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20231222132156.0 |
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231222s1999 xx ||||| 00| ||eng c |
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|a pubmed24n0348.xml
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|a (DE-627)NLM104279036
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|a (NLM)10497012
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|a DE-627
|b ger
|c DE-627
|e rakwb
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| 041 |
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|a eng
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| 100 |
1 |
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|a Caricchio, R
|e verfasserin
|4 aut
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| 245 |
1 |
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|a Apoptosis provoked by the oxidative stress inducer menadione (Vitamin K(3)) is mediated by the Fas/Fas ligand system
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|c 1999
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| 336 |
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|a Text
|b txt
|2 rdacontent
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| 337 |
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|a ohne Hilfsmittel zu benutzen
|b n
|2 rdamedia
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| 338 |
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|a Band
|b nc
|2 rdacarrier
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| 500 |
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|a Date Completed 05.11.1999
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| 500 |
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|a Date Revised 16.11.2017
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|a published: Print
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|a Citation Status MEDLINE
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| 520 |
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|a Copyright 1999 Academic Press.
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| 520 |
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|a Menadione, or vitamin K(3) (VK(3)), a potent oxidative stress inducer, has been recently used as an effective and remarkably safe cytotoxic drug for treatment of several human tumors. VK(3) induces apoptotic cell death through a poorly understood mechanism. Here we show for the first time that VK(3)-induced apoptosis requires the Fas/FasL system. Spleen cells from both Fas- and FasL-deficient mice (C57BL/6-lpr and C57BL/6-gld, respectively) had much lower levels of VK(3) apoptosis in vitro compared to cells from control C57BL/6 mice. VK(3) cytotoxicity toward mouse splenocytes was also blocked with a Fas-Fc fusion protein. VK(3) induced apoptosis in Jurkat cells, coincident with an increase in both Fas and FasL expression. A FasL-resistant variant of these Jurkat cells was also resistant to VK(3)-induced apoptosis. Furthermore, because VK(3) effects were inhibited by glutathione, a potent antioxidant, oxidative stress was linked to the Fas/FasL system. Moreover, since the Jurkat cell lines were p53 null, the activation of Fas/FasL system after oxidative stress apparently acted through a p53-independent pathway. The therapeutic relevance of the K vitamins has been growing in recent years; our findings offer new insight for improving and expanding their applications
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| 650 |
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4 |
|a Journal Article
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| 650 |
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4 |
|a Research Support, Non-U.S. Gov't
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| 650 |
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4 |
|a Research Support, U.S. Gov't, P.H.S.
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| 650 |
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|a FASLG protein, human
|2 NLM
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| 650 |
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7 |
|a Fas Ligand Protein
|2 NLM
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| 650 |
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7 |
|a Fasl protein, mouse
|2 NLM
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| 650 |
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7 |
|a Ligands
|2 NLM
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| 650 |
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7 |
|a Membrane Glycoproteins
|2 NLM
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| 650 |
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7 |
|a fas Receptor
|2 NLM
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| 650 |
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7 |
|a Vitamin K
|2 NLM
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| 650 |
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7 |
|a 12001-79-5
|2 NLM
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| 650 |
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7 |
|a Glutathione
|2 NLM
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| 650 |
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7 |
|a GAN16C9B8O
|2 NLM
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| 700 |
1 |
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|a Kovalenko, D
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Kaufmann, W K
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Cohen, P L
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 93(1999), 1 vom: 01. Okt., Seite 65-74
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
8 |
|g volume:93
|g year:1999
|g number:1
|g day:01
|g month:10
|g pages:65-74
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| 912 |
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|a GBV_USEFLAG_A
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|a SYSFLAG_A
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| 912 |
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|a GBV_NLM
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| 912 |
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|a GBV_ILN_11
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| 912 |
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|a GBV_ILN_24
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| 912 |
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|a GBV_ILN_350
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| 951 |
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|a AR
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| 952 |
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|d 93
|j 1999
|e 1
|b 01
|c 10
|h 65-74
|