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Signal transduction: multiple pathways, multiple options for therapy
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Ludwig Institute for Cancer Research.
2001 (English)In: Stem Cells, ISSN 1066-5099, Vol. 19, no 4, 295-303 p.Article in journal (Refereed) Published
Abstract [en]

Many aspects of cell behavior, such as growth, motility, differentiation, and apoptosis, are regulated by signals cells receive from their environment. Such signals are important, e.g., during embryonal development, wound healing, hematopoiesis, and in the regulation of the immune response, and may come from interactions with other cells or components of the extracellular matrix, or from binding of soluble signaling molecules to specific receptors at the cell membrane. Hereby different signaling pathways are initiated inside the cell. Perturbations of such signaling pathways are seen in several types of diseases, e.g., cancer, inflammatory conditions, and atherosclerosis. Thus, antagonists of several signaling pathways have potential clinical utility. Several such compounds are currently used or are in clinical trials; others are currently being analyzed in animal models.

Place, publisher, year, edition, pages
2001. Vol. 19, no 4, 295-303 p.
Keyword [en]
1-Phosphatidylinositol 3-Kinase/antagonists & inhibitors/metabolism, Diabetes Mellitus/drug therapy, Drug Design, Enzyme Inhibitors/therapeutic use, GTP-Binding Proteins/antagonists & inhibitors/metabolism, Humans, Neoplasms/drug therapy, Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism, Protein-Tyrosine Kinase/antagonists & inhibitors/metabolism, Receptors; Cell Surface/*physiology, Signal Transduction
National Category
Medical and Health Sciences
URN: urn:nbn:se:uu:diva-73346DOI: 10.1634/stemcells.19-4-295PubMedID: 11463949OAI: oai:DiVA.org:uu-73346DiVA: diva2:101256
Available from: 2005-06-02 Created: 2005-06-02 Last updated: 2013-10-31Bibliographically approved

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Publisher's full textPubMedhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Retrieve&list_uids=11463949&dopt=Citation

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Heldin, Carl-Henrik
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