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Anticancer drugs of tomorrow: apoptotic pathways as targets for drug design
Institute of Experimental Dermatology, University of Muenster, Germany.ORCID iD: 0000-0001-9518-1411
Institute of Experimental Dermatology, University of Muenster, Germany.
Institute of Experimental Dermatology, University of Muenster, Germany.
Dept of Tumor Biology Oncology Center, Maria Sklodowska-Curie Memorial Institute, Wybrzeze Armii Krajowej 15, PL-44100 Gliwice, Poland.
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2003 (English)In: Drug Discovery Today, ISSN 1359-6446, E-ISSN 1878-5832, Vol. 8, no 2, 67-77 p.Article in journal (Refereed) Published
Abstract [en]

Apoptosis or programmed cell death is a set of ordered events that enables the selective removal of cells from tissue and is essential for homeostasis and proper function of multicellular organisms. Components of this signaling network, which include ligands, such as CD95, tumor necrosis factor (TNF) and TNF-related apoptosis-inducing ligand, as well as downstream molecules, such as caspases, Bcl-2 family members, and inhibitor-of-apoptosis proteins, which trigger and regulate apoptosis, are crucial targets for conventional drug development and gene therapy of cancer and other diseases. Here, we focus on apoptotic pathways and propose new potential molecular targets that could prove effective in controlling cell death in the clinical setting.

Place, publisher, year, edition, pages
Elsevier, 2003. Vol. 8, no 2, 67-77 p.
Keyword [en]
bcl-2 protein family, caspase activation, cytochrome-c, interleukin-1-beta converting-enzyme, leukemia-cells, mice deficient, programmed cell-death, serine-protease, structural basis, trail-induced apoptosis
National Category
Cancer and Oncology Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
Identifiers
URN: urn:nbn:se:liu:diva-87007DOI: 10.1016/S1359-6446(02)02563-1ISI: 000180434100007OAI: oai:DiVA.org:liu-87007DiVA: diva2:584216
Available from: 2013-01-08 Created: 2013-01-08 Last updated: 2017-12-06

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Los, Marek Jan

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