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Molecular mechanism of pancreatic bicarbonate secretion

DC FieldValueLanguage
dc.contributor.author김경환-
dc.date.accessioned2016-05-16T11:20:46Z-
dc.date.available2016-05-16T11:20:46Z-
dc.date.issued2002-
dc.identifier.issn1226-4512-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/144346-
dc.description.abstractThanks to recent progress in availability of molecular and functional techniques it became possible to search for the basic molecular and cellular processes that mediate and control HCO3- and fluid secretion by the pancreatic duct. The coordinated action of various transporters on the luminal and basolateral membranes of polarized epithelial cells mediates the transepithelial HCO3- transport, which involves HCO3- absorption in the resting state and HCO3- secretion in the stimulated state. The overall process of HCO3- secretion can be divided into two steps. First, HCO3- in the blood enters the ductal epithelial cells across the basolateral membrane either by simple diffusion in the forms of CO2 and H2O or by the action of an Na+-coupled transporter, a Na+-HCO3- cotranporter (NBC) identified as pNBC1. Subsequently, the cells secrete HCO3- to the luminal space using at least two HCO3- exit mechanisms at the luminal membrane. One of the critical transporters needed for all forms of HCO3- secretion across the luminal membrane is the cystic fibrosis transmembrane conductance regulator (CFTR). In the resting state the pancreatic duct, and probably other HCO3- secretory epithelia, absorb HCO3-. Interestingly, CFTR also control this mechanism. In this review, we discuss recent progress in understanding epithelial HCO3- transport, in particular the nature of the luminal transporters and their regulation by CFTR.-
dc.description.statementOfResponsibilityopen-
dc.format.extent131~138-
dc.relation.isPartOfKOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleMolecular mechanism of pancreatic bicarbonate secretion-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Pharmacology (약리학)-
dc.contributor.googleauthorMin Goo Lee-
dc.contributor.googleauthorJe Woo Kim-
dc.contributor.googleauthorKyung Hwan Kim-
dc.contributor.googleauthorShmuel Muallem-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00311-
dc.relation.journalcodeJ02104-
dc.identifier.eissn2093-3827-
dc.subject.keywordPancreas-
dc.subject.keywordBicarbonate-
dc.subject.keywordCFTR-
dc.subject.keywordTransporter-
dc.contributor.alternativeNameKim, Kyung Hwan-
dc.contributor.affiliatedAuthorKim, Kyung Hwan-
dc.rights.accessRightsfree-
dc.citation.volume6-
dc.citation.number3-
dc.citation.startPage131-
dc.citation.endPage138-
dc.identifier.bibliographicCitationKOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY, Vol.6(3) : 131-138, 2002-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers

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