presented the case of his patient, Auguste D., a 51 year-old female admitted to the local asylum who presented with early memory impairments, psychoses, hallucinations and morbid jealousy. Dr. Alzheimer would argue that specific lesions that were present in and around neurons were responsible for dementia. In the ensuing decades, studies of the disorder that affected Auguste D., which would be named Alzheimer's disease (AD), were largely limited to descriptive neuropathological and psychological assessments of this disease, but with little understanding of the molecular and cellular mechanisms underlying neurodegeneration and dementia. This would change in the 1980s when the protein components of the major neuropathological hallmarks of the disease, senile plaques (and cerebral blood vessel amyloid) and neurofibrillary tangles were first determined. The identification of the ß-amyloid protein (Aß) and the microtubule-associated tau protein as the main components of plaques and tangles, respectively, would pave the way for the molecular genetic era of AD research. By the late-1980s, the genes encoding the ß-amyloid precursor protein (APP) and tau (MAPT) were identified and would subsequently be shown to harbor autosomal dominant mutations causing early-onset familial AD and frontal temporal dementia (FTD), respectively. In the early 1990s, the e4variant of the apoliprotein E gene (APOE) would be found to beassociated with increased risk for late-onset AD. APP mutations increased the generation and subsequent deposition of the neurotoxic peptide, Aß42, in brain while APOE-e4affected aggregation of Aß into fibrils and its clearance from brain. In 1995, genes encoding presenilin 1 and 2 (PSEN1, PSEN2) were identified, and mutations in MAPT were linked to frontal temporal dementia. Thus, by 1995, the stage was set for molecular studies of age-related dementias with APP, presenilin 1 and 2, APOE, and tau playing the major roles. The vast majority of studies addressing the molecular mechanisms underlying dementia would continue to focus on characterizing the five genes already firmly implicated in the etiology and pathogenesis of these dementing disorders, and these efforts have provided a firm foundation for translational studies that will hopefully serve to take these findings from the bench top to the bedside designing and developing novel ways to diagnose, treat, and prevent these diseases.

Taschenbuch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - As we approach the twenty-first century the problems of industrialization are evident: we find there is a greenhouse effect, the ozone layer is being depleted, the rain is acidified, and there is a terrible problem of increasing C0 concentrations in the atmo 2 sphere. The carbonic anhydrases are a unique family of enzymes that solve these problems in the human body: they are responsible for converting C0 (a gas) to 2 HC0-, which is the biggest intracellular buffer, with a concomitant decrease in a 3 hydroxyl ion. Globally, the functions of the carbonic anhydrases in photosynthesis in rain forests and in the algae and plankton that cover our oceans indicate that they are also of utmost importance in the maintenance of the acid-base balance on our planet. Although the whole field of C0 metabolism is enormous and still rapidly 2 expanding, because of the research interests of the editors this book is mainly concerned with mammalian carbonic anhydrases. However, if the interested reader intends to purify carbonic anhydrases from nonmammalian sources, Dr. Cheg widden has provided the necessary information in Chapter 7. The carbonic anhydrases were first discovered in 1933; until1976 there were thought to be only two isozymes. Since then CA ill, IY, V, VI, and Vll have been discovered and well characterized. There is, of course, no reason to believe that we have found them all.

