| Project/Area Number |
09671101
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Hematology
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| Research Institution | Niigata University |
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Principal Investigator |
FUSE Ichiro Niigata University School of Medicine, Associate Professor, 医学部, 助教授 (90242429)
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| Co-Investigator(Kenkyū-buntansha) |
HANAWA Haruo Niigata University Hospital, Assistant, 医学部附属病院, 助手 (40282983)
FUKUKAWA Tatsuo Niigata University Hospital, Associate Professor, 医学部附属病院, 助教授 (00272849)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1998: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1997: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Platelets / Thromboxane A_2 / Receptor / Platelet unresponsiveness to thrombxane A_2 |
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| Research Abstract |
We investigated the mutation of the thromboxane A_2 (TXA_2) receptor in six patients with platelet unresponsiveness to TXA_2, and found that all of the patients patients have the same abnormality of the TXR (Arg^<60> to Leu), although four patients are homozygous and two patients are heterozygous for this mutation. However, in the latter patients, TXA_2-induced IP_3 formation and Ca^<2+> mobilization were within normal limilts.
These results suggest that this mutation is the only abnormality which has been found in this platelet disorder, and that, in patients with heterozygous for this mutation, the mutant type TXR suppress the wild-type receptor mediated platelet aggregation by the mechanism independent of phospholipase C.
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