Bcl-2 Knockdown Accelerates T Cell Receptor-Triggered Activation-Induced Cell Death in Jurkat T Cells
The Korean Journal of Physiology and Pharmacology
; : 73-78, 2014.
Article
em En
| WPRIM
| ID: wpr-727592
Biblioteca responsável:
WPRO
ABSTRACT
Cell death and survival are tightly controlled through the highly coordinated activation/inhibition of diverse signal transduction pathways to insure normal development and physiology. Imbalance between cell death and survival often leads to autoimmune diseases and cancer. Death receptors sense extracellular signals to induce caspase-mediated apoptosis. Acting upstream of CED-3 family proteases, such as caspase-3, Bcl-2 prevents apoptosis. Using short hairpin RNAs (shRNAs), we suppressed Bcl-2 expression in Jurkat T cells, and this increased TCR-triggered AICD and enhanced TNFR gene expression. Also, knockdown of Bcl-2 in Jurkat T cells suppressed the gene expression of FLIP, TNF receptor-associated factors 3 (TRAF3) and TRAF4. Furthermore, suppressed Bcl-2 expression increased caspase-3 and diminished nuclear factor kappa B (NF-kappaB) translocation.
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WPRIM
Assunto principal:
Peptídeo Hidrolases
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Fisiologia
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Doenças Autoimunes
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Linfócitos T
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Transdução de Sinais
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Expressão Gênica
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NF-kappa B
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Morte Celular
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Apoptose
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RNA Interferente Pequeno
Limite:
Humans
Idioma:
En
Revista:
The Korean Journal of Physiology and Pharmacology
Ano de publicação:
2014
Tipo de documento:
Article