Literature DB >> 10386996

Expression of the SM-20 gene promotes death in nerve growth factor-dependent sympathetic neurons.

E A Lipscomb1, P D Sarmiere, R J Crowder, R S Freeman.   

Abstract

Sympathetic neurons undergo apoptosis when deprived of nerve growth factor (NGF). Inhibitors of RNA or protein synthesis block this death, suggesting that gene expression is important for apoptosis in this system. We have identified SM-20 as a new gene that increases in expression in sympathetic neurons after NGF withdrawal. Expression of SM-20 also increases during neuronal death caused by cytosine arabinoside or the phosphatidylinositol 3-kinase inhibitor LY294002. In addition, SM-20 protein synthesis is elevated in NGF-deprived neurons compared with neurons maintained with NGF. Importantly, expression of SM-20 in sympathetic neurons causes cell death in the presence of NGF. These results suggest that SM-20 may function to regulate cell death in neurons.

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Year:  1999        PMID: 10386996     DOI: 10.1046/j.1471-4159.1999.0730429.x

Source DB:  PubMed          Journal:  J Neurochem        ISSN: 0022-3042            Impact factor:   5.372


  31 in total

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Journal:  PLoS One       Date:  2011-11-08       Impact factor: 3.240

2.  Prolyl hydroxylase PHD3 activates oxygen-dependent protein aggregation.

Authors:  Krista Rantanen; Juha Pursiheimo; Heidi Högel; Virpi Himanen; Eric Metzen; Panu M Jaakkola
Journal:  Mol Biol Cell       Date:  2008-03-12       Impact factor: 4.138

3.  Pin1 promotes cell death in NGF-dependent neurons through a mechanism requiring c-Jun activity.

Authors:  Maria Cecilia Barone; Lynette A Desouza; Robert S Freeman
Journal:  J Neurochem       Date:  2008-04-14       Impact factor: 5.372

Review 4.  Role of hypoxia and HIF2α in development of the sympathoadrenal cell lineage and chromaffin cell tumors with distinct catecholamine phenotypic features.

Authors:  Susan Richter; Nan Qin; Karel Pacak; Graeme Eisenhofer
Journal:  Adv Pharmacol       Date:  2013

5.  The kinesin KIF1Bbeta acts downstream from EglN3 to induce apoptosis and is a potential 1p36 tumor suppressor.

Authors:  Susanne Schlisio; Rajappa S Kenchappa; Liesbeth C W Vredeveld; Rani E George; Rodney Stewart; Heidi Greulich; Kristina Shahriari; Nguyen V Nguyen; Pascal Pigny; Patricia L Dahia; Scott L Pomeroy; John M Maris; A Thomas Look; Matthew Meyerson; Daniel S Peeper; Bruce D Carter; William G Kaelin
Journal:  Genes Dev       Date:  2008-03-11       Impact factor: 11.361

6.  Prolyl hydroxylase inhibitors depend on extracellular glucose and hypoxia-inducible factor (HIF)-2alpha to inhibit cell death caused by nerve growth factor (NGF) deprivation: evidence that HIF-2alpha has a role in NGF-promoted survival of sympathetic neurons.

Authors:  David J Lomb; Lynette A Desouza; James L Franklin; Robert S Freeman
Journal:  Mol Pharmacol       Date:  2009-02-09       Impact factor: 4.436

7.  Biochemical purification and pharmacological inhibition of a mammalian prolyl hydroxylase acting on hypoxia-inducible factor.

Authors:  Mircea Ivan; Thomas Haberberger; David C Gervasi; Kristen S Michelson; Volkmar Günzler; Keiichi Kondo; Haifeng Yang; Irina Sorokina; Ronald C Conaway; Joan W Conaway; William G Kaelin
Journal:  Proc Natl Acad Sci U S A       Date:  2002-09-26       Impact factor: 11.205

8.  EGLN3 inhibition of NF-κB is mediated by prolyl hydroxylase-independent inhibition of IκB kinase γ ubiquitination.

Authors:  Jian Fu; Mark B Taubman
Journal:  Mol Cell Biol       Date:  2013-06-03       Impact factor: 4.272

9.  The von Hippel-Lindau protein sensitizes renal carcinoma cells to apoptotic stimuli through stabilization of BIM(EL).

Authors:  Y Guo; M C Schoell; R S Freeman
Journal:  Oncogene       Date:  2009-03-23       Impact factor: 9.867

Review 10.  Neuronal apoptosis by prolyl hydroxylation: implication in nervous system tumours and the Warburg conundrum.

Authors:  Susanne Schlisio
Journal:  J Cell Mol Med       Date:  2009-08-19       Impact factor: 5.310

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