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人类FK506结合蛋白:人FKBP19的特性

The human FK506-binding proteins: characterization of human FKBP19.

作者信息

Rulten Stuart L, Kinloch Ross A, Tateossian Hilda, Robinson Colin, Gettins Lucy, Kay John E

机构信息

Trafford Centre for Graduate Medical Education and Research, University of Sussex, Falmer, Brighton, BN1 9QG, UK.

出版信息

Mamm Genome. 2006 Apr;17(4):322-31. doi: 10.1007/s00335-005-0127-7. Epub 2006 Apr 4.

DOI:10.1007/s00335-005-0127-7
PMID:16596453
Abstract

Analysis of the human repertoire of the FK506-binding protein (FKBP) family of peptidyl-prolyl cis/trans isomerases has identified an expansion of genes that code for human FKBPs in the secretory pathway. There are distinct differences in tissue distribution and expression levels of each variant. In this article we describe the characterization of human FKBP19 (Entrez Gene ID: FKBP11), an FK506-binding protein predominantly expressed in vertebrate secretory tissues. The FKBP19 sequence comprises a cleavable N-terminal signal sequence followed by a putative peptidyl-prolyl cis/trans isomerase domain with homology to FKBP12. This domain binds FK506 weakly in vitro. FKBP19 mRNA is abundant in human pancreas and other secretory tissues and high levels of FKBP19 protein are detected in the acinar cells of mouse pancreas.

摘要

对肽基脯氨酰顺/反异构酶的FK506结合蛋白(FKBP)家族的人类基因库分析表明,在分泌途径中编码人类FKBP的基因有所扩增。每个变体在组织分布和表达水平上存在明显差异。在本文中,我们描述了人类FKBP19(Entrez基因ID:FKBP11)的特征,这是一种主要在脊椎动物分泌组织中表达的FK506结合蛋白。FKBP19序列包含一个可切割的N端信号序列,随后是一个与FKBP12具有同源性的假定肽基脯氨酰顺/反异构酶结构域。该结构域在体外与FK506的结合较弱。FKBP19 mRNA在人类胰腺和其他分泌组织中丰富,并且在小鼠胰腺的腺泡细胞中检测到高水平的FKBP19蛋白。

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Curr Top Med Chem. 2003;3(12):1315-47. doi: 10.2174/1568026033451862.
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Human genome. A low number wins the GeneSweep Pool.人类基因组。数字小者赢得基因扫描抽奖池。
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Identification and characterisation of Schizosaccharomyces pombe cyclophilin 3, a cyclosporin A insensitive orthologue of human USA-CyP.
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FK506-Binding Protein 11 Is a Novel Plasma Cell-Specific Antibody Folding Catalyst with Increased Expression in Idiopathic Pulmonary Fibrosis.FK506 结合蛋白 11 是一种新型浆细胞特异性抗体折叠催化剂,在特发性肺纤维化中表达增加。
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