Open Access

ARTICLE

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

CUIXIA CHEN^1*, 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.

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