دورية أكاديمية
Nerve growth factor inhibits apoptosis in memory B lymphocytes via inactivation of p38 MAPK, prevention of Bcl-2 phosphorylation, and cytochrome c release
| العنوان: | Nerve growth factor inhibits apoptosis in memory B lymphocytes via inactivation of p38 MAPK, prevention of Bcl-2 phosphorylation, and cytochrome c release |
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| المؤلفون: | Torcia M., De Chiara G., Nencioni L., Ammendola S., Labardi D., Lucibello M., Rosini P., Marlier L. N. J. L., Bonini P., Dello Sbarba P., Palamara A. T., Zambrano N., Russo T., Cozzolino F., GARACI, ENRICO |
| المساهمون: | Torcia, M, De Chiara, G, Nencioni, L, Ammendola, S, Labardi, D, Lucibello, M, Rosini, P, Marlier, Lnjl, Bonini, P, Dello Sbarba, P, Palamara, At, Zambrano, N, Russo, T, Garaci, E, Cozzolino, F |
| بيانات النشر: | AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC BETHESDA |
| سنة النشر: | 2001 |
| المجموعة: | Universitá degli Studi di Roma "Tor Vergata": ART - Archivio Istituzionale della Ricerca |
| مصطلحات موضوعية: | Bioassay, Cell, Enzyme, Mutagenesi, Nerve growth factor (NGF), Biochemistry, 4 (4 fluorophenyl) 2 (4 methylsulfinylphenyl) 5 (4 pyridyl)imidazole, cytochrome c, Janus kinase, mitogen activated protein kinase, nerve growth factor, protein bcl 2, serine, synaptophysin, threonine, DNA fragment, enzyme inhibitor, imidazole derivative, mitogen activated protein kinase kinase, mitogen activated protein kinase kinase 4, mitogen activated protein kinase p38, pyridine derivative, recombinant protein, stress activated protein kinase, animal cell, apoptosi, article, autocrine effect, B lymphocyte, cell survival |
| الوصف: | Survival of memory B lymphocytes is tightly linked to the integrity of the Bcl-2 protein and is regulated by a nerve growth factor (NGF) autocrine circuit. In factor-starved memory B cells, the addition of exogenous NGF promptly induced p38 mitogen-activated protein kinase (MAPK), but not c-Jun N-terminal kinase (JNK), dephosphorylation. Conversely, withdrawal of endogenous NGF was followed by p38 MAPK activation and translocation onto mitochondria, whereby it combined with and phosphorylated Bcl-2, as assessed by co-immunoprecipitation and kinase assays in vivo and in vitro. Mitochondria isolated from human memory B cells, then exposed to recombinant p38 MAPK, released cytochrome c, as did mitochondria from Bcl-2-negative MDCK cells loaded with recombinant Bcl-2. Apoptosis induced by NGF neutralization could be blocked by the specific p38 MAPK inhibitor SB203580 or by Bcl-2 mutations in Ser-87 or Thr-56. These data demonstrate that the molecular mechanisms underlying the survival factor function of NGF critically rely upon the continuous inactivation of p38 MAPK, a Bcl-2-modifying enzyme. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| العلاقة: | volume:276; issue:42; firstpage:39027; lastpage:39036; journal:THE JOURNAL OF BIOLOGICAL CHEMISTRY; http://hdl.handle.net/2108/52011Test |
| DOI: | 10.1074/jbc.M102970200 |
| الإتاحة: | https://doi.org/10.1074/jbc.M102970200Test http://hdl.handle.net/2108/52011Test |
| رقم الانضمام: | edsbas.8501EDA6 |
| قاعدة البيانات: | BASE |
| DOI: | 10.1074/jbc.M102970200 |
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