Deoxycholic acid delays the wound healing of colonic epithelial cells via transmembrane G‐protein‐coupled receptor 5
暂无分享,去创建一个
Y. Naito | T. Sugaya | K. Kamada | T. Takagi | K. Uchiyama | K. Mizushima | O. Dohi | Y. Itoh | N. Yoshida | T. Ishikawa | K. Inoue | Hikaru Hashimoto | S. Sugino | Toshifumi Doi | M. Kajiwara | H. Kitae | Y. Azuma | T. Torii | T. Yasuda | Kazuhiro Kamada | Ken Inoue | Yuka Azuma | Hiroaki Kitae | Satoshi Sugino | Naohisa Yoshida
[1] K. Schoonjans,et al. Bile Acids Signal via TGR5 to Activate Intestinal Stem Cells and Epithelial Regeneration. , 2020, Gastroenterology.
[2] C. Benoist,et al. Microbial bile acid metabolites modulate gut RORγ+ regulatory T cell homeostasis , 2019, Nature.
[3] Huawei Zeng,et al. Secondary Bile Acids and Short Chain Fatty Acids in the Colon: A Focus on Colonic Microbiome, Cell Proliferation, Inflammation, and Cancer , 2019, International journal of molecular sciences.
[4] P. Malhotra,et al. Bile Acid Receptors and Gastrointestinal Functions. , 2019, Liver research.
[5] J. Duan,et al. Scutellariae Radix and Coptidis Rhizoma Improve Glucose and Lipid Metabolism in T2DM Rats via Regulation of the Metabolic Profiling and MAPK/PI3K/Akt Signaling Pathway , 2018, International journal of molecular sciences.
[6] J. Walters,et al. Guts and Gall: Bile Acids in Regulation of Intestinal Epithelial Function in Health and Disease. , 2018, Physiological reviews.
[7] G. Zhu,et al. Effects of Metabolites Derived From Gut Microbiota and Hosts on Pathogens , 2018, Front. Cell. Infect. Microbiol..
[8] A. Neish,et al. Role of gut microbiota in intestinal wound healing and barrier function , 2018, Tissue barriers.
[9] S. Keely,et al. The bile acids, deoxycholic acid and ursodeoxycholic acid, regulate colonic epithelial wound healing. , 2018, American journal of physiology. Gastrointestinal and liver physiology.
[10] D. Francisci,et al. The Bile Acid Receptor GPBAR1 Regulates the M1/M2 Phenotype of Intestinal Macrophages and Activation of GPBAR1 Rescues Mice from Murine Colitis , 2017, The Journal of Immunology.
[11] Cong Guo,et al. TGR5, Not Only a Metabolic Regulator , 2016, Front. Physiol..
[12] Y. Naito,et al. Partially hydrolyzed guar gum enhances colonic epithelial wound healing via activation of RhoA and ERK1/2. , 2016, Food & function.
[13] O. Dormond,et al. PI3K and AKT: Unfaithful Partners in Cancer , 2015, International journal of molecular sciences.
[14] B. Finlay,et al. Chemical communication in the gut: Effects of microbiota-generated metabolites on gastrointestinal bacterial pathogens. , 2015, Anaerobe.
[15] T. Denning,et al. Wound repair: role of immune–epithelial interactions , 2015, Mucosal Immunology.
[16] H. Kuniyasu,et al. Significance of AKT in gastric cancer (Review). , 2014, International journal of oncology.
[17] K. Schoonjans,et al. TGR5 reduces macrophage migration through mTOR-induced C/EBPβ differential translation. , 2014, The Journal of clinical investigation.
[18] N. Bunnett. Neuro‐humoral signalling by bile acids and the TGR5 receptor in the gastrointestinal tract , 2014, The Journal of physiology.
[19] Jesse D. Martinez,et al. Differential Regulation of EGFR–MAPK Signaling by Deoxycholic Acid (DCA) and Ursodeoxycholic Acid (UDCA) in Colon Cancer , 2014, Digestive Diseases and Sciences.
[20] Y. Taché,et al. The bile acid TGR5 membrane receptor: from basic research to clinical application. , 2014, Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver.
[21] H. Kiyono,et al. Mucosal innate immune cells regulate both gut homeostasis and intestinal inflammation , 2013, European journal of immunology.
[22] P. Edwards,et al. Pleiotropic roles of bile acids in metabolism. , 2013, Cell metabolism.
[23] H. Sokol,et al. Connecting dysbiosis, bile-acid dysmetabolism and gut inflammation in inflammatory bowel diseases , 2012, Gut.
[24] H. Kiyono,et al. Epithelial barrier: an interface for the cross‐communication between gut flora and immune system , 2012, Immunological reviews.
[25] S. Spiegel,et al. Conjugated bile acids activate the sphingosine‐1‐phosphate receptor 2 in primary rodent hepatocytes , 2012, Hepatology.
[26] M. Iizuka,et al. Wound healing of intestinal epithelial cells. , 2011, World journal of gastroenterology.
[27] S. Kwon,et al. Bile acid regulates MUC2 transcription in colon cancer cells via positive EGFR/PKC/Ras/ERK/CREB, PI3K/Akt/IkappaB/NF-kappaB and p38/MSK1/CREB pathways and negative JNK/c-Jun/AP-1 pathway. , 2010, International journal of oncology.
[28] J. Auwerx,et al. TGR5-mediated bile acid sensing controls glucose homeostasis. , 2009, Cell metabolism.
[29] R. Stubbs,et al. Reproducibility, sensitivity and compatibility of the ProteoExtract® subcellular fractionation kit with saturation labeling of laser microdissected tissues , 2009, Proteomics.
[30] G. Tseng,et al. Mechanisms of hepatocyte growth factor–mediated and epidermal growth factor–mediated signaling in transdifferentiation of rat hepatocytes to biliary epithelium , 2008, Hepatology.
[31] A. Dignass,et al. Epithelial restitution and wound healing in inflammatory bowel disease. , 2008, World journal of gastroenterology.
[32] M. Vatn,et al. Mucosal healing in inflammatory bowel disease: results from a Norwegian population-based cohort. , 2007, Gastroenterology.
[33] S. Spiegel,et al. Conjugated bile acids promote ERK1/2 and AKT activation via a pertussis toxin–sensitive mechanism in murine and human hepatocytes , 2005, Hepatology.
[34] D. Guertin,et al. Phosphorylation and Regulation of Akt/PKB by the Rictor-mTOR Complex , 2005, Science.
[35] Masataka Harada,et al. A G Protein-coupled Receptor Responsive to Bile Acids* , 2003, The Journal of Biological Chemistry.
[36] Takao Nakamura,et al. Identification of membrane-type receptor for bile acids (M-BAR). , 2002, Biochemical and biophysical research communications.
[37] D. Podolsky,et al. Cytokine modulation of intestinal epithelial cell restitution: central role of transforming growth factor beta. , 1993, Gastroenterology.
[38] W. Tremaine,et al. Coated oral 5-aminosalicylic acid therapy for mildly to moderately active ulcerative colitis. A randomized study. , 1987, The New England journal of medicine.
[39] G PLACITELLI,et al. [Ulcerative colitis]. , 1958, La Riforma medica.