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논문 기본 정보

자료유형
학술저널
저자정보
Sang-Hoon Lee (Konyang University) Pyeung-Hyeun Kim (Kangwon National University) Sang-Muk Oh (Konyang University) Jung-Hwan Park (Konyang University) Yung-Choon Yoo (Konyang University) Junglim Lee (Konyang University) Seok-Rae Park (Konyang University)
저널정보
대한면역학회 Immune Network Immune Network Vol.14 No.6
발행연도
2014.12
수록면
321 - 327 (7page)

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초록· 키워드

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TGF-β induces IgA class switching by B cells. We previously reported that Smad3 and Smad4, pivotal TGF-β signal-transducing transcription factors, mediate germline (GL) α transcription induced by TGF-β1, resulting in IgA switching by mouse B cells. Post-translational sumoylation of Smad3 and Smad4 regulates TGF-β-induced transcriptional activation in certain cell types. In the present study, we investigated the effect of sumoylation on TGF-β1-induced, Smad3/4-mediated GLα transcription and IgA switching by mouse B cell line, CH12F3-2A. Overexpression of small ubiquitin-like modifier (SUMO)-1, SUMO-2 or SUMO-3 did not affect TGF-β1-induced, Smad3/4-mediated GLα promoter activity, expression of endogenous GLα transcripts, surface IgA expression, and IgA production. Next, we tested the effect of the E3 ligase PIASy on TGF-β1-induced, Smad3/4-mediated GLα promoter activity. We found that PIASy overexpression suppresses the GLα promoter activity in cooperation with histone deacetylase 1. Taken together, these results suggest that SUMO itself does not affect regulation of GLα transcription and IgA switching induced by TGF-β1/ Smad3/4, while PIASy acts as a repressor.

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INTRODUCTION
MATERIALS AND METHODS
RESULTS AND DISCUSSION
REFERENCES

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UCI(KEPA) : I410-ECN-0101-2016-511-001754224