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整合型牛白血病病毒基因组侧翼细胞序列的特征分析

Characterization of cellular sequences flanking an integrated bovine leukemia virus genome.

作者信息

Gelmann E P, Burny A, Kettmann R

出版信息

J Virol. 1984 Dec;52(3):988-90. doi: 10.1128/JVI.52.3.988-990.1984.

DOI:10.1128/JVI.52.3.988-990.1984
PMID:6092727
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC254626/
Abstract

We cloned a 20.2-kilobase fragment, including the unique proviral integration site, from the tumor tissue DNA of a bovine leukemia virus-induced lymphoma (tumor 1351). This clone contained 5.5 kilobases of flanking sequences at either side of the full-length integrated viral genome. Hybridization analysis of both 3' and 5' cellular flanking regions provided no evidence for rearrangements at this locus in other tumors, RNA transcription from either flanking region, or homology to eight known onc genes.

摘要

我们从一头牛白血病病毒诱导的淋巴瘤（肿瘤1351）的肿瘤组织DNA中克隆了一个20.2千碱基的片段，其中包括独特的原病毒整合位点。该克隆在全长整合病毒基因组的两侧各包含5.5千碱基的侧翼序列。对3'和5'细胞侧翼区域的杂交分析未发现其他肿瘤中该位点发生重排、侧翼区域有RNA转录或与八个已知癌基因存在同源性的证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59dc/254626/885d729a3c86/jvirol00129-0276-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59dc/254626/b13b7fe12119/jvirol00129-0275-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59dc/254626/0853fd6be203/jvirol00129-0275-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59dc/254626/ad133128c453/jvirol00129-0275-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59dc/254626/885d729a3c86/jvirol00129-0276-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59dc/254626/b13b7fe12119/jvirol00129-0275-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59dc/254626/0853fd6be203/jvirol00129-0275-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59dc/254626/ad133128c453/jvirol00129-0275-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59dc/254626/885d729a3c86/jvirol00129-0276-a.jpg

相似文献

1
Characterization of cellular sequences flanking an integrated bovine leukemia virus genome.整合型牛白血病病毒基因组侧翼细胞序列的特征分析
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本文引用的文献

1
Isolation and characterization of full-length cDNA clones for human alpha-, beta-, and gamma-actin mRNAs: skeletal but not cytoplasmic actins have an amino-terminal cysteine that is subsequently removed.人α-、β-和γ-肌动蛋白mRNA全长cDNA克隆的分离与鉴定：骨骼肌肌动蛋白而非细胞质肌动蛋白具有一个随后会被去除的氨基端半胱氨酸。
Mol Cell Biol. 1983 May;3(5):787-95. doi: 10.1128/mcb.3.5.787-795.1983.
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Structure of 3' terminal region of type II human T lymphotropic virus: evidence for new coding region.人类嗜T淋巴细胞病毒II型3'末端区域的结构：新编码区的证据
Science. 1984 Jul 27;225(4660):419-21. doi: 10.1126/science.6330894.
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Different bovine leukemia virus-induced tumors harbor the provirus in different chromosomes.
不同的牛白血病病毒诱导的肿瘤在不同染色体中含有前病毒。
J Virol. 1984 Apr;50(1):275-9. doi: 10.1128/JVI.50.1.275-279.1984.
4
Mode of proviral activation of a putative mammary oncogene (int-1) on mouse chromosome 15.小鼠15号染色体上一个假定的乳腺癌基因（int-1）的原病毒激活模式。
Nature. 1984;307(5947):131-6. doi: 10.1038/307131a0.
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Chromosome integration domain for bovine leukemia provirus in tumors.肿瘤中牛白血病原病毒的染色体整合结构域
J Virol. 1983 Jul;47(1):146-50. doi: 10.1128/JVI.47.1.146-150.1983.
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Lack of expression of cellular homologues of retroviral onc genes in bovine tumors.
Haematol Blood Transfus. 1983;28:218-21. doi: 10.1007/978-3-642-68761-7_42.
7
Human adult T-cell leukemia virus: complete nucleotide sequence of the provirus genome integrated in leukemia cell DNA.人类成人T细胞白血病病毒：整合于白血病细胞DNA中的前病毒基因组的完整核苷酸序列。
Proc Natl Acad Sci U S A. 1983 Jun;80(12):3618-22. doi: 10.1073/pnas.80.12.3618.
8
Leukemogenesis by bovine leukemia virus: proviral DNA integration and lack of RNA expression of viral long terminal repeat and 3' proximate cellular sequences.牛白血病病毒引发的白血病：前病毒DNA整合以及病毒长末端重复序列和3' 近端细胞序列的RNA表达缺失
Proc Natl Acad Sci U S A. 1982 Apr;79(8):2465-9. doi: 10.1073/pnas.79.8.2465.
9
Experiments with cloned complete tumor-derived bovine leukemia virus information prove that the virus is totally exogenous to its target animal species.对克隆的完整肿瘤源性牛白血病病毒信息进行的实验证明，该病毒对于其目标动物物种而言完全是外源性的。
J Virol. 1981 Nov;40(2):605-9. doi: 10.1128/JVI.40.2.605-609.1981.
10
Restriction endonuclease mapping of linear unintegrated proviral DNA of bovine leukemia virus.牛白血病病毒线性未整合前病毒DNA的限制性内切酶图谱分析
J Virol. 1981 Apr;38(1):27-33. doi: 10.1128/JVI.38.1.27-33.1981.