| Project/Area Number |
08556044
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
Applied animal science
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| Research Institution | Meiji University |
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Principal Investigator |
HARIGAYA Toshio Meiji University, Dept.of Agriculture, Professor, 農学部, 教授 (70135557)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAGI Hiroaki Higeta Shoyu CO.LTD,Research Institute, Researcher, 研究所, 研究員
SAKAI Senkichi Tokyo University, Dept.of Agriculture, Professor, 大学院・農学生命科学研究科, 教授 (80114487)
SATO Eimei Touhoku University, Dept.of Agriculture, Professor, 農学部, 教授 (80093243)
SHIMADA Seiji Nagoya University, Dept.of Agriculture, Professor, 農学部, 教授 (40065579)
山本 真則 帝人(株), 研究所, 研究員
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥12,700,000 (Direct Cost: ¥12,700,000)
Fiscal Year 1997: ¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 1996: ¥8,700,000 (Direct Cost: ¥8,700,000)
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| Keywords | prolactin / mouse / gene targetting / recombinant |
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| Research Abstract |
1) Cloning and nucleotide sequence analysis of mouse prolactin gene.
To investigate the structural analysis of Prolactin gene, a partial DNA of prolactin gene was obtained by PCR and the nucleotide sequence of this DNA clone contained intron 2 was analyzed.
2) VIP receptor for prolactin gene expression.
Unlike mammals, synthesis and secretion of PRL in birds is controlled predominantly by the hypothalamic releasing factor rather than inhibiting factor. VIP is proposed to be such a factor and specific receptor must mediate VIP actions for PRL synthesis and release between extracellular and intracellular regions. Localization of PRL-producing cell in the cephalic lobe of anterior pituitary gland is attributable, at least in part, to localized expression of VIP receptor gene. The cAMP-PKA system is an intracellular messenger for PRL gene expression in the cephalic lobe of the pituitary gland in the chicken.
3) Prolactin receptor gene expression at lactogenesis.
In the mouse mammary gland, the level of prolactin receptor mRNA decreased about 60% during the first 5 days of pregnancy, and its low levels were maintained until 10 : 00 on day 18 of pregnancy. The level of prolactin receptor mRNA increased about 6 folds during the next 12 h period. The high level was maintaind on day zero of lactation. The increase in the prolactin receptor mRNA was caused by the increase in corticosterone in vivo and in vitro. The similar changes were found in the ovariectomized midpregnant mouse mammary gland. It is concluded that the prolactin receptor gene expresses about 12 h before the onset of parturition.
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