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一个富含鸟嘌呤-胞嘧啶的元件赋予胃泌素启动子转录对表皮生长因子的响应性。

A GC-rich element confers epidermal growth factor responsiveness to transcription from the gastrin promoter.

作者信息

Merchant J L, Demediuk B, Brand S J

机构信息

Gastrointestinal Unit, Massachusetts General Hospital, Boston.

出版信息

Mol Cell Biol. 1991 May;11(5):2686-96. doi: 10.1128/mcb.11.5.2686-2696.1991.

DOI:10.1128/mcb.11.5.2686-2696.1991
PMID:2017173
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC360038/
Abstract

Epidermal growth factor (EGF) and transforming growth factor alpha are important determinants of mucosal integrity in the gastrointestinal tract, and they act both directly and indirectly to prevent ulceration in the stomach. Consistent with this physiological role, EGF stimulates transcription of gastrin, a peptide hormone which regulates gastric acid secretion and mucosal growth. EGF stimulation of gastrin transcription is mediated by a GC-rich gastrin EGF response element (gERE) (GGGGCGGGGTGGGGGG) which lies between -54 and -68 in the human gastrin promoter. The gERE sequence also confers weaker responsiveness to phorbol ester stimulation. The gERE sequence differs from previously described EGF response elements. The gERE DNA sequence specifically interacts with a GH4 DNA-binding protein distinct from previously described transcription factors (Egr-1 and AP2) which bind GC-rich sequences and mediate transcriptional activation by growth factors. Furthermore, the gERE element does not bind the Sp1 transcription factor even though the gERE sequence contains a high-affinity Sp1-binding site (GGCGGG).

摘要

表皮生长因子（EGF）和转化生长因子α是胃肠道黏膜完整性的重要决定因素，它们直接或间接发挥作用以预防胃黏膜溃疡。与这一生理作用一致，EGF刺激胃泌素的转录，胃泌素是一种调节胃酸分泌和黏膜生长的肽类激素。EGF对胃泌素转录的刺激由富含GC的胃泌素EGF反应元件（gERE）（GGGGCGGGGTGGGGGG）介导，该元件位于人胃泌素启动子的-54至-68之间。gERE序列对佛波酯刺激也具有较弱的反应性。gERE序列不同于先前描述的EGF反应元件。gERE DNA序列与一种GH4 DNA结合蛋白特异性相互作用，该蛋白不同于先前描述的结合富含GC序列并介导生长因子转录激活的转录因子（Egr-1和AP2）。此外，尽管gERE序列包含一个高亲和力的Sp1结合位点（GGCGGG），但gERE元件并不结合Sp1转录因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74fd/360038/18f7412ae0b8/molcellb00139-0369-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74fd/360038/23dd965978bc/molcellb00139-0364-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74fd/360038/fb8a73b21a89/molcellb00139-0366-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74fd/360038/e0f2bb69ec58/molcellb00139-0367-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74fd/360038/ac45627242fe/molcellb00139-0368-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74fd/360038/18f7412ae0b8/molcellb00139-0369-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74fd/360038/23dd965978bc/molcellb00139-0364-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74fd/360038/fb8a73b21a89/molcellb00139-0366-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74fd/360038/e0f2bb69ec58/molcellb00139-0367-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74fd/360038/ac45627242fe/molcellb00139-0368-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74fd/360038/18f7412ae0b8/molcellb00139-0369-a.jpg

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