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由爱泼斯坦-巴尔病毒编码并与蛋白质复合的两种小RNA被系统性红斑狼疮患者的抗体沉淀下来。

Two small RNAs encoded by Epstein-Barr virus and complexed with protein are precipitated by antibodies from patients with systemic lupus erythematosus.

作者信息

Lerner M R, Andrews N C, Miller G, Steitz J A

出版信息

Proc Natl Acad Sci U S A. 1981 Feb;78(2):805-9. doi: 10.1073/pnas.78.2.805.

DOI:10.1073/pnas.78.2.805
PMID:6262773
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC319891/
Abstract

Primate cells harboring the Epstein-Barr virus (EBV) genome synthesize large amounts of two small RNAs:EBER 1 and EBER 2 (EBV-encoded RNA). These RNAs are approximately 180 nucleotides long, possess 5' pppA termini, and lack poly(A). They have different T1 and pancreatic RNase digestion fingerprints. They are not found in normal B lymphocytes, in transformed B lymphocytes that lack EBV DNA, in T lymphocytes transformed by Herpesvirus ateles, or in a variety of other nonlymphoid mammalian cells. Hybridization analyses indicate that EBER 1 and EBER 2 are encoded by the EcoRI-J fragment of EBV (B95-8) DNA. In vivo both RNAs are associated with protein(s), allowing their specific precipitation by the systemic lupus erythematosus-associated antibody anti-La. The La antigen in uninfected mammalian cells consists of a heterogeneous class of small ribonucleoprotein particles, some of whose RNA components exhibit sequence homology with a highly repetitive, interspersed class of human DNA designated the Alu family. Possible functions for EBER 1 and EBER 2 in infection and cell transformation by EBV and their potential relationship to the pathogenesis of systemic lupus erythematosus are discussed.

摘要

携带爱泼斯坦 - 巴尔病毒(EBV)基因组的灵长类细胞会合成大量两种小RNA:EBER 1和EBER 2(EBV编码RNA)。这些RNA长度约为180个核苷酸,具有5' pppA末端,且无poly(A)。它们具有不同的T1和胰核糖核酸酶消化指纹图谱。在正常B淋巴细胞、缺乏EBV DNA的转化B淋巴细胞、被蛛猴疱疹病毒转化的T淋巴细胞或多种其他非淋巴哺乳动物细胞中均未发现它们。杂交分析表明,EBER 1和EBER 2由EBV(B95 - 8)DNA的EcoRI - J片段编码。在体内,这两种RNA均与蛋白质结合,可被系统性红斑狼疮相关抗体抗 - La特异性沉淀。未感染的哺乳动物细胞中的La抗原由一类异质性的小核糖核蛋白颗粒组成,其中一些RNA成分与一类高度重复、散布的人类DNA(称为Alu家族)具有序列同源性。文中讨论了EBER 1和EBER 2在EBV感染和细胞转化中的可能功能及其与系统性红斑狼疮发病机制的潜在关系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83b/319891/c5fd43a0a909/pnas00653-0172-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83b/319891/c12a4f78c004/pnas00653-0170-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83b/319891/c572b56c2092/pnas00653-0171-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83b/319891/d7f4fe91d641/pnas00653-0172-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83b/319891/c5fd43a0a909/pnas00653-0172-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83b/319891/c12a4f78c004/pnas00653-0170-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83b/319891/c572b56c2092/pnas00653-0171-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83b/319891/d7f4fe91d641/pnas00653-0172-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b83b/319891/c5fd43a0a909/pnas00653-0172-b.jpg

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