Cited 5 times in
Shank2 mutant mice display a hypersecretory response to cholera toxin
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 노신혜 | - |
dc.contributor.author | 박준희 | - |
dc.contributor.author | 이민구 | - |
dc.contributor.author | 이정수 | - |
dc.contributor.author | 정은석 | - |
dc.contributor.author | 정진세 | - |
dc.contributor.author | 지헌영 | - |
dc.date.accessioned | 2015-01-06T16:49:33Z | - |
dc.date.available | 2015-01-06T16:49:33Z | - |
dc.date.issued | 2014 | - |
dc.identifier.issn | 0022-3751 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/98842 | - |
dc.description.abstract | Shank2 is a PDZ (PSD-95/discs large/ZO-1)-based adaptor that has been suggested to regulate membrane transporting proteins in the brain and epithelial tissues. Here, we report that Shank2 mutant (Shank2(-/-)) mice exhibit aberrant fluid and ion transport in the intestine. Molecular characterization using epithelial tissues from Shank2(+/+) and Shank2(-/-) mice revealed that a long spliceoform of Shank2 (Shank2E) is predominantly expressed in the pancreatic, renal and intestinal epithelia. In functional assays, deletion of Shank2 increased the cystic fibrosis transmembrane conductance regulator (CFTR)-dependent short-circuit currents by 84% (P < 0.05) and 101% (P < 0.05) in the mouse colon and rectum, respectively. Disruption of the CFTR-Shank2-phosphodiesterase 4D protein complex appeared to be mostly responsible for the changes in CFTR activities. Notably, Shank2 deletion profoundly increased cholera toxin-induced fluid accumulation in the mouse intestine (∼90%, P < 0.01). Analyses with chemical inhibitors confirmed that the hyperactivation of CFTR channel function is responsible for the increased response to cholera toxin. These results suggest that Shank2 is a key molecule that participates in epithelial homeostasis, in particular to prevent overt secretory responses caused by epithelial pathogens. | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 1809~1821 | - |
dc.relation.isPartOf | JOURNAL OF PHYSIOLOGY-LONDON | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Chlorides/metabolism | - |
dc.subject.MESH | Cholera Toxin/pharmacology* | - |
dc.subject.MESH | Colon/cytology | - |
dc.subject.MESH | Colon/metabolism | - |
dc.subject.MESH | Cyclic Nucleotide Phosphodiesterases, Type 4/metabolism | - |
dc.subject.MESH | Cystic Fibrosis Transmembrane Conductance Regulator/antagonists & inhibitors | - |
dc.subject.MESH | Cystic Fibrosis Transmembrane Conductance Regulator/metabolism | - |
dc.subject.MESH | HEK293 Cells | - |
dc.subject.MESH | Homeostasis | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Intestinal Mucosa/drug effects | - |
dc.subject.MESH | Intestinal Mucosa/metabolism* | - |
dc.subject.MESH | Intestinal Mucosa/secretion | - |
dc.subject.MESH | Ion Transport | - |
dc.subject.MESH | Mice | - |
dc.subject.MESH | Mutation* | - |
dc.subject.MESH | Nerve Tissue Proteins/genetics | - |
dc.subject.MESH | Nerve Tissue Proteins/metabolism* | - |
dc.subject.MESH | Protein Binding | - |
dc.subject.MESH | Protein Isoforms/genetics | - |
dc.subject.MESH | Protein Isoforms/metabolism | - |
dc.subject.MESH | Rectum/cytology | - |
dc.subject.MESH | Rectum/metabolism | - |
dc.title | Shank2 mutant mice display a hypersecretory response to cholera toxin | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Pharmacology (약리학) | - |
dc.contributor.googleauthor | Eun Suk Jung | - |
dc.contributor.googleauthor | Joonhee Park | - |
dc.contributor.googleauthor | Heon Yung Gee | - |
dc.contributor.googleauthor | Jinsei Jung | - |
dc.contributor.googleauthor | Shin Hye Noh | - |
dc.contributor.googleauthor | Jung‐Soo Lee | - |
dc.contributor.googleauthor | Wito Richter | - |
dc.contributor.googleauthor | Wan Namkung | - |
dc.contributor.googleauthor | Min Goo Lee | - |
dc.identifier.doi | 10.1113/jphysiol.2013.268631 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A03686 | - |
dc.contributor.localId | A01285 | - |
dc.contributor.localId | A01678 | - |
dc.contributor.localId | A02781 | - |
dc.contributor.localId | A03110 | - |
dc.contributor.localId | A03743 | - |
dc.contributor.localId | A03971 | - |
dc.relation.journalcode | J01710 | - |
dc.identifier.eissn | 1469-7793 | - |
dc.identifier.pmid | 24445315 | - |
dc.identifier.url | http://jp.physoc.org/content/592/8/1809.long | - |
dc.contributor.alternativeName | Noh, Shin Hye | - |
dc.contributor.alternativeName | Park, Joonhee | - |
dc.contributor.alternativeName | Lee, Min Goo | - |
dc.contributor.alternativeName | Lee, Jung Soo | - |
dc.contributor.alternativeName | Jung, Eun Suk | - |
dc.contributor.alternativeName | Jung, Jin Sei | - |
dc.contributor.alternativeName | Gee, Heon Yung | - |
dc.contributor.affiliatedAuthor | Jung, Eun Suk | - |
dc.contributor.affiliatedAuthor | Noh, Shin Hye | - |
dc.contributor.affiliatedAuthor | Park, Joonhee | - |
dc.contributor.affiliatedAuthor | Lee, Min Goo | - |
dc.contributor.affiliatedAuthor | Lee, Jung Soo | - |
dc.contributor.affiliatedAuthor | Jung, Jin Sei | - |
dc.contributor.affiliatedAuthor | Gee, Heon Yung | - |
dc.rights.accessRights | free | - |
dc.citation.volume | 592 | - |
dc.citation.number | 8 | - |
dc.citation.startPage | 1809 | - |
dc.citation.endPage | 1821 | - |
dc.identifier.bibliographicCitation | JOURNAL OF PHYSIOLOGY-LONDON, Vol.592(8) : 1809-1821, 2014 | - |
dc.identifier.rimsid | 38820 | - |
dc.type.rims | ART | - |
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