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Modulation of cell death pathways to apoptosis and necrosis of H2O2-treated rat thymocytes by lipocortin I.

Authors: Sakamoto, T  Repasky, WT  Uchida, K  Hirata, A  Hirata, F 
Citation: Sakamoto T, etal., Biochem Biophys Res Commun. 1996 Mar 27;220(3):643-7.
Pubmed: (View Article at PubMed) PMID:8607818
DOI: Full-text: DOI:10.1006/bbrc.1996.0457

Lipocortin I, also called annexin I, a calcium and phospholipid binding protein, protected rat thymocytes from H2O2-elicited necrosis and facilitated H2O2-induced apoptosis, while anti-lipocortin I antibody enhanced H202-elicited necrosis by blocking H202-induced apoptosis. Essentially similar results were obtained with phospholipase A2 inhibitors and activators such as 3,4-octyadecyl-benzylacrylic acid and melittin, respectively. Available evidence suggests that lipocortin I modulates signals for cell death pathways of H2O2-treated rat thymocytes to apoptosis and necrosis by regulating cellular phospholipase A2 activities but not by inhibiting membrane lipid peroxidation.


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CRRD Object Information
CRRD ID: 2306955
Created: 2009-05-12
Species: All species
Last Modified: 2009-05-12
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.