【摘 要】
：
As one of the best-characterized transcription factors,nuclear factor-κB(NF-κB)plays a wide role in the regulation of biological responses,but growing evidences support a major function in neurodegene
【机 构】
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School of medicine,Shandong University,No.44 West Wenhua Road,Jinan 250011,Shandong Province,China
【出 处】
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第九届海内外华人神经科学家研讨会(The 9th Symposium for Chinese Neuroscientis
论文部分内容阅读
As one of the best-characterized transcription factors,nuclear factor-κB(NF-κB)plays a wide role in the regulation of biological responses,but growing evidences support a major function in neurodegeneration.NF-κB regulates the expression of genes involved in the development and progression of neurodegeneration,such as mitochondrial function of neuronal cell.Adenine nucleotide translocator 1(ANT1),a critical component of mitochondrial function and the most abundant protein in the mitochondrial inner membrane,catalyzes the exchange of cytosolic ADP for mitochondrial ATP.We found that NF-κB represses the gene expression of ANT1 both in mRNA and protein level,and tumour necrosis factor α(TNFα),a stimulator of NF-κB activation,also diminishes the ANT1 expression.Furthermore,we identified NF-κB responsive elements(NREs)in ANT1 promoter by EMSA and CH-IP.We also determined that TNFα-induced NF-κB nuclear localization impairs ANT1-dependent ATP/ADP exchange in neuron and glial cells.In addition,NF-κB decreases mitochondria-associated ATP production and increases reactive oxygen species(ROS)generation in neuron and glial cells by negatively regulating ANT1.In conclusion,TNFα Induced NF-κB activation could alter mitochondrial function of neuron and glial cells by reducing ATP level and increasing ROS production via down-regulating the ANT1 expression,making NF-κB a regulator in mitochondrial functions.
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