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Structure-activity relationship between carboxylic acids and T cell cycle blockade.

机译：羧酸与T细胞周期阻滞之间的构效关系。

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This study was designed to examine the potential structure-activity relationship between carboxylic acids, histone acetylation and T cell cycle blockade. Toward this goal a series of structural homologues of the short-chain carboxylic acid n-butyrate were studied for their ability to block the IL-2-stimulated proliferation of cloned CD4+ T cells. The carboxylic acids were also tested for their ability to inhibit histone deacetylation. In addition, Western blotting was used to examine the relative capacity of the carboxlic acids to upregulate the cyclin kinase-dependent inhibitor p21cip1 in T cells. As shown earlier n-butyrate effectively inhibited histone deacetylation. The increased acetylation induced by n-butyrate was associated with the upregulation of the cyclin-dependent kinase inhibitor p21cip1 and the cell cycle blockade of CD4+ T cells. Of the other carboxylic acids studied, the short chain acids, C3-C5, without branching were the best inhibitors of histone deacetylase. This inhibition correlated with increased expression of the cell cycle blocker p21cip1, and the associated suppression of CD4+ T cell proliferation. The branched-chain carboxylic acids tested were ineffective in all the assays. These results underline the relationship between the ability of a carboxylic acid to inhibit histone deacetylation, and their ability to block T cell proliferation, and suggests that branching inhibits these effects.
机译：本研究旨在检查羧酸，组蛋白乙酰化和T细胞周期阻滞之间潜在的构效关系。为了实现这个目标，研究了短链羧酸正丁酸酯的一系列结构同源物，它们具有阻断IL-2刺激的克隆CD4 + T细胞增殖的能力。还测试了羧酸抑制组蛋白脱乙酰基的能力。此外，蛋白质印迹法被用来检验羧酸在T细胞中上调细胞周期蛋白激酶依赖性抑制剂p21cip1的相对能力。如前所述，正丁酸酯有效抑制组蛋白脱乙酰基作用。正丁酸诱导的乙酰化增加与细胞周期蛋白依赖性激酶抑制剂p21cip1的上调和CD4 + T细胞的细胞周期阻滞有关。在研究的其他羧酸中，无支链的短链酸C3-C5是组蛋白脱乙酰基酶的最佳抑制剂。这种抑制与细胞周期阻滞剂p21cip1的表达增加以及CD4 + T细胞增殖的相关抑制有关。测试的支链羧酸在所有测定中均无效。这些结果强调了羧酸抑制组蛋白脱乙酰基的能力与它们阻断T细胞增殖的能力之间的关系，并表明分支抑制了这些作用。

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