کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8292302 | 1536727 | 2018 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
TSG101 interacts with the androgen receptor and attenuates its expression through the endosome/lysosome pathway
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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![عکس صفحه اول مقاله: TSG101 interacts with the androgen receptor and attenuates its expression through the endosome/lysosome pathway TSG101 interacts with the androgen receptor and attenuates its expression through the endosome/lysosome pathway](/preview/png/8292302.png)
چکیده انگلیسی
The androgen receptor (AR) signaling pathway plays a vital role in the normal development and function of the male reproductive organs. Dysregulation of the androgen-AR signaling pathway has been linked to prostate cancer. Here, we demonstrate that tumor susceptibility gene 101 (TSG101) regulates AR expression level via the endosome/lysosome degradation pathway. In LNCaP cells, TSG101 overexpression recruits the AR to TSG101-containing cytoplasmic vesicles resulting in reduced AR protein level and AR transactivation activity downregulation. Immunofluorescence microscopy demonstrated that TSG101-decorated cytoplasmic vesicles are associated with late endosomes/lysosomes and the AR could be found within the Lamp2 positive TSG101 vesicles upon lysosomal protease inhibitor treatment. Furthermore, chloroquine or bafilomycin A1 treatment was able to restore TSG101-mediated AR expression reduction. Based on these data, we conclude that the interaction of the AR and TSG101 leads to AR recruitment to TSG101-containing cytoplasmic vesicles and induces AR-attenuated expression through the late endosome/lysosome degradation pathway.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 503, Issue 1, 3 September 2018, Pages 157-164
Journal: Biochemical and Biophysical Research Communications - Volume 503, Issue 1, 3 September 2018, Pages 157-164
نویسندگان
Yen-Ming Lin, Pao-Hsien Chu, Pin Ouyang,