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PIM-1基因的转录衰减

Transcriptional attenuation of PIM-1 gene.

作者信息

Nagarajan L, Narayana L

机构信息

Department of Hematology, University of Texas M. D. Anderson Cancer Center, Houston 77030.

出版信息

Biochem Biophys Res Commun. 1993 Jan 29;190(2):435-9. doi: 10.1006/bbrc.1993.1066.

DOI:10.1006/bbrc.1993.1066
PMID:8427586
Abstract

Levels of the mRNA for PIM-1, a protooncogene encoding a cytoplasmic serine threonine kinase show a wide variation among tissues and cell lines, although this gene is transcribed from a GC- rich housekeeping promoter. Previous studies have failed to identify tissue specific elements in the PIM-1 promoter raising the possibility that these elements might reside within the gene. Transient transfections of Luciferase reporter gene constructs into the chronic myelogenous leukemia cell line K562 (which expresses high levels of PIM-1 mRNA) demonstrate that the 1.7kbp PIM-1 promoter sequences alone were three times more efficient than constructs driven by the promoter+PIM-1 genomic sequences. Nuclear run on assays of nascent RNA from K562 cells revealed premature transcriptional termination within the PIM-1 gene. Thus, PIM-1 gene may be constitutively transcribed in all tissues and transcriptional attenuation could be one of the mechanisms regulating the observed differences in steady state levels of mRNA.

摘要

原癌基因PIM-1编码一种细胞质丝氨酸苏氨酸激酶,其mRNA水平在不同组织和细胞系中存在很大差异,尽管该基因是从富含GC的管家启动子转录而来。先前的研究未能在PIM-1启动子中鉴定出组织特异性元件,这增加了这些元件可能存在于基因内部的可能性。将荧光素酶报告基因构建体瞬时转染到慢性粒细胞白血病细胞系K562(该细胞系表达高水平的PIM-1 mRNA)中,结果表明单独的1.7kbp PIM-1启动子序列的效率比由启动子+PIM-1基因组序列驱动的构建体高三倍。对来自K562细胞的新生RNA进行的核转录分析揭示了PIM-1基因内的过早转录终止。因此,PIM-1基因可能在所有组织中组成性转录,转录衰减可能是调节观察到的mRNA稳态水平差异的机制之一。

相似文献

1
Transcriptional attenuation of PIM-1 gene.PIM-1基因的转录衰减
Biochem Biophys Res Commun. 1993 Jan 29;190(2):435-9. doi: 10.1006/bbrc.1993.1066.
2
pim-1 proto-oncogene expression in anti-CD3-mediated T cell activation is associated with protein kinase C activation and is independent of Raf-1.抗CD3介导的T细胞活化过程中pim-1原癌基因的表达与蛋白激酶C活化相关,且不依赖于Raf-1。
J Immunol. 1996 Jan 15;156(2):549-57.
3
Ubiquitous expression and cell cycle regulation of the protein kinase PIM-1.蛋白激酶PIM-1的广泛表达与细胞周期调控
Arch Biochem Biophys. 1996 Jun 15;330(2):259-65. doi: 10.1006/abbi.1996.0251.
4
The human Pim-1 gene is selectively transcribed in different hemato-lymphoid cell lines in spite of a G + C-rich housekeeping promoter.尽管人类Pim-1基因拥有富含鸟嘌呤和胞嘧啶的管家启动子,但它在不同的血液淋巴细胞系中仍被选择性转录。
Mol Cell Biol. 1990 Apr;10(4):1680-8. doi: 10.1128/mcb.10.4.1680-1688.1990.
5
Stability changes in pim-1 proto-oncogene mRNA after mitogen stimulation of normal lymphocytes.正常淋巴细胞经有丝分裂原刺激后pim-1原癌基因mRNA的稳定性变化
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6
Targeting PIM kinases impairs survival of hematopoietic cells transformed by kinase inhibitor-sensitive and kinase inhibitor-resistant forms of Fms-like tyrosine kinase 3 and BCR/ABL.靶向PIM激酶会损害由激酶抑制剂敏感型和激酶抑制剂耐药型Fms样酪氨酸激酶3及BCR/ABL转化的造血细胞的存活。
Cancer Res. 2006 Apr 1;66(7):3828-35. doi: 10.1158/0008-5472.CAN-05-2309.
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Pim kinases promote cell cycle progression by phosphorylating and down-regulating p27Kip1 at the transcriptional and posttranscriptional levels.Pim激酶通过在转录和转录后水平上磷酸化并下调p27Kip1来促进细胞周期进程。
Cancer Res. 2008 Jul 1;68(13):5076-85. doi: 10.1158/0008-5472.CAN-08-0634.
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Expression of the pim-1 protooncogene: differential inducibility between alpha/beta- and gamma/delta-T cells and B cells.原癌基因pim-1的表达:α/β与γ/δ T细胞及B细胞之间的诱导差异
Cell Immunol. 1995 Apr 15;162(1):123-30. doi: 10.1006/cimm.1995.1059.
9
Alterations in pim-1 and c-myc expression associated with sodium butyrate-induced growth factor dependency in autonomous rat Nb2 lymphoma cells.与丁酸钠诱导的自主大鼠Nb2淋巴瘤细胞生长因子依赖性相关的pim-1和c-myc表达改变。
Cell Growth Differ. 1996 Dec;7(12):1713-21.
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Transcriptional regulation of the mouse PNRC2 promoter by the nuclear factor Y (NFY) and E2F1.核因子Y(NFY)和E2F1对小鼠PNRC2启动子的转录调控。
Gene. 2005 Nov 21;361:89-100. doi: 10.1016/j.gene.2005.07.012. Epub 2005 Sep 21.

引用本文的文献

1
Cryptic promoter activity in the DNA sequence corresponding to the pim-1 5'-UTR.与pim-1 5'-非翻译区相对应的DNA序列中的隐蔽启动子活性。
Nucleic Acids Res. 2005 Apr 20;33(7):2248-58. doi: 10.1093/nar/gki523. Print 2005.