相似文献
1
SL3-3 enhancer factor 1 transcriptional activators are required for tumor formation by SL3-3 murine leukemia virus.SL3-3增强子因子1转录激活因子是SL3-3小鼠白血病病毒形成肿瘤所必需的。
J Virol. 1991 Aug;65(8):4177-81. doi: 10.1128/JVI.65.8.4177-4181.1991.
2
Binding of SL3-3 enhancer factor 1 transcriptional activators to viral and chromosomal enhancer sequences.SL3-3增强子因子1转录激活因子与病毒和染色体增强子序列的结合。
J Virol. 1991 Jan;65(1):42-50. doi: 10.1128/JVI.65.1.42-50.1991.
3
Importance of a c-Myb binding site for lymphomagenesis by the retrovirus SL3-3.c-Myb结合位点对逆转录病毒SL3-3致淋巴瘤作用的重要性
J Virol. 1997 Feb;71(2):1213-9. doi: 10.1128/JVI.71.2.1213-1219.1997.
4
Stability of AML1 (core) site enhancer mutations in T lymphomas induced by attenuated SL3-3 murine leukemia virus mutants.减毒SL3-3小鼠白血病病毒突变体诱导的T淋巴瘤中AML1（核心）位点增强子突变的稳定性
J Virol. 1997 Jul;71(7):5080-7. doi: 10.1128/JVI.71.7.5080-5087.1997.
5
Transcriptional activity of core binding factor-alpha (AML1) and beta subunits on murine leukemia virus enhancer cores.核心结合因子α（AML1）和β亚基对鼠白血病病毒增强子核心的转录活性。
J Virol. 1995 May;69(5):2898-906. doi: 10.1128/JVI.69.5.2898-2906.1995.
6
Second-site proviral enhancer alterations in lymphomas induced by enhancer mutants of SL3-3 murine leukemia virus: negative effect of nuclear factor 1 binding site.SL3-3小鼠白血病病毒增强子突变体诱导的淋巴瘤中第二位点前病毒增强子改变：核因子1结合位点的负面影响
J Virol. 1997 Feb;71(2):1196-206. doi: 10.1128/JVI.71.2.1196-1206.1997.
7
Increased lymphomagenicity and restored disease specificity of AML1 site (core) mutant SL3-3 murine leukemia virus by a second-site enhancer variant evolved in vivo.通过在体内进化出的第二位点增强子变体，AML1位点（核心）突变的SL3-3鼠白血病病毒的淋巴瘤致瘤性增加且疾病特异性得以恢复。
J Virol. 1997 Oct;71(10):7273-80. doi: 10.1128/JVI.71.10.7273-7280.1997.
8
Increased induction of osteopetrosis, but unaltered lymphomagenicity, by murine leukemia virus SL3-3 after mutation of a nuclear factor 1 site in the enhancer.在增强子中的核因子1位点发生突变后，鼠白血病病毒SL3-3对骨硬化症的诱导作用增强，但对淋巴瘤发生的影响未改变。
J Virol. 1999 Dec;73(12):10406-15. doi: 10.1128/JVI.73.12.10406-10415.1999.
9
Mutation of all Runx (AML1/core) sites in the enhancer of T-lymphomagenic SL3-3 murine leukemia virus unmasks a significant potential for myeloid leukemia induction and favors enhancer evolution toward induction of other disease patterns.致T淋巴细胞性SL3-3鼠白血病病毒增强子中所有Runx（AML1/核心）位点的突变揭示了诱导髓系白血病的巨大潜力，并有利于增强子向诱导其他疾病模式的方向进化。
J Virol. 2004 Dec;78(23):13216-31. doi: 10.1128/JVI.78.23.13216-13231.2004.
10
CBF, Myb, and Ets binding sites are important for activity of the core I element of the murine retrovirus SL3-3 in T lymphocytes.CBF、Myb和Ets结合位点对于鼠逆转录病毒SL3-3的核心I元件在T淋巴细胞中的活性很重要。
J Virol. 1998 Apr;72(4):3129-37. doi: 10.1128/JVI.72.4.3129-3137.1998.
引用本文的文献
1
A novel enhancer RNA, Hmrhl, positively regulates its host gene, in chronic myelogenous leukemia.一种新型增强子RNA，Hmrhl，在慢性粒细胞白血病中对其宿主基因起正向调控作用。
Noncoding RNA Res. 2019 Aug 8;4(3):96-108. doi: 10.1016/j.ncrna.2019.08.001. eCollection 2019 Sep.
2
Recombinant Origins of Pathogenic and Nonpathogenic Mouse Gammaretroviruses with Polytropic Host Range.具有多嗜性宿主范围的致病性和非致病性小鼠γ逆转录病毒的重组起源
J Virol. 2017 Oct 13;91(21). doi: 10.1128/JVI.00855-17. Print 2017 Nov 1.
3
Gene expression profiling of murine T-cell lymphoblastic lymphoma identifies deregulation of S-phase initiating genes.鼠 T 细胞淋巴母细胞淋巴瘤的基因表达谱分析鉴定出 S 期起始基因的失调。
Leuk Res. 2013 Oct;37(10):1383-90. doi: 10.1016/j.leukres.2013.04.012. Epub 2013 Jul 26.
4
Antisense transcription in gammaretroviruses as a mechanism of insertional activation of host genes.γ逆转录病毒中的反义转录作为一种插入激活宿主基因的机制。
J Virol. 2010 Apr;84(8):3780-8. doi: 10.1128/JVI.02088-09. Epub 2010 Feb 3.
