| Project/Area Number |
13556044
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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 | 展開研究 |
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| Research Field |
Applied animal science
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| Research Institution | HOKKAIDO UNIVERSITY (2002)
The University of Tokyo (2001) |
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Principal Investigator |
INABA Mutsumi Graduate School of Veterinary Medicine, Professor, 大学院・獣医学研究科, 教授 (00183179)
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| Co-Investigator(Kenkyū-buntansha) |
IMAGAWA Kazuhiko Graduate School of Agriculture and Life Sciences, University of Tokyo, Associate Professor, 大学院・農学生命科学研究科, 助教授 (00291956)
OGAWA Hiroyuki Graduate School of Agriculture and Life Sciences, University of Tokyo, Professor, 大学院・農学生命科学研究科, 教授 (30012016)
MAEDE Yoshimitsu Graduate School of Veterinary Medicine, Professor, 大学院・獣医学研究科, 教授 (40002084)
INANAMI Osamu Graduate School of Veterinary Medicine, Associate Professor, 大学院・獣医学研究科, 助教授 (10193559)
KOBAYASHI Masato YamagataTechnopolis for Agriculture, Chief Scientist, 主任研究員
小野 憲一郎 東京大学, 大学院・農学生命科学研究科, 教授 (50111480)
印牧 美佐生 (社)家畜改良事業団, 家畜改良技術研究所, 遺伝子検査部長(研究職)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥13,700,000 (Direct Cost: ¥13,700,000)
Fiscal Year 2002: ¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2001: ¥10,200,000 (Direct Cost: ¥10,200,000)
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| Keywords | genetic disorders / beef quality / beef cattle / band 3 deficiency / claudin-16 deficiency / quantitative traits / red cells / kidney / 牛腎尿細管形成不全症 |
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| Research Abstract |
A putative relationship between phenotypes for band 3 deficiency with the R664X mutation and contents of saturated/unsaturated fatty acids, which predominantly affect flavor and taste of beef, was evaluated. There was no direct linkage between phenotype/genotype and beef quality although carriers for band 3 deficiency appeared to have unsaturated fatty acids such as oleic acid at levels higher than normal animals. Moreover, we could not obtain direct evidence for remarkable advantage of homozygous/heterozygous states for claudin-16 deficiency. Present study, however, demonstrated a genetic factor that would regulate fatty acid contents located in chromosome 19, and suggested its linkage with fatnecrosis.
The findings on molecular pathobiology of band 3 deficiency indicated that the mutant band 3 (bebRX) plays a dominant-negative role on the expression of normal band 3 and a partner in the membrane skeleton, ankyrin, and the interaction of band 3 with ankyrin occurs on the ER membrane soon after band 3 synthesis is started during erythroid development. Total or partial deficiency of band 3 in erythroid and renal tubular cells appeared to cause acidosis, leading to downregulation of cell metabolism. Claudin-16 expressed in MDCK cells displayed overall reduction in paracellular transport of ions and solutes including calcium ion, while it appeared to form intercellular pathway for calcium, suggesting that heterophilic combinations of claudin-16 and other claudin proteins other than claudin-1/4 would be essential to formation of molecular pores for calcium.
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