Identification of novel regulatory NFAT and TFII-I binding elements in the calbindin-D28k promoter in response to serum deprivation
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- 作者：Asghar Hajibeigia ; 1 ; Elhadji M. Dioumb ; 1 ; elhadjimamadou.dioum@rd.nestle.com" class="auth_mail" title="E-mail the corresponding author ; Jianfei Guoa ; Orhan K. Ö ; za ; orhan.oz@utsouthwestern.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：Apoptosis ; Calbindin-D28k ; Calcium binding proteins ; NFAT transcription factors ; Serum deprivation ; TFII-I
- 刊名：Biochemical and Biophysical Research Communications
- 出版年：2015
- 出版时间：25 September 2015
- 年：2015
- 卷：465
- 期：3
- 页码：414-420
- 全文大小：991 K
文摘
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Calbindin-D28k (D28k) promoter activity in kidney and pancreatic beta cells increases in response to serum withdrawal.
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Cis-elements downstream within +2/+139 are necessary for full promoter activity.
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A 23nt sequence, +117/+139, is critical for basal transcription.
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NFAT and TFII-I binding sites in the proximal promoter contribute to transcriptional control of D28k expression.
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Discovery of a novel regulatory mechanism of D28k expression by CN/NFAT may lead to new methods to modulate cell survival.