Home FOR AUTHORS Neoplasma 2005 Neoplasma Vol.52, p.18-24, 2005

Journal info


6 times a year.
Founded: 1954
ISSN 0028-2685
ISSN 1338-4317 (online)

Published in English

Editorial Info
Abstracted and Indexed
Submission Guidelines

Select Journal







Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

Neoplasma Vol.52, p.18-24, 2005

Title: An antigen recognized on cells in apoptosis detected by monoclonal antibody 2E12*
Author: G., STIBRIKOVA ; I., MARINOV ; P., STOCKBAUER ;

Abstract: Monoclonal antibody 2E12 was prepared by immunization of mice with cells of a chronic myeloid leukemia cell line MOLM-7. Human hematopoietic cell lines JURKAT, HPB-ALL, RC2A and MOLM-7 were induced to receptor mediated apoptosis by the treatment with anti- Fas monoclonal antibody 7C11 and subsequently tested for reactivity with 2E12 antibody in comparison to staining with annexin V-FITC and PI in the two-color immunofluorescence and flow cytometry. After 2, 5, 24, and 48 hours of induction, a gradual increase of the percentage of 2E12 positive cells in all cell lines was observed, which partially correlated with an increase of annexin V-FITC binding with a delay of about 12 hours. In the two- color fluorescence microscopy the 2E12 antibody positivity was restricted to the annexin V positive cells, but their number was lower. The binding of 2E12 did not induce apoptosis nor influenced the binding of annexin V. We suppose that the antibody 2E12 detects an antigen expressed on a subpopulation of cells in death. Therefore it can be useful as a new marker for further dissection between living, apoptotic and necrotic cellular populations in vitro.

Keywords: antibody 2E12, cell lines, apoptosis, anti-Fas, annexin V
Year: 2005, Volume: 52, Issue: Page From: 18, Page To: 24



download file



© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.