Nuclear Smad6 promotes gliomagenesis by negatively regulating PIAS3-mediated STAT3 inhibition - Jiao, Jiantong; Zhang, Rui; Li, Zheng; Yin, Ying; Fang, Xiangming; Ding, Xiaopeng; Cai, Ying; Yang, Shudong; Mu, Huijun; Zong, Da; Chen, Yuexin; Zhang, Yansong; et al. (Nature communications, 2018)
Keywords: 13/105; 13/51; 13/95; 631/67/1922; 631/67/2195; 82/80; Adult; Aged; Aged, 80 and over; Animals; Brain; Brain - pathology; Brain Neoplasms - genetics; Brain Neoplasms - mortality; Brain Neoplasms - pathology; Carcinogenesis - pathology; Cell Line, Tumor; Cell Nucleus - metabolism; Cell Proliferation - genetics; Cohort Studies; Degradation; Down-Regulation; Female; Gene expression; Gene Expression Regulation, Neoplastic; Glioma; Glioma - genetics; Glioma - mortality; Glioma - pathology; Glioma cells; Growth factors; HEK293 Cells; Homology; Hospitals; Humanities and Social Sciences; Humans; Infant; Kinases; Localization; Male; Medical prognosis; Mice; Mice, Inbred BALB C; Mice, Nude; Middle Aged; Molecular chains; Molecular Chaperones - metabolism; multidisciplinary; Neurosurgery; Nuclei; Nuclei (cytology); Pathology; Patients; Protein Domains; Protein expression; Protein Inhibitors of Activated STAT - metabolism; Proteins; Proteolysis; Rings (mathematics); Science; Science (multidisciplinary); Signal Transduction - genetics; Smad6 Protein - metabolism; Stat3 protein; STAT3 Transcription Factor - metabolism; Survival Rate; Transcription activation; Tumorigenesis; Tumors; Ubiquitin-Protein Ligases; Ubiquitination; Ubiquitination - genetics; Up-Regulation; Xenograft Model Antitumor Assays; Young Adult