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人转录因子IIB自身抗体的鉴定

Identification of human autoantibodies to transcription factor IIB.

作者信息

Abendroth F D, Peterson S R, Galman M, Suwa A, Hardin J A, Dynan W S

机构信息

Department of Chemistry and Biochemistry, University of Colorado, Boulder 80309, USA.

出版信息

Nucleic Acids Res. 1995 Jul 25;23(14):2770-4. doi: 10.1093/nar/23.14.2770.

DOI:10.1093/nar/23.14.2770
PMID:7651839
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC307103/
Abstract

We have characterized the ability of various human autoimmune sera to react with RNA polymerase II transcription factors. One serum, which strongly inhibited transcription in a cell-free system, was shown to contain antibodies directed against human TFIIB. The serum did not show reactivity against the other general transcription factors, including human TBP, TFIIE and TFIIF. The inhibition of transcription was directly attributable to depletion of TFIIB activity, as demonstrated by reconstitution of activity with recombinant TFIIB. It has long been recognized that components of the RNA processing machinery are major human autoantigens. The present results show that at least one general transcription factor required for messenger RNA synthesis is an autoantigen as well.

摘要

我们已经对多种人类自身免疫血清与RNA聚合酶II转录因子发生反应的能力进行了表征。其中一种血清在无细胞系统中强烈抑制转录,结果显示该血清含有针对人类TFIIB的抗体。该血清对其他通用转录因子,包括人类TBP、TFIIE和TFIIF,未表现出反应性。转录抑制直接归因于TFIIB活性的耗尽,重组TFIIB恢复活性证明了这一点。长期以来人们已经认识到,RNA加工机制的成分是主要的人类自身抗原。目前的结果表明,信使RNA合成所需的至少一种通用转录因子也是一种自身抗原。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f823/307103/abdcb4d9eb5d/nar00014-0211-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f823/307103/dd097fbe0f5c/nar00014-0209-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f823/307103/08009d03f11b/nar00014-0210-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f823/307103/6beaca9277db/nar00014-0210-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f823/307103/abdcb4d9eb5d/nar00014-0211-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f823/307103/dd097fbe0f5c/nar00014-0209-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f823/307103/08009d03f11b/nar00014-0210-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f823/307103/6beaca9277db/nar00014-0210-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f823/307103/abdcb4d9eb5d/nar00014-0211-a.jpg

相似文献

1
Identification of human autoantibodies to transcription factor IIB.人转录因子IIB自身抗体的鉴定
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2
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3
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Factors involved in specific transcription by mammalian RNA polymerase II: identification of general transcription factor TFIIG.哺乳动物RNA聚合酶II特异性转录所涉及的因子:通用转录因子TFIIG的鉴定。
Proc Natl Acad Sci U S A. 1990 Dec;87(23):9158-62. doi: 10.1073/pnas.87.23.9158.

本文引用的文献

1
Autoantibody reactive with three classes of RNA polymerases in sera from patients with systemic sclerosis.系统性硬化症患者血清中与三类RNA聚合酶发生反应的自身抗体。
J Clin Invest. 1993 Apr;91(4):1399-404. doi: 10.1172/JCI116343.
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Identification of autoantibodies to RNA polymerase II. Occurrence in systemic sclerosis and association with autoantibodies to RNA polymerases I and III.RNA聚合酶II自身抗体的鉴定。在系统性硬化症中的出现及其与RNA聚合酶I和III自身抗体的关联。
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Autoantibodies to RNA polymerase II are common in systemic lupus erythematosus and overlap syndrome. Specific recognition of the phosphorylated (IIO) form by a subset of human sera.抗RNA聚合酶II自身抗体在系统性红斑狼疮和重叠综合征中很常见。一部分人血清能特异性识别磷酸化(IIO)形式。
J Clin Invest. 1994 Nov;94(5):1981-9. doi: 10.1172/JCI117550.
7
Stimulation of the DNA-dependent protein kinase by RNA polymerase II transcriptional activator proteins.RNA聚合酶II转录激活蛋白对DNA依赖性蛋白激酶的刺激作用。
J Biol Chem. 1995 Jan 20;270(3):1449-54. doi: 10.1074/jbc.270.3.1449.
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A small nuclear ribonucleoprotein is required for splicing of adenoviral early RNA sequences.腺病毒早期RNA序列的剪接需要一种小核核糖核蛋白。
Proc Natl Acad Sci U S A. 1981 Mar;78(3):1371-5. doi: 10.1073/pnas.78.3.1371.
9
Splicing of messenger RNA precursors is inhibited by antisera to small nuclear ribonucleoprotein.信使核糖核酸前体的剪接受到针对小核核糖核蛋白的抗血清的抑制。
Cell. 1983 Nov;35(1):101-7. doi: 10.1016/0092-8674(83)90212-x.
10
Characterization by human antibodies of two HeLa cell proteins which are related to Xenopus laevis transcription factor TFIIIA.用人抗体对两种与非洲爪蟾转录因子TFIIIA相关的海拉细胞蛋白进行表征。
Nucleic Acids Res. 1988 Mar 25;16(6):2473-87. doi: 10.1093/nar/16.6.2473.