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在体细胞中抑制c-mos转录的负调控元件的鉴定。

Identification of a negative regulatory element that inhibits c-mos transcription in somatic cells.

作者信息

Zinkel S S, Pal S K, Szeberényi J, Cooper G M

机构信息

Dana-Farber Cancer Institute, Boston, Massachusetts.

出版信息

Mol Cell Biol. 1992 May;12(5):2029-36. doi: 10.1128/mcb.12.5.2029-2036.1992.

Abstract

We have used transient expression assays to identify a cis-acting region in the 5' flanking sequence of murine c-mos which, when deleted, allows expression from the c-mos promoter in NIH 3T3 cells. This negative regulatory sequence, located 400 to 500 nucleotides upstream of the c-mos ATG, also inhibited expression from a heterologous promoter. In addition to NIH 3T3 cells, the c-mos negative regulatory sequence was active in BALB/3T3 cells, PC12 rat pheochromocytoma cells, and A549 human lung carcinoma cells. Site-specific mutagenesis identified three possibly interacting regions that were involved in negative regulatory activity, located around -460, -425, and -405 with respect to the ATG. RNase protection analysis indicated that once the negative regulatory sequences were deleted, transcription in NIH 3T3 cells initiated from the same transcription initiation sites normally utilized in spermatocytes, approximately 280 nucleotides upstream of the ATG. Deletions beyond the spermatocyte promoter, however, allowed transcription initiation from progressively downstream c-mos sequences. Deletion or mutation of sequences surrounding the oocyte promoter at -53 also had little effect on expression of c-mos constructs in NIH 3T3 cells. Therefore, the major determinant of c-mos expression in NIH 3T3 cells was removal of the negative regulatory sequence rather than the utilization of a unique promoter. The c-mos negative regulatory sequences thus appear to play a significant role in tissue-specific c-mos expression by inhibiting transcription in somatic cells.

摘要

我们利用瞬时表达分析鉴定了小鼠c-mos基因5'侧翼序列中的一个顺式作用区域,该区域缺失后可使c-mos启动子在NIH 3T3细胞中表达。这个负调控序列位于c-mos起始密码子上游400至500个核苷酸处,它也抑制异源启动子的表达。除了NIH 3T3细胞外,c-mos负调控序列在BALB/3T3细胞、PC12大鼠嗜铬细胞瘤细胞和A549人肺癌细胞中也有活性。位点特异性诱变确定了三个可能相互作用的区域参与负调控活性,相对于起始密码子分别位于约-460、-425和-405处。核糖核酸酶保护分析表明,一旦负调控序列被删除,NIH 3T3细胞中的转录从精母细胞中正常使用的相同转录起始位点开始,该位点位于起始密码子上游约280个核苷酸处。然而,超出精母细胞启动子的缺失允许转录从逐渐下游的c-mos序列起始。-53处卵母细胞启动子周围序列的缺失或突变对NIH 3T3细胞中c-mos构建体的表达也几乎没有影响。因此,NIH 3T3细胞中c-mos表达的主要决定因素是负调控序列的去除,而不是独特启动子的利用。因此,c-mos负调控序列似乎通过抑制体细胞中的转录在组织特异性c-mos表达中发挥重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f881/364373/ff2e798e73c9/molcellb00027-0139-a.jpg

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