Cellular mechanisms of intestinal bicarbonate transport: Molecular regulation and physiological function of the apical Cl'/HCOs" exchanger SLC26A6

• Antragstellerin: Professorin Dr. Ursula Seidler
• Fachliche Zuordnung: Gastroenterologie
• Förderung: Förderung von 1999 bis 2010
• Projektkennung: Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 5160094

• Erstellungsjahr: 2014

Zusammenfassung der Projektergebnisse

Keine Zusammenfassung vorhanden

Projektbezogene Publikationen (Auswahl)

• CFTR and its key role in in vivo resting and lu-minal acid-induced duodenal HCO3- secretion. Acta Physiologica, Vol. 193. 2008, Issue 4, pp. 357–365.
  Singh AK, Sjoblom M, Zheng W, et al.
  
• Fructose-induced hypertension: essential role of chlo-ride and fructose absorbing transporters PAT1 and Glut5. Kidney International, Vol. 74. 2008, pp. 438–447.
  Singh AK, Amlal H, Haas PJ, et al.
  
• Sodium and chloride absorptive defects in the small intestine in Slc26a6 null mice. Pflügers Archiv - European Journal of Physiology, Vol. 455. 2008, Issue 4, pp 757-766.
  Seidler U, Rottinghaus I, Hillesheim J, et al.
  
• The switch of intestinal Slc26 exchangers from ani-on absorptive to HCO3- secretory mode is dependent on CFTR anion channel function. American Journal of Physiology - Cell Physiology, Vol. 298. 2010, no. 5, C1057-C1065.
  Singh AK, Riederer B, Chen M, et al.
  
• New therapeutic targets in ulcerative colitis: the importance of ion transporters in the human colon. Inflammatory Bowel Diseases, Vol. 17. 2011, Issue 4, pp. 884–898.
  Farkas K, Yeruva S, Rakonczay Z,Jr, et al.
  
• Loss of downregulated in adenoma (DRA) impairs mucosal HCO3(-) secretion in murine ileocolonic inflammation. Inflammatory Bowel Diseases, Vol. 18. 2012, Issue 1, pp. 101–111.
  Xiao F, Juric M, Li J, et al.
  
• Telomere shortening is associated with reduced duodenal HCO3- secretory but normal gastric acid secretory capacity in aging mice. American Journal of Physiology - Gastrointestinal and Liver Physiology, Vol. 303. 2012, no. 12, G1312-G1321.
  Tuo B, Ju Z, Riederer B, et al.
  
• Increased epithelial permeability is the primary cause for bicarbonate loss in inflamed murine colon. Inflammatory Bowel Diseases, Vol. 19. 2013, Issue 5, pp. 904–911.
  Juric M, Xiao F, Amasheh S, et al.
  
• Molecular transport machinery involved in orchestrat-ing luminal acid-induced duodenal bicarbonate secretion in vivo. The Journal of Physiology, Vol. 591. 2013, Issue 21, pp. 5377–5391.
  Singh AK, Liu Y, Riederer B, et al.
  
• The PDZ-interaction of the intestinal anion exchanger downregulated in adenoma (DRA; SLC26A3) facilitates its movement into Rab11a-positive recycling endosomes. American Journal of Physiology - Gastrointestinal and Liver Physiology, Vol. 304. 2013, no. 11, G980-G990.
  Lissner S, Hsieh CJ, Nold L, et al.
  
• Lysophosphatidic acid increases SLC26A3 expression in inflamed intestine and reduces diarrheal severity in C57BL/6 mice with dextran-sodium-sulfateinduced colitis. Chinese Medical Journal, Vol. 127. 2014, Issue 9, pp. 1737-1743.
  Xu L, Xiao F, He J, et al.
  
• Lysophosphatidic acid increases SLC26A3 expression in inflamed intestine and reduces diarrheal severity in C57BL/6 mice with dextran-sodium-sulfateinduced colitis. Chinese Medical Journal, Vol. 127. 2014, Issue 9, pp. 1737-1743.
  Xu L, Xiao F, He J, et al.
  
• Lysophosphatidic acid increases SLC26A3 expression in inflamed intestine and reduces diarrheal severity in C57BL/6 mice with dextran-sodium-sulfateinduced colitis. Chinese Medical Journal, Vol. 127. 2014, Issue 9, pp. 1737-1743.
  Xu L, Xiao F, He J, et al.
  
• Slc26a3 deficiency is associated with loss of colonic HCO3 (-)secretion, absence of a firm mucus layer and barrier impairment in mice. Acta Physiologica, Vol. 211. 2014, Issue 1, pp. 161–175.
  Xiao F, Yu Q, Li J, et al.
  
• The distinct roles of anion transporters Slc26a3 (DRA) and Slc26a6 (PAT-1) in fluid and electrolyte absorption in the murine small intestine. Pflügers Archiv - European Journal of Physiology, Vol. 466. 2014, Issue 8, pp 1541-1556.
  Xia W, Yu Q, Riederer B, et al.