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调节醛缩酶B基因肝脏特异性表达的转录因子的发育表现。

Developmental appearance of transcription factors that regulate liver-specific expression of the aldolase B gene.

作者信息

Tsutsumi K, Ito K, Ishikawa K

机构信息

Department of Biochemistry, Yamagata University School of Medicine, Japan.

出版信息

Mol Cell Biol. 1989 Nov;9(11):4923-31. doi: 10.1128/mcb.9.11.4923-4931.1989.

DOI:10.1128/mcb.9.11.4923-4931.1989
PMID:2601701
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC363643/
Abstract

The region from -202 to -1 of the rat aldolase B (AldB) promoter directs tissue-specific transcription in vitro. Deletion of the half of this promoter distal to its origin reduced its ability for tissue-specific expression. Two protein-binding sites in this distal element have been identified and characterized. One bound a factor named AIF-A, which is probably identical to previously characterized liver-specific factors HNF-1 and APF. The other, containing a CCAAT motif, bound a factor named AIF-B. These two factors were considerably enriched in liver cells compared with other cells not expressing AldB. In the liver, these two factors increased prior to the activation of the AldB gene during development. Liver-specific in vitro transcription assays indicated that the binding of both factors to their target sequences was required for AldB transcription. These results suggest that AIF-A and AIF-B are positively acting transcription factors that regulate tissue-specific and development stage-specific activation of the AldB gene.

摘要

大鼠醛缩酶B（AldB）启动子从-202至-1的区域在体外指导组织特异性转录。该启动子起源远端的一半缺失会降低其组织特异性表达能力。已在该远端元件中鉴定并表征了两个蛋白质结合位点。一个位点结合了一种名为AIF-A的因子，它可能与先前表征的肝脏特异性因子HNF-1和APF相同。另一个包含CCAAT基序的位点结合了一种名为AIF-B的因子。与不表达AldB的其他细胞相比，这两种因子在肝细胞中显著富集。在肝脏中，这两种因子在发育过程中先于AldB基因激活而增加。肝脏特异性体外转录分析表明，这两种因子与其靶序列的结合是AldB转录所必需的。这些结果表明，AIF-A和AIF-B是正向作用的转录因子，它们调节AldB基因的组织特异性和发育阶段特异性激活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1805/363643/1142a4f1e8d0/molcellb00059-0353-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1805/363643/b72715447171/molcellb00059-0348-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1805/363643/4825cad69839/molcellb00059-0349-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1805/363643/a9e91dbd4292/molcellb00059-0350-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1805/363643/af4b42771eb1/molcellb00059-0351-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1805/363643/1fbc0480daa1/molcellb00059-0352-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1805/363643/1142a4f1e8d0/molcellb00059-0353-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1805/363643/b72715447171/molcellb00059-0348-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1805/363643/4825cad69839/molcellb00059-0349-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1805/363643/a9e91dbd4292/molcellb00059-0350-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1805/363643/af4b42771eb1/molcellb00059-0351-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1805/363643/1fbc0480daa1/molcellb00059-0352-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1805/363643/1142a4f1e8d0/molcellb00059-0353-a.jpg

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