Buch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - Alzheimer's Disease: Advances in Genetics, Cellular and Molecular Biology provides exciting, comprehensive and up-to-date summaries of the most important recent advances in the genetic, molecular, biochemical, and cell biological studies of AD. The studies and advances described in this volume will help to accelerate the process of rational drug discovery and soon serve to extend and enhance the mental health and lifespan of our burgeoning elderly population.In 1906, Dr. Alois Alzheimer presented the case of his patient, Auguste D., a 51 year-old female admitted to the local asylum who presented with early memory impairments, psychoses, hallucinations and morbid jealousy. Dr. Alzheimer would argue that specific lesions that were present in and around neurons were responsible for dementia. In the ensuing decades, studies of the disorder that affected Auguste D., which would be named Alzheimer's disease (AD), were largely limited to descriptive neuropathological and psychological assessments of this disease, but with little understanding of the molecular and cellular mechanisms underlying neurodegeneration and dementia. This would change in the 1980s when the protein components of the major neuropathological hallmarks of the disease, senile plaques (and cerebral blood vessel amyloid) and neurofibrillary tangles were first determined. The identification of the ß-amyloid protein (Aß) and the microtubule-associated tau protein as the main components of plaques and tangles, respectively, would pave the way for the molecular genetic era of AD research. By the late-1980s, the genes encoding the ß-amyloid precursor protein (APP) and tau (MAPT) were identified and would subsequently be shown to harbor autosomal dominant mutations causing early-onset familial AD and frontal temporal dementia (FTD), respectively. In the early 1990s, the e4variant of the apoliprotein E gene (APOE) would be found to beassociated with increased risk for late-onset AD. APP mutations increased the generation and subsequent deposition of the neurotoxic peptide, Aß42, in brain while APOE-e4affected aggregation of Aß into fibrils and its clearance from brain. In 1995, genes encoding presenilin 1 and 2 (PSEN1, PSEN2) were identified, and mutations in MAPT were linked to frontal temporal dementia. Thus, by 1995, the stage was set for molecular studies of age-related dementias with APP, presenilin 1 and 2, APOE, and tau playing the major roles. The vast majority of studies addressing the molecular mechanisms underlying dementia would continue to focus on characterizing the five genes already firmly implicated in the etiology and pathogenesis of these dementing disorders, and these efforts have provided a firm foundation for translational studies that will hopefully serve to take these findings from the bench top to the bedside designing and developing novel ways to diagnose, treat, and prevent these diseases.

Buch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - As we approach the twenty-first century the problems of industrialization are evident: we find there is a greenhouse effect, the ozone layer is being depleted, the rain is acidified, and there is a terrible problem of increasing C0 concentrations in the atmo 2 sphere. The carbonic anhydrases are a unique family of enzymes that solve these problems in the human body: they are responsible for converting C0 (a gas) to 2 HC0-, which is the biggest intracellular buffer, with a concomitant decrease in a 3 hydroxyl ion. Globally, the functions of the carbonic anhydrases in photosynthesis in rain forests and in the algae and plankton that cover our oceans indicate that they are also of utmost importance in the maintenance of the acid-base balance on our planet. Although the whole field of C0 metabolism is enormous and still rapidly 2 expanding, because of the research interests of the editors this book is mainly concerned with mammalian carbonic anhydrases. However, if the interested reader intends to purify carbonic anhydrases from nonmammalian sources, Dr. Cheg widden has provided the necessary information in Chapter 7. The carbonic anhydrases were first discovered in 1933; until1976 there were thought to be only two isozymes. Since then CA ill, IY, V, VI, and Vll have been discovered and well characterized. There is, of course, no reason to believe that we have found them all.

Paperback. Zustand: Brand New. reprint edition. 397 pages. 9.26x6.11x0.91 inches. In Stock.

Hardcover. Zustand: Brand New. 1st edition. 286 pages. 9.50x6.25x1.00 inches. In Stock.

Zustand: New. In.

Hardcover. Zustand: As New. First Edition. Fine-looking, structurally sound hardcover, little discernible wear to the glossy pictorial cloth over boards, bright interior, unmarked. From the publisher's blurb, "Helicobacter pylori is an important human pathogen that infects up to 50% of the human population. As the leading cause of peptic ulcers, gastritis and gastric cancer worldwide, the organism has been the subject of intensive research to unravel the mysteries of its genetics and cellular biology. In fact the number of publications in this field has risen dramatically in recent years making it extremely difficult for even the most diligent reader to stay abreast of progress. This book distills the most important cutting-edge findings in the field to produce a timely and comprehensive review. With contributions from leading international helicobacter researchers, topics include: lipopolysaccharides, outer membrane proteins, motility and chemotaxis, type IV secretions systems, metal metabolism, molecular mechanisms of host adaptation, genomotyping, and proteonomics. A useful introduction to the subject for new researchers and an invaluable reference for the experienced researcher, this book is essential reading for all researchers working with Helicobacter and related organisms." Contributions to the study of Helicobacter Pylori by the editor, Yoshio Yamaoka, and by Anthony P. Moran and M. Stephen Trent, Melanie Rust, Tobias Schweinitzer, Christin Josenhands, George Sachs, Yi Wen, David R. Scott and many others. Volume contains scholarly apparatus in the form of, e.g., notes, index, and bibliography. [9], 10-261 pp.Member, I.O.B.A., C.B.A., and adherent to the highest ethical standards. Additional postage may be required for oversize or especially heavy volumes, and for sets.

