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Quantification of aminopeptidase N mRNA in T cells by competitive PCR.

作者信息

Wex T, Lendeckel U, Wex H, Frank K, Ansorge S

机构信息

Department of Internal Medicine, University of Magdeburg, Germany.

出版信息

FEBS Lett. 1995 Nov 6;374(3):341-4. doi: 10.1016/0014-5793(95)01139-6.

DOI:10.1016/0014-5793(95)01139-6
PMID:7589567
Abstract

The aminopeptidase N (CD13, EC 3.4.11.2) is a well-characterized surface molecule expressed in a variety of cell types and species. Recent data indicate an expression of the APN mRNA and the corresponding aminopeptidase activity in human peripheral T cells and related cell lines as well. Here, the sensitive method of competitive PCR was used to quantify low amounts of APN mRNA in T cell lines. An APN cDNA fragment enshortened by a deletion of 87 bp was used as an internal APN-specific standard. The myelo-monocytic cell line U937 and the lymphoid T cell lines HuT78 and H9 contain 2.3 x 10(7), 5.9 x 10(6) and 5.6 x 10(6) copies/micrograms total RNA, corresponding to 160, 70 and 50 copies/cell, respectively. These data have been confirmed by determination of the APN activity, that represents a fraction only of the total cellular neutral aminopeptidase activity in hematopoetic cells. In the case of the CD13-positive cell line U937, approximately 60-70% of the total neutral aminopeptidase activity could be attributed to APN. In contrast, only a minor fraction (5-20%) of the cellular neutral aminopeptidase activity in the T cell lines H9 and HuT78 represents APN. The results suggest that APN gene expression within the hematopoetic system is not restricted to myelo-monocytic cells, instead a low APN expression may be a common feature of lymphocytes, at least of T cells, too.

摘要

相似文献

1
Quantification of aminopeptidase N mRNA in T cells by competitive PCR.
FEBS Lett. 1995 Nov 6;374(3):341-4. doi: 10.1016/0014-5793(95)01139-6.
2
The main neutral aminopeptidase activity of human lymphoid tumour cell lines does not originate from the aminopeptidase N-(APN; CD13) gene.人类淋巴瘤细胞系的主要中性氨肽酶活性并非源自氨肽酶N(APN;CD13)基因。
Biochim Biophys Acta. 1997 Feb 4;1355(2):147-54. doi: 10.1016/s0167-4889(96)00132-2.
3
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引用本文的文献

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Addition of an aminopeptidase N-binding sequence to human endostatin improves inhibition of ovarian carcinoma growth.将氨肽酶N结合序列添加到人类内皮抑素中可增强对卵巢癌生长的抑制作用。
Cancer. 2005 Jul 15;104(2):321-31. doi: 10.1002/cncr.21149.
2
Regulation of aminopeptidase N (EC 3.4.11.2; APN; CD13) by interferon-gamma on the HL-60 cell line.γ干扰素对HL-60细胞系中氨肽酶N(EC 3.4.11.2;APN;CD13)的调节作用
Life Sci. 2005 Apr 22;76(23):2681-97. doi: 10.1016/j.lfs.2004.09.040.
3
Identification of acute myeloid leukemia patients with diminished expression of CD13 myeloid transcripts by competitive reverse transcription polymerase chain reaction (RT-PCR).
通过竞争性逆转录聚合酶链反应(RT-PCR)鉴定CD13髓系转录本表达降低的急性髓系白血病患者。
Leuk Res. 2000 Jun;24(6):497-506. doi: 10.1016/s0145-2126(00)00021-7.
4
The activation-dependent induction of APN-(CD13) in T-cells is controlled at different levels of gene expression.T细胞中APN-(CD13)的激活依赖性诱导在基因表达的不同水平受到调控。
FEBS Lett. 1997 Jul 21;412(1):53-6. doi: 10.1016/s0014-5793(97)00738-2.
5
Rapid mitogen-induced aminopeptidase N surface expression in human T cells is dominated by mechanisms independent of de novo protein biosynthesis.在人T细胞中,丝裂原快速诱导的氨肽酶N表面表达主要由独立于从头蛋白质生物合成的机制所主导。
Immunobiology. 1997 Jun;197(1):55-69. doi: 10.1016/S0171-2985(97)80057-5.
6
An enhancer with cell-type dependent activity is located between the myeloid and epithelial aminopeptidase N (CD 13) promoters.一种具有细胞类型依赖性活性的增强子位于髓样和上皮氨肽酶N(CD13)启动子之间。
Biochem J. 1997 Mar 15;322 ( Pt 3)(Pt 3):899-908. doi: 10.1042/bj3220899.
7
The main neutral aminopeptidase activity of human lymphoid tumour cell lines does not originate from the aminopeptidase N-(APN; CD13) gene.人类淋巴瘤细胞系的主要中性氨肽酶活性并非源自氨肽酶N(APN;CD13)基因。
Biochim Biophys Acta. 1997 Feb 4;1355(2):147-54. doi: 10.1016/s0167-4889(96)00132-2.
8
Induction of the membrane alanyl aminopeptidase gene and surface expression in human T-cells by mitogenic activation.有丝分裂原激活诱导人T细胞中膜丙氨酰氨基肽酶基因的表达及表面表达。
Biochem J. 1996 Nov 1;319 ( Pt 3)(Pt 3):817-21. doi: 10.1042/bj3190817.