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Volumn 18, Issue 3, 2008, Pages 284-291

Signaling by death receptors in the nervous system

Author keywords

[No Author keywords available]

Indexed keywords

DEATH RECEPTOR; FAS LIGAND; FOLIC ACID; NEUROTROPHIN RECEPTOR P75; SOMATOMEDIN C; THALIDOMIDE; TUMOR NECROSIS FACTOR ALPHA;

EID: 53949108541     PISSN: 09594388     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.conb.2008.07.013     Document Type: Review
Times cited : (86)

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    • •] are significant because they clearly demonstrate the concept of active killing of motor neurons by glia in the mutant SOD1 mouse model of familial ALS.
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    • This paper provides two types of evidence for a role for Fas receptor in neurodegeneration in ALS model mice. First, the authors show increased expression in SOD mice of Fas and its downstream signaling intermediates, and report that Fas-FADD interactions are intensified at one stage of the disease. In addition, they report that lithium can prevent neurodegeneration and lead to modest increases in lifespan of SOD1 mice. Lithium also strongly inhibits the expression of Fas and FADD, though it still needs to be determined whether this underlies its neuroprotective activity.
    • Shin J.H., Cho S.I., Lim H.R., Lee J.K., Lee Y.A., Noh J.S., Joo I.S., Kim K.W., and Gwag B.J. Concurrent administration of Neu2000 and lithium produces marked improvement of motor neuron survival, motor function, and mortality in a mouse model of amyotrophic lateral sclerosis. Mol Pharmacol 71 (2007) 965-975. This paper provides two types of evidence for a role for Fas receptor in neurodegeneration in ALS model mice. First, the authors show increased expression in SOD mice of Fas and its downstream signaling intermediates, and report that Fas-FADD interactions are intensified at one stage of the disease. In addition, they report that lithium can prevent neurodegeneration and lead to modest increases in lifespan of SOD1 mice. Lithium also strongly inhibits the expression of Fas and FADD, though it still needs to be determined whether this underlies its neuroprotective activity.
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    • Tumor necrosis factor p55 and p75 receptors are involved in chemical-induced apoptosis of dentate granule neurons
    • This study investigates the role of TNF in neuronal damage induced by neuroinflammation. The toxin trimethyltin was known to induce a microglial response and an increase in TNFα, and is shown to induce cell death of hippocampal neurons. Genetic ablation of TNFR1 and/or TNFR2, or the use of antibodies to TNFα, both provide significant protection against the effects of toxin treatment.
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    • Minocycline attenuates microglial activation but fails to mitigate striatal dopaminergic neurotoxicity: role of tumor necrosis factor-alpha
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* 이 정보는 Elsevier사의 SCOPUS DB에서 KISTI가 분석하여 추출한 것입니다.