eprintid: 10432
rev_number: 174
eprint_status: archive
userid: 598
dir: disk0/00/01/04/32
datestamp: 2008-11-05 12:01:36
lastmod: 2021-10-04 00:54:43
status_changed: 2008-11-05 12:01:36
type: article
metadata_visibility: show
item_issues_count: 0
creators_name: Parkinson, DB
creators_name: Dong, ZP
creators_name: Bunting, H
creators_name: Whitfield, J
creators_name: Meier, C
creators_name: Marie, H
creators_name: Mirsky, R
creators_name: Jeesen, KR
title: Transforming growth factor beta (TGF beta) mediates schwann cell death in vitro and in vivo: Examination of c-jun activation, interactions with survival signals, and the relationship of TGF beta-mediated death to schwann cell differentiation
subjects: 8900
divisions: UCL
divisions: B02
divisions: C08
divisions: D09
divisions: F96
keywords: autocrine signals, apoptosis, nerve development, peripheral nerve, nerve injury, nerve regeneration, MESSENGER-RNA EXPRESSION, V-JUN, TRANSCRIPTION FACTOR, SYMPATHETIC NEURONS, PROTEIN-KINASES, NGF-RECEPTOR, HA-RAS, APOPTOSIS, NERVE, PHOSPHORYLATION
abstract: In some situations, cell death in the nervous system is controlled by an interplay between survival factors and negative survival signals that actively induce apoptosis. The present work indicates that the survival of Schwann cells is regulated by such a dual mechanism involving the negative survival signal transforming growth factor beta (TGF beta), a family of growth factors that is present in the Schwann cells themselves. We analyze the interactions between this putative autocrine death signal and previously defined paracrine and autocrine survival signals and show that expression of a dominant negative c-Jun inhibits TGF beta -induced apoptosis. This and other findings pinpoint activation of c-Jun as a key downstream event in TGF beta -induced Schwann cell death. The ability of TGF beta to kill Schwann cells, like normal Schwann cell death in vivo, is under a strong developmental regulation, and we show that the decreasing ability of TGF beta to kill older cells is attributable to a decreasing ability of TGF beta to phosphorylate c-Jun in more differentiated cells.
date: 2001-11-01
publisher: SOC NEUROSCIENCE
id_number: PMID: 11606645
vfaculties: VFLS
rae2008: 14
oa_status: green
primo: open
primo_central: open_green
article_type_text: Article
verified: verified_batch
elements_source: Web of Science
elements_id: 4777
lyricists_name: Jessen, Kristjan
lyricists_name: Mirsky, Rhona
lyricists_name: PARKINSON, DAVID
lyricists_id: KRJES88
lyricists_id: RMIRS78
lyricists_id: DBPAR23
full_text_status: public
publication: J NEUROSCI
volume: 21
number: 21
pagerange: 8572 - 8585
refereed: TRUE
issn: 0270-6474
citation:        Parkinson, DB;    Dong, ZP;    Bunting, H;    Whitfield, J;    Meier, C;    Marie, H;    Mirsky, R;           Parkinson, DB;  Dong, ZP;  Bunting, H;  Whitfield, J;  Meier, C;  Marie, H;  Mirsky, R;  Jeesen, KR;   - view fewer <#>    (2001)    Transforming growth factor beta (TGF beta) mediates schwann cell death in vitro and in vivo: Examination of c-jun activation, interactions with survival signals, and the relationship of TGF beta-mediated death to schwann cell differentiation.                   J NEUROSCI , 21  (21)   8572 - 8585.          Green open access   
 
document_url: https://discovery.ucl.ac.uk/id/eprint/10432/1/10432.pdf