Protein carbonylation, cellular dysfunction, and disease progression.
Protein carbonylation, cellular dysfunction, and disease progression.
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DOI：
10.1111/j.1582-4934.2006.tb00407.x
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发表时间：
2006-04
影响因子：
5.3
通讯作者：
Milzani A
中科院分区：
文献类型：
--
作者：
Dalle-Donne I;Aldini G;Carini M;Colombo R;Rossi R;Milzani A
蛋白质的羰基化是一种不可逆的氧化损伤，通常导致蛋白质功能丧失，这被认为是严重氧化损伤和疾病引起的蛋白质功能障碍的广泛指标。中度羰基化的蛋白质会被蛋白酶体系统降解，而重度羰基化的蛋白质往往会形成高分子量的聚集体，这些聚集体能够抵抗降解并以受损或未折叠的蛋白质形式积累。这种羰基化蛋白质的聚集体可以抑制蛋白酶体活性。许多神经退行性疾病与组织中羰基化蛋白质的抗蛋白水解聚集体的积累直接相关。功能受损的特定羰基化蛋白质的鉴定和选择性羰基阻断剂的开发应导致对蛋白质羰基化在疾病发作和/或进展中的因果、相关或后果作用的明确评估，可能提供新的治疗方法。
Carbonylation of proteins is an irreversible oxidative damage, often leading to a loss of protein function, which is considered a widespread indicator of severe oxidative damage and disease-derived protein dysfunction. Whereas moderately carbonylated proteins are degraded by the proteasomal system, heavily carbonylated proteins tend to form high-molecular-weight aggregates that are resistant to degradation and accumulate as damaged or unfolded proteins. Such aggregates of carbonylated proteins can inhibit proteasome activity. A large number of neurodegenerative diseases are directly associated with the accumulation of proteolysis-resistant aggregates of carbonylated proteins in tissues. Identification of specific carbonylated protein(s) functionally impaired and development of selective carbonyl blockers should lead to the definitive assessment of the causative, correlative or consequential role of protein carbonylation in disease onset and/or progression, possibly providing new therapeutic aproaches.
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影响因子：
11.4
作者：
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通讯作者：
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影响因子：
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DOI：
10.1073/pnas.0404650101
发表时间：
2004-08-17
影响因子：
11.1
作者：
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通讯作者：
Kretzschmar, H