Hardcover. Zustand: gut. 2011 | 6., aktualisierte Auflage. Die Molekularbiologie als eigenständige Disziplin der Biologie existiert exakt so lange wie dieses Buch, dessen erste Auflage 1965 das Gebiet und seine Aufgaben gültig definierte. In allen Folgeauflagen ist es stets das Standardwerk der Molekularbiologie geblieben. Auch die vorliegende 6. Auflage besticht durch Aktualität und die Fähigkeit, ein komplettes und lebendiges Bild der Molekularbiologie auf knappem Raum zu entwerfen. Die genaue Darstellung von Schlüsselexperimenten und den wichtigsten Arbeitstechniken belegt, warum die Molekularbiologie heute das aufregendste Feld in den Life Sciences ist. Zahlreiche Bezüge zu medizinischen Anwendungen, aktuelle Literaturhinweise, ein Glossar und umfangreiche animierte Übungseinheiten auf der Website machen die Wissenschaft von den Biomolekülen zum echten Erlebnis. AUS DEM INHALT: TEIL I Chemie und Genetik * Das Mendel'sche Weltbild * Nucleinsäuren als Träger der genetischen Information * Die Bedeutung der schwachen chemischen Wechselwirkungen * Die Bedeutung energiereicher Bindungen * Schwache und starke Bindungen bestimmen makromolekulare Strukturen TEIL II Erhaltung des Genoms * Die Strukturen von DNA und RNA * Genomstruktur, Chromatin und Nucleosomen * Die Replikation der DNA * Die Mutabilität und Reparatur der DNA * Die Homologe Rekombination auf molekularer Ebene * Sequenzspezifische Rekombination und Transposition von DNA TEIL III Expression des Genoms * Kapitel 12 Mechanismen der Transkription * Kapitel 13 Das Spleißen von RNA * Kapitel 14 Translation * Kapitel 15 Der genetische Code TEIL IV Regulation * Kapitel 16 Transkriptionelle Regulation in Prokaryonten * Kapitel 17 Transkriptionelle Regulation in Eukaryonten * Kapitel 18 Regulatorische RNAs * Kapitel 19 Genregulation in Entwicklung und Evolution Über die Autoren: James D. Watson entschlüsselte 1953 zusammen mit Francis Crick die Struktur der DNA und erhielt dafür 1962 den Nobelpreis. Er lehrte und forschte an der Harvard University und am Cold Spring Harbor Laboratory und war u.a. Mitinitiator des Human Genome Project. Reihe/Serie: Pearson Studium - Biologie Pearson Studium - Biology Verlagsort München Sprache: deutsch Gewicht: 3560 g Einbandart: gebunden Naturwissenschaften Biologie Genetik Molekularbiologie DNA Genetik Genom Molekular Molekularbiologie; Handbuch Lehrbuch Zellbiologie ISBN-10: 3-86894-029-4 / 3868940294 ISBN-13: 978-3-86894-029-9 / 9783868940299 Tania A. Baker und Stephen P. Bell sind Biologie-Professoren am renommierten Massachusetts Institute of Technology (MIT). Alexander Gann arbeitet zusammen mit Watson am Cold Spring Harbor Laboratory. Michael Levine ist Professor für Molekulare Zellbiologie an der University of California, Berkeley. Richard Losick arbeitet am Howard Hughes Medical Institute in Harvard. Auf der Companion-Website: Für Dozenten * Alle Abbildungen des Buches Für Studenten * Übungsaufgaben mit Lösungsvorschlägen zu den einzelnen Kapiteln * Ausführliche Struktur-Tutorien mit interaktiven und animierten Molekülmodellen zu 14 ausgewählten Biomolekülen Autor: James D. Watson, geboren 1928 in Chicago, ist Biochemiker. Mit Francis H. Crick entwickelte er in Cambridge das Molekül-Modell der DNA. Dafür erhielten beide 1962 den Medizin-Nobelpreis. Er ist Mitinitiator des »Human Genome Project«. Sein Buch »Die Doppelhelix« wurde zum Bestseller. Molecular biology cells DNA RNA proteins genetics biochemistry cellular processes gene expression regulatory mechanisms In deutscher Sprache. 918 pages.