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Title: c-Jun induces apoptosis of starved BM2 monoblasts by activating cyclin A-CDK2

Abstract

c-Jun is one of the major components of the activating protein-1 (AP-1), the transcription factor that participates in regulation of proliferation, differentiation, and apoptosis. In this study, we explored functional interactions of the c-Jun protein with several regulators of the G1/S transition in serum-deprived v-myb-transformed chicken monoblasts BM2. We show that the c-Jun protein induces expression of cyclin A, thus up-regulating activity of cyclin A-associated cyclin-dependent kinase 2 (CDK2), and causing massive programmed cell death of starved BM2cJUN cells. Specific inhibition of CDK2 suppresses frequency of apoptosis of BM2cJUN cells. We conclude that up-regulation of cyclin A expression and CDK2 activity can represent important link between the c-Jun protein, cell cycle machinery, and programmed cell death pathway in leukemic cells.

Authors:
 [1];  [2];  [3];  [3];  [4];  [1]
  1. Institute of Experimental Biology, Faculty of Science, Masaryk University, Brno (Czech Republic)
  2. Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm (Sweden)
  3. Institute of Biophysics, Academy of Sciences of the Czech Republic, Brno (Czech Republic)
  4. Institute of Biology, Faculty of Medicine, Masaryk University, Brno (Czech Republic)
Publication Date:
OSTI Identifier:
20857978
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 353; Journal Issue: 1; Other Information: DOI: 10.1016/j.bbrc.2006.11.124; PII: S0006-291X(06)02611-8; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; APOPTOSIS; CELL CYCLE; CELL PROLIFERATION; CHICKENS; GENE REGULATION; INHIBITION; TRANSCRIPTION FACTORS

Citation Formats

Vanhara, Petr, Bryja, Vitezslav, Horvath, Viktor, Kozubik, Alois, Hampl, Ales, Center for Cell Therapy and Tissue Repair, Charles University, Prague, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, and Smarda, Jan. c-Jun induces apoptosis of starved BM2 monoblasts by activating cyclin A-CDK2. United States: N. p., 2007. Web. doi:10.1016/j.bbrc.2006.11.124.
Vanhara, Petr, Bryja, Vitezslav, Horvath, Viktor, Kozubik, Alois, Hampl, Ales, Center for Cell Therapy and Tissue Repair, Charles University, Prague, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, & Smarda, Jan. c-Jun induces apoptosis of starved BM2 monoblasts by activating cyclin A-CDK2. United States. https://doi.org/10.1016/j.bbrc.2006.11.124
Vanhara, Petr, Bryja, Vitezslav, Horvath, Viktor, Kozubik, Alois, Hampl, Ales, Center for Cell Therapy and Tissue Repair, Charles University, Prague, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, and Smarda, Jan. 2007. "c-Jun induces apoptosis of starved BM2 monoblasts by activating cyclin A-CDK2". United States. https://doi.org/10.1016/j.bbrc.2006.11.124.
@article{osti_20857978,
title = {c-Jun induces apoptosis of starved BM2 monoblasts by activating cyclin A-CDK2},
author = {Vanhara, Petr and Bryja, Vitezslav and Horvath, Viktor and Kozubik, Alois and Hampl, Ales and Center for Cell Therapy and Tissue Repair, Charles University, Prague and Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague and Smarda, Jan},
abstractNote = {c-Jun is one of the major components of the activating protein-1 (AP-1), the transcription factor that participates in regulation of proliferation, differentiation, and apoptosis. In this study, we explored functional interactions of the c-Jun protein with several regulators of the G1/S transition in serum-deprived v-myb-transformed chicken monoblasts BM2. We show that the c-Jun protein induces expression of cyclin A, thus up-regulating activity of cyclin A-associated cyclin-dependent kinase 2 (CDK2), and causing massive programmed cell death of starved BM2cJUN cells. Specific inhibition of CDK2 suppresses frequency of apoptosis of BM2cJUN cells. We conclude that up-regulation of cyclin A expression and CDK2 activity can represent important link between the c-Jun protein, cell cycle machinery, and programmed cell death pathway in leukemic cells.},
doi = {10.1016/j.bbrc.2006.11.124},
url = {https://www.osti.gov/biblio/20857978}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 1,
volume = 353,
place = {United States},
year = {Fri Feb 02 00:00:00 EST 2007},
month = {Fri Feb 02 00:00:00 EST 2007}
}