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Sökning: onr:"swepub:oai:DiVA.org:liu-47470" > Induction of cancer...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004226naa a2200469 4500
001oai:DiVA.org:liu-47470
003SwePub
008091011s2001 | |||||||||||000 ||eng|
024a https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-474702 URI
024a https://doi.org/10.1096/fj.00-0251com2 DOI
040 a (SwePub)liu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Neuzil, J.u Institute for Prevention of Cardiovascular Diseases and Medical Policlinic, Ludwig-Maximilians-University, Munich, Germany, Institute for Prevention of Cardiovascular Diseases, Pettenkoferstrasse 9, 80336 Munich, Germany4 aut
2451 0a Induction of cancer cell apoptosis by a-tocopheryl succinate :b Molecular pathways and structural requirements
264 c 2001-02
264 1b Wiley,c 2001
338 a print2 rdacarrier
520 a The vitamin E analog a-tocopheryl succinate (a-TOS) can induce apoptosis. We show that the proapoptotic activity of a-TOS in hematopoietic and cancer cell lines involves inhibition of protein kinase C (PKC), since phorbol myristyl acetate prevented a-TOS-triggered apoptosis. More selective effectors indicated that a-TOS reduced PKCa isotype activity by increasing protein phosphatase 2A (PP2A) activity. The role of PKCa inhibition in a-TOS-induced apoptosis was confirmed using antisense oligonucleotides or PKCa overexpression. Gain- or loss-of-function bcl-2 mutants implied modulation of bcl-2 activity by PKC/PP2A as a mitochondrial target of a-TOS-induced proapoptotic signals. Structural analogs revealed that a-tocopheryl and succinyl moieties are both required for maximizing these effects. In mice with colon cancer xenografts, a-TOS suppressed tumor growth by 80%. This epitomizes cancer cell killing by a pharmacologically relevant compound without known side effects.
653 a Colon cancer
653 a Programmed cell death
653 a Protein kinase C
653 a Vitamin E succinate
653 a MEDICINE
653 a MEDICIN
700a Weber, T.u Institute for Prevention of Cardiovascular Diseases and Medical Policlinic, Ludwig-Maximilians-University, Munich, Germany4 aut
700a Schroder, A.u Schröder, A., Institute for Prevention of Cardiovascular Diseases and Medical Policlinic, Ludwig-Maximilians-University, Munich, Germany4 aut
700a Lu, M.u Medical Center North, Vanderbilt University, Nashville, TN, United States4 aut
700a Ostermann, G.u Institute for Prevention of Cardiovascular Diseases and Medical Policlinic, Ludwig-Maximilians-University, Munich, Germany4 aut
700a Gellert, N.u Institute for Prevention of Cardiovascular Diseases and Medical Policlinic, Ludwig-Maximilians-University, Munich, Germany4 aut
700a Mayne, G.C.u Flinders University of South Australia, Adelaide, SA, Australia4 aut
700a Olejnicka, Beatau Linköpings universitet,Hälsouniversitetet,Experimentell patologi4 aut0 (Swepub:liu)beaol03
700a Negre-Salvayre, A.u Nègre-Salvayre, A., Biochemistry Department, INSERM, Toulouse, France4 aut
700a Sticha, M.u Stícha, M., Faculty of Science, Charles University, Prague, Czech Republic4 aut
700a Coffey, R.J.u Medical Center North, Vanderbilt University, Nashville, TN, United States4 aut
700a Weber, C.u Institute for Prevention of Cardiovascular Diseases and Medical Policlinic, Ludwig-Maximilians-University, Munich, Germany, Institute for Prevention of Cardiovascular Diseases, Pettenkoferstrasse 9, 80336 Munich, Germany4 aut
710a Institute for Prevention of Cardiovascular Diseases and Medical Policlinic, Ludwig-Maximilians-University, Munich, Germany, Institute for Prevention of Cardiovascular Diseases, Pettenkoferstrasse 9, 80336 Munich, Germanyb Institute for Prevention of Cardiovascular Diseases and Medical Policlinic, Ludwig-Maximilians-University, Munich, Germany4 org
773t The FASEB Journald : Wileyg 15:2, s. 403-415q 15:2<403-415x 0892-6638x 1530-6860
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-47470
8564 8u https://doi.org/10.1096/fj.00-0251com

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