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1
Genetic control of radiation leukemia virus-induced tumorigenesis II. Influence of Srlv-1, a locus not linked to H-2.辐射白血病病毒诱导肿瘤发生的遗传控制II. Srlv-1位点的影响，该位点与H-2不连锁
J Exp Med. 1977 Oct 1;146(4):1088-95. doi: 10.1084/jem.146.4.1088.
2
Genetic control of radiation leukemia virus-induced tumorigenesis. I. Role of the major murine histocompatibility complex, H-2.辐射白血病病毒诱导肿瘤发生的遗传控制。I. 主要小鼠组织相容性复合体H-2的作用。
J Exp Med. 1977 Oct 1;146(4):1079-87. doi: 10.1084/jem.146.4.1079.
3
Resistance genes to murine leukemia in the I immune response gene region of the H-2 complex.H-2复合体I免疫反应基因区域中对鼠白血病的抗性基因。
J Exp Med. 1977 Oct 1;146(4):1164-8. doi: 10.1084/jem.146.4.1164.
4
H-21-linked control of immunological resistance to viral leukemogenesis as a response to preleukemic cells.作为对白血病前期细胞的一种反应，H-21连锁的对病毒性白血病发生的免疫抗性控制。
Immunogenetics. 1981 Mar 1;12(5-6):423-32. doi: 10.1007/BF01561685.
5
A role for elevated H-2 antigen expression in resistance to neoplasia caused by radiation-induced leukemia virus. Enhancement of effective tumor surveillance by killer lymphocytes.H-2抗原表达升高在抵抗辐射诱导的白血病病毒所致肿瘤形成中的作用。杀伤淋巴细胞增强有效的肿瘤监测。
J Exp Med. 1979 Apr 1;149(4):898-909. doi: 10.1084/jem.149.4.898.
6
Cell surface antigens of murine leukemias induced by radiation leukemia virus. Recognition of individually distinct cell surface antigens by cytotoxic T cells on leukemias expressing crossreactive transplantation antigens.辐射白血病病毒诱导的小鼠白血病的细胞表面抗原。表达交叉反应移植抗原的白血病上的细胞毒性T细胞对个体独特细胞表面抗原的识别。
J Exp Med. 1986 Feb 1;163(2):452-7. doi: 10.1084/jem.163.2.452.
7
Increased synthesis and expression of H-2 antigens on thymocytes as a result of radiation leukemia virus infection: a possible mechanism for H-2 linked control of virus-induced neoplasia.辐射白血病病毒感染导致胸腺细胞上H-2抗原的合成与表达增加：H-2连锁控制病毒诱导肿瘤形成的一种可能机制。
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[Genetic aspects of leukemogenesis in mice (author's transl)].
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9
Bone marrow phenotype determines genetic resistance to RadLV-induced leukemia in radiation chimeric mice.
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10
A new gene that controls the type of leukemia induced by Friend murine leukemia virus.一种控制由弗瑞德鼠白血病病毒诱导的白血病类型的新基因。
J Exp Med. 1983 Aug 1;158(2):493-505. doi: 10.1084/jem.158.2.493.

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1
Growth of SJL/J-derived transplantable reticulum cell sarcoma as related to its ability to induce T-cell proliferation in the host. I. Dominant negative genetic influences of other parent haplotype in F1 hybrids of SJL/J mice.SJL/J 衍生的可移植性网状细胞肉瘤的生长与其在宿主体内诱导 T 细胞增殖能力的关系。I. SJL/J 小鼠 F1 杂交种中其他亲本单倍型的显性负性遗传影响。
J Exp Med. 1980 Feb 1;151(2):347-61. doi: 10.1084/jem.151.2.347.
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Therapeutic agents with dramatic antiretroviral activity and little toxicity at effective doses: aromatic polycyclic diones hypericin and pseudohypericin.具有显著抗逆转录病毒活性且在有效剂量下毒性极小的治疗药物：芳香多环二酮金丝桃素和假金丝桃素。
Proc Natl Acad Sci U S A. 1988 Jul;85(14):5230-4. doi: 10.1073/pnas.85.14.5230.
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Proc Natl Acad Sci U S A. 1989 Aug;86(15):5963-7. doi: 10.1073/pnas.86.15.5963.
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Enhanced gene expression of the murine ecotropic retroviral receptor and its human homolog in proliferating cells.小鼠嗜亲性逆转录病毒受体及其人类同源物在增殖细胞中的基因表达增强。
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Proc Natl Acad Sci U S A. 1979 Jan;76(1):425-9. doi: 10.1073/pnas.76.1.425.
6
Genetics of resistance of animals to viruses: I. Introduction and studies in mice.动物对病毒的抗性遗传学：I. 引言及小鼠研究
Adv Virus Res. 1978;23:269-348. doi: 10.1016/s0065-3527(08)60102-5.
7
Increased synthesis and expression of H-2 antigens on thymocytes as a result of radiation leukemia virus infection: a possible mechanism for H-2 linked control of virus-induced neoplasia.辐射白血病病毒感染导致胸腺细胞上H-2抗原的合成与表达增加：H-2连锁控制病毒诱导肿瘤形成的一种可能机制。
J Exp Med. 1978 Feb 1;147(2):470-87. doi: 10.1084/jem.147.2.470.

