期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 503, 期 3, 页码 1674-1681出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2018.07.098
关键词
LncRNA MALATI; CD80; NF-kappa B; Gene transcription regulation
资金
- project of postgraduate scientific research innovation project of Jiangsu Province [KYCX17_1244]
CD80 has been known to be a co-stimulatory factor expressed in antigen presenting cells (APCs) involved in T-cell activation. It can be expressed in non-bone marrow-derived cells induced by lipopolysaccharide (LPS) or other stimulators, and directly involved in the pathogenesis following T cell activation. However, the intricate transcription mechanisms that underlying the upregulation of CD80 expression levels in LPS-activated non-bone marrow-derived cells is still unknown. LncRNAs are confirmed to be involved in transcriptional regulation by influencing transcription factors. Therefore, we wanted to determine whether the IncRNA MALAT1, which has been found to be related to LPS-induced inflammation, could regulate the transcription of CD80. Our results showed that CD80 was upregulated in low-dose LPS-activated A549 cells in a NF-kappa B-dependent manner. The IncRNA MALAT1 can interfere with NF-kappa B activation and disrupt its binding efficiency with the CD80 promoter. Thus, the IncRNA MALAT1 can regulate CD80 transcription via the NF-kappa B signaling pathway in the LPS-activated A549 cell line. (C) 2018 Elsevier Inc. All rights reserved.
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