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NFAT regulates CSF-1 gene transcription triggered by L-selectin crosslinking

CUIXIA CHEN1*, LINGLING CUI2, XIN SHANG2, XIANLU ZENG2
1. Centre for Bioengineering and Biotechnology, China University of Petroleum (East China), Qingdao 266555, P. R. China.
2. Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, P. R. China.
*Address correspondence to: Cuixia Chen. E-mail:

BIOCELL 2010, 34(2), 57-64. https://doi.org/10.32604/biocell.2010.34.057

Abstract

L-selectin is a member of the selectin family that play an important role both in mediating the initial capture and subsequent rolling of leukocytes along the endothelial cells. Furthermore, L-selectin can function as a signal molecule. In our previous studies, we reported that L-selectin ligation could regulate CSF-1 (colony-stimulating factor-1) gene transcription, in which AP-1 acts as a crucial transcriptional factor. Here we investigated the function of the NFAT in the CSF-1 gene transcriptional events. We found that overexpression of WT NFAT induce CSF-1 gene transcription greatly in the activated Jurkat cells. Furthermore, we found that NFAT can be recruited to the nucleus after L-selectin ligation, and the nuclear NFAT interacts with the CSF-1 promoter region to regulate CSF-1 gene transcription in the L-selectin ligation activated Jurkat cells. These results indicate that nuclear NFAT can activate CSF-1 gene transcription by connecting with the CSF-1 promoter in the signaling events induced by L-selectin ligation.

Keywords

signal transduction, gene transcription, nuclear transcriptional factor

Cite This Article

CHEN, C., CUI, L., SHANG, X., ZENG, X. (2010). NFAT regulates CSF-1 gene transcription triggered by L-selectin crosslinking. BIOCELL, 34(2), 57–64.

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This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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