5
Loss of MicroRNA targets in the 3' untranslated region as a mechanism of retroviral insertional activation of growth factor independence 1.3'非翻译区中微小RNA靶标的缺失作为逆转录病毒插入激活生长因子独立性1的一种机制。
J Virol. 2009 Aug;83(16):8051-61. doi: 10.1128/JVI.00427-09. Epub 2009 May 27.
6
Control of pathogenicity and disease specificity of a T-lymphomagenic gammaretrovirus by E-box motifs but not by an overlapping glucocorticoid response element.通过E-box基序而非重叠的糖皮质激素反应元件来控制致T淋巴瘤γ逆转录病毒的致病性和疾病特异性。
J Virol. 2009 Jan;83(1):336-46. doi: 10.1128/JVI.01368-08. Epub 2008 Oct 22.
7
Activation of an oncogenic microRNA cistron by provirus integration.前病毒整合激活致癌性微小RNA顺反子。
Proc Natl Acad Sci U S A. 2006 Dec 5;103(49):18680-4. doi: 10.1073/pnas.0609030103. Epub 2006 Nov 22.
8
Analysis of wild-type and mutant SL3-3 murine leukemia virus insertions in the c-myc promoter during lymphomagenesis reveals target site hot spots, virus-dependent patterns, and frequent error-prone gap repair.对淋巴瘤发生过程中c-myc启动子区域野生型和突变型SL3-3鼠白血病病毒插入情况的分析揭示了靶位点热点、病毒依赖模式以及频繁的易错缺口修复。
J Virol. 2005 Jan;79(1):67-78. doi: 10.1128/JVI.79.1.67-78.2005.
9
Mutation of all Runx (AML1/core) sites in the enhancer of T-lymphomagenic SL3-3 murine leukemia virus unmasks a significant potential for myeloid leukemia induction and favors enhancer evolution toward induction of other disease patterns.致T淋巴细胞性SL3-3鼠白血病病毒增强子中所有Runx（AML1/核心）位点的突变揭示了诱导髓系白血病的巨大潜力，并有利于增强子向诱导其他疾病模式的方向进化。
J Virol. 2004 Dec;78(23):13216-31. doi: 10.1128/JVI.78.23.13216-13231.2004.
10
The use of retroviral vectors for gene therapy-what are the risks? A review of retroviral pathogenesis and its relevance to retroviral vector-mediated gene delivery.用于基因治疗的逆转录病毒载体——风险有哪些？逆转录病毒发病机制及其与逆转录病毒载体介导的基因递送相关性综述。
Genet Vaccines Ther. 2004 Aug 13;2(1):9. doi: 10.1186/1479-0556-2-9.
本文引用的文献
1
2
Oncogenic retrovirus from spontaneous murine osteomas. I. Isolation and biological characterization.源自自发性小鼠骨瘤的致癌逆转录病毒。I. 分离与生物学特性
J Gen Virol. 1984 Dec;65 ( Pt 12):2237-48. doi: 10.1099/0022-1317-65-12-2237.
3
Murine T lymphomas in which the cellular myc oncogene has been activated by retroviral insertion.细胞原癌基因myc已通过逆转录病毒插入而被激活的小鼠T淋巴瘤。
Cell. 1984 May;37(1):113-22. doi: 10.1016/0092-8674(84)90306-4.
4
Proviruses are adjacent to c-myc in some murine leukemia virus-induced lymphomas.在某些鼠白血病病毒诱导的淋巴瘤中，前病毒与c-myc相邻。
Proc Natl Acad Sci U S A. 1984 Apr;81(7):2097-101. doi: 10.1073/pnas.81.7.2097.
5
Determination of the leukaemogenicity of a murine retrovirus by sequences within the long terminal repeat.通过长末端重复序列内的序列测定鼠逆转录病毒的致白血病性。
Nature. 1984;308(5958):467-70. doi: 10.1038/308467a0.
6
A common region for proviral DNA integration in MoMuLV-induced rat thymic lymphomas.莫洛尼鼠白血病病毒（MoMuLV）诱导的大鼠胸腺淋巴瘤中前病毒DNA整合的常见区域。
Nature. 1983;302(5907):445-9. doi: 10.1038/302445a0.
7
Novel leukaemogenic retroviruses isolated from cell line derived from spontaneous AKR tumour.从自发的AKR肿瘤衍生的细胞系中分离出的新型致白血病逆转录病毒。
Nature. 1981 Jul 9;292(5819):167-70. doi: 10.1038/292167a0.
8
Tissue-specific transcription preference as a determinant of cell tropism and leukaemogenic potential of murine retroviruses.组织特异性转录偏好作为小鼠逆转录病毒细胞嗜性和白血病发生潜力的决定因素。
Nature. 1984;312(5990):159-62. doi: 10.1038/312159a0.
9
A new technique for the assay of infectivity of human adenovirus 5 DNA.一种检测人腺病毒5型DNA感染性的新技术。
Virology. 1973 Apr;52(2):456-67. doi: 10.1016/0042-6822(73)90341-3.
10
Oncogenic retrovirus from spontaneous murine osteomas. II. Molecular cloning and genomic characterization.源自自发性小鼠骨瘤的致癌逆转录病毒。II. 分子克隆与基因组特征分析。
Virology. 1986 Apr 15;150(1):96-105. doi: 10.1016/0042-6822(86)90269-2.
Zotero 插件