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肿瘤坏死因子受体相关因子2（TRAF2）通过调节Krüppel样因子LKLF的表达发挥其抗凋亡作用。

TRAF2 exerts its antiapoptotic effect by regulating the expression of Krüppel-like factor LKLF.

作者信息

Lin Yong, Ryan Jennifer, Lewis Joseph, Wani Maqsood A, Lingrel Jerry B, Liu Zheng-Gang

机构信息

Cell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

出版信息

Mol Cell Biol. 2003 Aug;23(16):5849-56. doi: 10.1128/MCB.23.16.5849-5856.2003.

DOI:10.1128/MCB.23.16.5849-5856.2003
PMID:12897154
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC166344/
Abstract

Tumor necrosis factor receptor (TNFR)-associated factor 2 (TRAF2) is one of the key factors that mediate TNF signaling. The deletion of TRAF2 renders cells more sensitive to TNF-induced apoptosis. Although TRAF2 is known to be required for TNF-induced JNK and NF-kappaB activation, the underlying mechanism of the increased sensitivity of TRAF2 null cells (TRAF2(-/-)) to TNF-induced apoptosis is not fully understood. To study the underlying mechanism, we examined the difference in gene expression between TRAF2(-/-) and wild-type fibroblast cells by using microarray technology. We found that one of the genes whose expression was dramatically decreased in TRAF2(-/-) cells was the lung Krüppel-like factor (LKLF). Our results indicate that the expression of LKLF requires TRAF2 but is independent of TNF signaling. Although it appears that TRAF2 regulates the expression of the LKLF gene at the transcription level, TRAF2 does not function as a transcription factor itself. Our results suggest that TRAF2 regulates LKLF expression through the mitogen-activated protein kinase p38 pathway. More importantly, ectopic expression of LKLF in TRAF2(-/-) cells protected cells against TNF-induced apoptosis. These results reveal a novel aspect of TRAF2 function: by regulating the expression of genes, such as LKLF, TRAF2 controls cell sensitivity to apoptosis.

摘要

肿瘤坏死因子受体（TNFR）相关因子2（TRAF2）是介导TNF信号传导的关键因子之一。TRAF2的缺失使细胞对TNF诱导的凋亡更加敏感。尽管已知TRAF2是TNF诱导的JNK和NF-κB激活所必需的，但TRAF2基因敲除细胞（TRAF2（-/-））对TNF诱导的凋亡敏感性增加的潜在机制尚未完全了解。为了研究其潜在机制，我们使用微阵列技术检测了TRAF2（-/-）和成纤维细胞之间基因表达的差异。我们发现，在TRAF2（-/-）细胞中表达显著降低的基因之一是肺Krüppel样因子（LKLF）。我们的结果表明，LKLF的表达需要TRAF2，但与TNF信号传导无关。尽管TRAF2似乎在转录水平上调节LKLF基因的表达，但TRAF2本身并不作为转录因子发挥作用。我们的结果表明，TRAF2通过丝裂原活化蛋白激酶p38途径调节LKLF的表达。更重要的是，在TRAF2（-/-）细胞中异位表达LKLF可保护细胞免受TNF诱导的凋亡。这些结果揭示了TRAF2功能的一个新方面：通过调节诸如LKLF等基因的表达，TRAF2控制细胞对凋亡的敏感性。