Gregory R. Bock & Joan Marsh 
Molecular Control of Haemopoiesis [PDF ebook] 

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The many different kinds of blood cells found in the human body are derived from multi-potential stem cells, which are induced to differentiate into one or another cell type by the action of regulatory proteins or growth factors. This volume looks at the way that binding of these proteins to specific receptors causes changes in gene expression in the nucleus and the activity of certain enzymes in the cytoplasm, committing the cell to a particular developmental pathway. Also discussed are recently established clinical applications and clinical trials of new techniques.

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Table des matières

Partial table of contents:
The Proteins That Control Hemopoiesis and Leukemia (L.
Sachs).
Protein Factors That Regulate the Growth and Differentiation of
Mouse Myeloid Leukemia Cells (M. Hozumi, et al.).
Responses of Neutrophils to Myeloid Growth Factors (D. Golde,
et al.).
Signal-Response Coupling Mediated by the Transduced
Colony-Stimulating Factor-1 Receptor and Its Oncogenic fms
Variants in Naive Cells (C. Sherr, et al.).
Hemopoietic Growth Factor Regulation of Protein Kinases and
Genes Associated with Cell Proliferation (W. Farrar, et
al.).
Contributions of Autocrine and Non-Autocrine Mechanisms to
Tumorigenicity in a Murine Model for Leukemia (A. Dunn & A.
Wilks).
Retroviral Infection and Hemopoiesis (J. Groopman).
The Use of Recombinant Human Erythropoietin in Humans (J.
Adamson & J. Eschbach).
General Discussion.
Index of Contributors.
Subject Index.

A propos de l’auteur

The Novartis Foundation is an international scientific and educational charity which promotes the study and general knowledge of science and in particular encourages international co-operation in scientific research.

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Langue Anglais ● Format PDF ● Pages 242 ● ISBN 9780470513897 ● Taille du fichier 14.7 MB ● Éditeur Gregory R. Bock & Joan Marsh ● Maison d’édition John Wiley & Sons ● Publié 2008 ● Téléchargeable 24 mois ● Devise EUR ● ID 2318935 ● Protection contre la copie Adobe DRM
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