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首页> 外文期刊>Molecular and Cellular Biology >Selective Cooperation between Fatty Acid Binding Proteins and Peroxisome Proliferator-Activated Receptors in Regulating Transcription
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Selective Cooperation between Fatty Acid Binding Proteins and Peroxisome Proliferator-Activated Receptors in Regulating Transcription

机译：脂肪酸结合蛋白和过氧化物酶体增殖物激活的受体之间的选择性合作调节转录。

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Lipophilic compounds such as retinoic acid and long-chain fatty acids regulate gene transcription by activating nuclear receptors such as retinoic acid receptors (RARs) and peroxisome proliferator-activated receptors (PPARs). These compounds also bind in cells to members of the family of intracellular lipid binding proteins, which includes cellular retinoic acid-binding proteins (CRABPs) and fatty acid binding proteins (FABPs). We previously reported that CRABP-II enhances the transcriptional activity of RAR by directly targeting retinoic acid to the receptor. Here, potential functional cooperation between FABPs and PPARs in regulating the transcriptional activities of their common ligands was investigated. We show that adipocyte FABP and keratinocyte FABP (A-FABP and K-FABP, respectively) selectively enhance the activities of PPARγ and PPARβ, respectively, and that these FABPs massively relocate to the nucleus in response to selective ligands for the PPAR isotype which they activate. We show further that A-FABP and K-FABP interact directly with PPARγ and PPARβ and that they do so in a receptor- and ligand-selective manner. Finally, the data demonstrate that the presence of high levels of K-FABP in keratinocytes is essential for PPARβ-mediated induction of differentiation of these cells. Taken together, the data establish that A-FABP and K-FABP govern the transcriptional activities of their ligands by targeting them to cognate PPARs in the nucleus, thereby enabling PPARs to exert their biological functions.
机译：亲脂性化合物（例如视黄酸和长链脂肪酸）通过激活核受体（例如视黄酸受体（RAR）和过氧化物酶体增殖物激活受体（PPAR））来调节基因转录。这些化合物还可以在细胞中与细胞内脂质结合蛋白家族的成员结合，其中包括细胞视黄酸结合蛋白（CRABPs）和脂肪酸结合蛋白（FABPs）。我们先前曾报道CRABP-II通过将视黄酸直接靶向受体来增强RAR的转录活性。在此，研究了FABP和PPAR之间潜在的功能合作，以调节其共同配体的转录活性。我们显示，脂肪细胞FABP和角质形成细胞FABP（分别为A-FABP和K-FABP）分别选择性地增强PPARγ和PPARβ的活性，并且这些FABPs响应于他们所选择的PPAR同种型的选择性配体而大量迁移至细胞核。启用。我们进一步表明，A-FABP和K-FABP与PPARγ和PPARβ直接相互作用，并且它们以受体和配体选择性的方式相互作用。最后，数据表明角质形成细胞中高水平的K-FABP的存在对于PPARβ介导的这些细胞的分化诱导至关重要。两者合计，数据确定A-FABP和K-FABP通过将配体靶向细胞核中的PPAR关联来控制其配体的转录活性，从而使PPAR发挥其生物学功能。

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