本文引用的文献

1
ASSAY FOR FRIEND LEUKEMIA VIRUS: RAPID QUANTITATIVE METHOD BASED ON ENUMERATION OF MACROSCOPIC SPLEEN FOCI IN MICE.Friend白血病病毒检测：基于小鼠脾脏肉眼可见病灶计数的快速定量方法。
Virology. 1964 Nov;24:513-8. doi: 10.1016/0042-6822(64)90199-0.
2
POTENTIATION OF VIRUS LEUKAEMOGENESIS IN C57BL MICE BY X-IRRADIATION OR URETHANE.X射线照射或氨基甲酸乙酯对C57BL小鼠病毒白血病发生的增强作用
Nature. 1964 Jul 25;203:420-2. doi: 10.1038/203420b0.
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Leukemogenic activity of filtrates from radiation-induced lymphoid tumors of mice.小鼠辐射诱导淋巴肿瘤滤液的致白血病活性。
Science. 1959 Aug 14;130(3372):387-8. doi: 10.1126/science.130.3372.387.
4
Cell-free transmission in adult Swiss mice of a disease having the character of a leukemia.具有白血病特征的疾病在成年瑞士小鼠中的无细胞传播。
J Exp Med. 1957 Apr 1;105(4):307-18. doi: 10.1084/jem.105.4.307.
5
Susceptibility to two strains of Friend leukemia virus in mice.小鼠对两种Friend白血病病毒株的易感性。
Science. 1967 Jan 27;155(3761):461-2. doi: 10.1126/science.155.3761.461.
6
The G-IX system. A cell surface allo-antigen associated with murine leukemia virus; implications regarding chromosomal integration of the viral genome.G-IX系统。一种与鼠白血病病毒相关的细胞表面同种异体抗原；关于病毒基因组染色体整合的意义。
J Exp Med. 1971 Jun 1;133(6):1334-55. doi: 10.1084/jem.133.6.1334.
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On the natural history of the murine leukemias: presidential address.论鼠白血病的自然史：主席致辞
Cancer Res. 1967 Aug;27(8):1325-40.
8
Studies of genetic transmission of murine leukemia virus by AKR mice. II. Crosses with Fv-1 b strains of mice.AKR小鼠对鼠白血病病毒的遗传传递研究。II. 与Fv-1 b系小鼠的杂交
J Exp Med. 1972 Nov 1;136(5):1286-301. doi: 10.1084/jem.136.5.1286.
9
Studies of genetic transmission of murine leukemia virus by AKR mice. I. Crosses with Fv-1 n strains of mice.AKR小鼠对鼠白血病病毒的遗传传递研究。I. 与Fv-1 n系小鼠的杂交。
J Exp Med. 1972 Nov 1;136(5):1272-85. doi: 10.1084/jem.136.5.1272.
10
A major genetic locus affecting resistance to infection with murine leukemia viruses. II. Apparent identity to a major locus described for resistance to friend murine leukemia virus.一个影响对鼠白血病病毒感染抗性的主要基因位点。II. 与描述的对弗氏鼠白血病病毒抗性的主要位点明显相同。
J Exp Med. 1971 Jun 1;133(6):1234-41. doi: 10.1084/jem.133.6.1234.

辐射白血病病毒诱导肿瘤发生的遗传控制II. Srlv-1位点的影响，该位点与H-2不连锁

Genetic control of radiation leukemia virus-induced tumorigenesis II. Influence of Srlv-1, a locus not linked to H-2.

作者信息

Meruelo D, Lieberman M, Deak B, McDevitt H O

出版信息

J Exp Med. 1977 Oct 1;146(4):1088-95. doi: 10.1084/jem.146.4.1088.

DOI:10.1084/jem.146.4.1088
PMID:197196
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2180817/
Abstract

A single locus, tentatively denoted Srlv-1 (susceptibility to radiation leukemia virus [RadLV]-1), confers dominant susceptibility to RadLV-induced leukemogenesis. Srlv-1 is not linked to H-2, and appears to be distinct from Fv-1 and Fv-2. Preliminary data suggest that Srlv-1 affected virus proliferation. A striking feature of this system is that Srlv-1 overrides the protection afforded by the H2D-associated dominant resistance to RadLV-induced neoplasia.

摘要

一个暂定名为Srlv-1（对辐射白血病病毒[RadLV]-1易感）的单一基因座赋予对RadLV诱导白血病发生的显性易感性。Srlv-1与H-2不连锁，且似乎与Fv-1和Fv-2不同。初步数据表明Srlv-1影响病毒增殖。该系统的一个显著特征是Srlv-1克服了由H2D相关的对RadLV诱导肿瘤形成的显性抗性所提供的保护作用。