Correction: Dehydroepiandrosterone Sulfate Stimulates Expression of Blood-Testis-Barrier Proteins Claudin-3 and -5 and Tight Junction Formation via a Gnα11-Coupled Receptor in Sertoli Cells.
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The following information is missing from the Funding section: This study was supported by a grant from the Deutsche Forschungsgemeinschaft (SCHE 307/7-1) to GSB. The publisher apologies for this error. open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
منابع مشابه
Dehydroepiandrosterone Sulfate Stimulates Expression of Blood-Testis-Barrier Proteins Claudin-3 and -5 and Tight Junction Formation via a Gnα11-Coupled Receptor in Sertoli Cells
Dehydroepiandrosterone sulfate (DHEAS) is a circulating sulfated steroid considered to be a pro-androgen in mammalian physiology. Here we show that at a physiological concentration (1 μM), DHEAS induces the phosphorylation of the kinase Erk1/2 and of the transcription factors CREB and ATF-1 in the murine Sertoli cell line TM4. This signaling cascade stimulates the expression of the tight juncti...
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AIM The present study aims to investigate the NALP3 system and its effect on claudins in Sertoli cells using a mouse adult Sertoli cell line as a model. We focus on the Sertoli cell biology looking for the possible implications for male reproductive functions. MATERIALS AND METHODS Adult Sertoli cells were transfected with NAPL3 siRNA and treated with NOD1 (ie-DAP) and NOD2 (MDP) receptor lig...
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Tissue integrity relies on barriers formed between epithelial cells. In the testis, the barrier is formed at the initiation of puberty by a tight junction complex between adjacent Sertoli cells, thereby defining an adluminal compartment where meiosis and spermiogenesis occur. Claudin 11 is an obligatory protein for tight junction formation and barrier integrity in the testis. It is expressed by...
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ورودعنوان ژورنال:
- PloS one
دوره 11 4 شماره
صفحات -
تاریخ انتشار 2016