Molecular biological changes of ADP/ATP carrier in cardiomypathic hamster
Molecular biological changes of ADP/ATP carrier in cardiomypathic hamster
批准号:
06670745
负责人:
KATO Mitsutoshi
金额:
$1.09万
依托单位国家:
日本
项目类别:
Grant-in-Aid for General Scientific Research (C)
财政年份:
1994
资助国家:
日本
项目状态:
已结题
起止时间:
1994 至 1995
中文摘要
ADP/ATP载体蛋白(AAC)是存在于线粒体内膜上的一种重要蛋白质,负责ADP和ATP在细胞质和线粒体内的交换。在J-2-N仓鼠中AAC含量显著降低。通过分子生物学分析,采用噬斑杂交法克隆了金黄地鼠AAC cDNA。AACcDNA与AACmRNA特异性杂交,进行RNA斑点杂交。在对照仓鼠中观察到最高的AAC mRNA水平,其次是具有轻度心肌损伤的J-2-N仓鼠、具有严重心肌损伤的J-2-N仓鼠和Bio 14.6心肌病仓鼠。这些结果表明,AAC含量减少可能有助于心肌病的发病机制,AAC mRNA水平的降低可能解释了AAC在J-2-N心肌病仓鼠的异常。
英文摘要
ADP/ATP carrier protein (AAC) is an integral protein present in the inner mitochondrial membrane that performs the exchange of cytoplasmic and intramitochondrial ADP and ATP.AAC content of myocardium was studied in J-2-N cardiomyopathic hamsters. The AAC content was significantly decreased in the J-2-N hamsters. By molecular biological analysis, hamster AAC cDNA was cloned by the plaque hybridization method. The AAC cDNA hybridized specifically with AAC mRNA,so RNA dot-blot hybridization was performed. The highest AAC mRNA level was observed in control hamsters followed by J-2-N hamsters with mild myocardial damage, J-2-N hamsters with severe myocardial damage and Bio 14.6 cardiomyopathic hamsters. These results suggest that a decreased AAC content may contribute to the pathogenesis of cardiomyopathy and that a decrease of AAC mRNA levels may explain the abnormalities of AAC in J-2-N cardiomyopathic hamsters.
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Nagano M,Kato M.: "Pathophysiological Aspects of the Cardioimyopathic J-2-N Hamster." The Cardiomyopathic Heart.157-164 (1994)
Nagano M,Kato M.:“心肌病 J-2-N 仓鼠的病理生理学方面。”
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KATO M: "Molecular biological changes of adenine nucleotide translocator in J-2-N cardiomyopathic hamsters" Mechanisms of Heart Failure. (in press). (1995)
加藤 M:“J-2-N 心肌病仓鼠中腺嘌呤核苷酸易位子的分子生物学变化”心力衰竭的机制。
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KATO M: "Molecular biological changes of adenine nucleotide translocator in J-2-N cardiomyopathic hamsters" Mechanisms of Heart Failure. 197-202 (1994)
加藤 M:“J-2-N 心肌病仓鼠中腺嘌呤核苷酸易位子的分子生物学变化”心力衰竭的机制。
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Takeda N,Kato M.: "Pharmacological modulation of cardiac hypertrophy in hypertensive patients." Raven Press,New York. The Adapted Heart.403-414 (1994)
Takeda N,Kato M.:“高血压患者心脏肥大的药理学调节。”
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KATO M: "Quantitative abnormalities of ADP/ATP carrier protein in cardiomyopathic hamsters." The Adaptes Heart. Chap7. 91-98 (1994)
KATO M:“心肌病仓鼠中 ADP/ATP 载体蛋白的数量异常。”
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共 25 条
Quantitative abnormalities and molecular biological investigation of the ADP/ATP carrier protein in J-2-N cardiomyopathic hamsters
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批准号:04670559
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项目类别:Grant-in-Aid for General Scientific Research (C)
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资助金额:$1.34万
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财政年份:1992
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负责人:KATO Mitsutoshi
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依托单位:
海外基金