NGF withdrawal induces apoptosis in CESS B cell line through p38 MAPK activation and Bcl-2 phosphorylation

Paolo Rosini, Giovanna De Chiara, Maria Lucibello, Enrico Garaci, Federico Cozzolino, Maria Torcia

Research output: Contribution to journalArticlepeer-review


The sIgG+ lymphoblastoid B cell line CESS spontaneously produces a high amount of NGF and expresses both high affinity (p140(Trk-A)) and low affinity (p75(NTR)) NGF receptors. Blocking NGF signals with neutralizing antibodies or specific Trk-A inhibitors induces a rapid phosphorylation of antiapoptotic Bcl-2 protein, followed by caspase activation, and apoptotic death of CESS cells. Bcl-2 phosphorylation in several sites within a ≃60 aa 'loop' domain of protein is known to regulate its antiapoptotic function. Accordingly, CESS cells expressing the loop deletional mutant cDNA constructs Bcl-2 Δ40-91 were completely resistant to apoptosis induced by NGF withdrawal, indicating that Bcl-2 phosphorylation is a critical event. NGF withdrawal induces p38 MAPK, but not JNK, activation in CESS cells, and SB203580, a specific inhibitor of p38 MAPK, is able to prevent both Bcl-2 phosphorylation and apoptosis, indicating that p38 MAPK is the enzyme responsible for these events. (C) 2000 Academic Press.

Original languageEnglish
Pages (from-to)753-759
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number3
Publication statusPublished - Nov 30 2000


  • Apoptosis
  • Bcl-2
  • Lymphoblastoid cells
  • Nerve growth factor
  • p38 MAPK
  • Phosphorylation

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology


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