التفاصيل البيبلوغرافية
| العنوان: |
Smad7 enables STAT3 activation and promotes pluripotency independent of TGF-β signaling. |
| المؤلفون: |
Shuchen Gu, Wenjian Li, Fenfang Chen, Mu Xiao, Lei Wang, Dewei Xu, Ye Li, Zongping Xia, Sheng Ye, Pinglong Xu, Bin Zhao, Yi Yu, Xin-Hua Feng, Ye-Guang Chen, Xia Lin, Chuang Sun, Yi Li, Chen Ding, Jun Qin |
| المصدر: |
Proceedings of the National Academy of Sciences of the United States of America; 9/19/2017, Vol. 114 Issue 38, p10113-10118, 6p |
| مصطلحات موضوعية: |
TRANSFORMING growth factors, CYTOKINES, LEUKEMIA inhibitory factor, EMBRYONIC stem cells, LIGANDS (Biochemistry) |
| مستخلص: |
Smad7 is a negative feedback product of TGF-β superfamily signaling and fine tunes a plethora of pleiotropic responses induced by TGF-β ligands. However, its noncanonical functions independent of TGF-β signaling remain to be elucidated. Here, we show that Smad7 activates signal transducers and activators of transcription 3 (STAT3) signaling in maintaining mouse embryonic stem cell pluripotency in a manner independent of the TGF-β receptors, yet dependent on the leukemia inhibitory factor (LIF) coreceptor glycoprotein 130 (gp130). Smad7 directly binds to the intracellular domain of gp130 and disrupts the SHP2-gp130 or SOCS3-gp130 complex, thereby amplifying STAT3 activation. Consequently, Smad7 facilitates LIF-mediated self-renewal of mouse ESCs and is also critical for induced pluripotent stem cell reprogramming. This finding illustrates an uncovered role of the Smad7-STAT3 interplay in maintaining cell pluripotency and also implicates a mechanism involving Smad7 underlying cytokine-dependent regulation of cancer and inflammation. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
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