| Project/Area Number |
16390044
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Medical pharmacy
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| Research Institution | Doshisha Women's College of Liberal Arts (2005-2006)
National Institute of Health Sciences (2004) |
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Principal Investigator |
URUSHIDANI Tetsuro Doshisha Women's College of Liberal Arts, Department of Pharmaceutical Sciences, Professor, 薬学部病態生理学研究室, 教授 (40262159)
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| Co-Investigator(Kenkyū-buntansha) |
KANNO Jun National Institute of Health Sciences, Department of Molecular Toxicology, Head, 毒性部, 部長 (90186172)
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| Project Period (FY) |
2004 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥14,900,000 (Direct Cost: ¥14,900,000)
Fiscal Year 2006: ¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥4,300,000 (Direct Cost: ¥4,300,000)
Fiscal Year 2004: ¥7,000,000 (Direct Cost: ¥7,000,000)
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| Keywords | parchorin / knockout mouse / gastric acid secretion / water movement / transcriptome / コンディショナルノックアウト |
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| Research Abstract |
We previously cloned a new protein from rabbit brain choroid plexus and named as parchorin. This protein had been identified by us as a phosphoprotein which translocated from cytosol to secretory membrane of rabbit parietal cell in association with stimulation of acid secretion. Subsequent works revealed that parchorin was specifically expressed in various tissues involving in water movement, such as choroid plexus. As the C-terminal of parchorin has common sequence to that found in CLIC family proteins, which are considered to be intracellular chloride channel, it is suggested that this molecule is regulating water movement via the control of chloride conductance. We then produced parchorin knock-out mouse, which is the first one for CLIC family. Contrary to our expectation, the mouse did not show any apparent phenotypes. Especially, the mouse showed normal acid secretory capacity although acid-secreting cell shows the highest parchorin expression. This could be due either to the expression of compensatory protein(s) during the process of growth, or to a possible physiological function that is totally unexpected. We then performed transcriptome analysis of the gastric mucosa and choroid plexus of wild and knock-out mice using GeneChip. In the gastric mucosa, some genes related to gastric acid secretion were differentially expressed, and in the choroid plexus, many genes related to various ion channels. Furthermore, it was suggested that unknown splicing variant (s) could be expressed at least in the choroid plexus. In a separate study, syntenin was identified as parchorin-interacting protein. Syntenin has two PDZ domains and suggested to be involved in intracellular traffic.
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