Please use this identifier to cite or link to this item: https://repositorio.uca.edu.ar/handle/123456789/9271
Título : GNAI1 and GNAI3 reduce colitis-associated tumorigenesis in mice by blocking IL6 signaling and down-regulating expression of GNAI2
Autor : Li, Zhi-Wei 
Sun, Beicheng 
Gong, Ting 
Guo, Sheng 
Zhang, Jianhua 
Wang, Junlong 
Sugawara, Atsushi 
Jiang, Meisheng 
Yan, Junjun 
Gurary, Alexandra 
Zheng, Xin 
Gao, Bifeng 
Xiao, Shu-Yuan 
Chen, Wenlian 
Ma, Chi 
Farrar, Christine 
Zhu, Chenjun 
Chan, Owen T. M. 
Xin, Can 
Winnicki, Andrew 
Winnicki, John 
Tang, Mingxin 
Park, Ryan 
Winnicki, Mary 
Diener, Katrina 
Wang, Zhanwei 
Liu, Qicai 
Chu, Catherine H. 
Arter, Zhaohui L. 
Yue, Peibin 
Alpert, Lindsay 
Hui, George S. 
Fei, Peiwen 
Turkson, James 
Yang, Wentian 
Wu, Guangyu 
Tao, Ailin 
Ramos, Joe W. 
Moisyadi, Stefan 
Holcombe, Randall F. 
Jia, Wei 
Birnbaumer, Lutz 
Zhou, Xiqiao 
Chu, Wen-Ming 
Palabras clave : CANCERTUMORESCOLITISCARCINOGENESIS
Fecha de publicación : 2019
Editorial : Elsevier
Cita : Li, Z. et al. GNAI1 and GNAI3 reduce colitis-associated tumorigenesis in mice by blocking IL6 signaling and down-regulating expression of GNAI2 [en línea]. Gastroenterology. 2019, 156(8). doi:10.1053/j.gastro.2019.02.040 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/9271
Resumen : Abstract: Interleukin 6 (IL6) and tumor necrosis factor contribute to the development of colitis-associated cancer (CAC). We investigated these signaling pathways and the involvement of G protein subunit alpha i1 (GNAI1), GNAI2, and GNAI3 in the development of CAC in mice and humans. GNAI1;3 suppresses DSS-plus-AOM–induced colon tumor development in mice, whereas expression of GNAI2 in CD11c+ cells and IL6 in CD4+/CD11b+ DCs appears to promote these effects. Strategies to induce GNAI1;3, or block GNAI2 and IL6, might be developed for the prevention or therapy of CAC in patients.
URI : https://repositorio.uca.edu.ar/handle/123456789/9271
ISSN : 0016-5085
Disciplina: MEDICINA
DOI: 10.1053/j.gastro.2019.02.040
Derechos: Acceso abierto
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