Importance of a c-Myb binding site for lymphomagenesis by the retrovirus SL3-3.
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ALY is a common coactivator of RUNX1 and c-Myb on the type B leukemogenic virus enhancerRegulation of FeLV-945 by c-Myb binding and CBP recruitment to the LTRAntisense transcription in gammaretroviruses as a mechanism of insertional activation of host genesSequence-specific and/or stereospecific constraints of the U3 enhancer elements of MCF 247-W are important for pathogenicity.Gene expression profiling of murine T-cell lymphoblastic lymphoma identifies deregulation of S-phase initiating genes.Increased induction of osteopetrosis, but unaltered lymphomagenicity, by murine leukemia virus SL3-3 after mutation of a nuclear factor 1 site in the enhancerType B leukemogenic virus has a T-cell-specific enhancer that binds AML-1.Disruption of hematopoiesis and thymopoiesis in the early premalignant stages of infection with SL3-3 murine leukemia virus.Genome-based identification of cancer genes by proviral tagging in mouse retrovirus-induced T-cell lymphomasStability of AML1 (core) site enhancer mutations in T lymphomas induced by attenuated SL3-3 murine leukemia virus mutants.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.The feline leukemia virus long terminal repeat contains a potent genetic determinant of T-cell lymphomagenicityAn SL3-3 murine leukemia virus enhancer variant more pathogenic than the wild type obtained by assisted molecular evolution in vivoControl of pathogenicity and disease specificity of a T-lymphomagenic gammaretrovirus by E-box motifs but not by an overlapping glucocorticoid response elementLoss of MicroRNA targets in the 3' untranslated region as a mechanism of retroviral insertional activation of growth factor independence 1.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.Selection of reversions and suppressors of a mutation in the CBF binding site of a lymphomagenic retrovirusSuppressor mutations within the core binding factor (CBF/AML1) binding site of a T-cell lymphomagenic retrovirus.CBF, Myb, and Ets binding sites are important for activity of the core I element of the murine retrovirus SL3-3 in T lymphocytes.The secondary structure of the R region of a murine leukemia virus is important for stimulation of long terminal repeat-driven gene expression.Tissue distribution and timing of appearance of polytropic envelope recombinants during infection with SL3-3 murine leukemia virus or its weakly pathogenic SL3DeltaMyb5 mutant.
P2860
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P2860
Importance of a c-Myb binding site for lymphomagenesis by the retrovirus SL3-3.
description
1997 nî lūn-bûn
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1997年の論文
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1997年学术文章
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1997年学术文章
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1997年学术文章
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1997年学术文章
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1997年学术文章
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1997年學術文章
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1997年學術文章
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name
Importance of a c-Myb binding site for lymphomagenesis by the retrovirus SL3-3.
@en
Importance of a c-Myb binding site for lymphomagenesis by the retrovirus SL3-3.
@nl
type
label
Importance of a c-Myb binding site for lymphomagenesis by the retrovirus SL3-3.
@en
Importance of a c-Myb binding site for lymphomagenesis by the retrovirus SL3-3.
@nl
prefLabel
Importance of a c-Myb binding site for lymphomagenesis by the retrovirus SL3-3.
@en
Importance of a c-Myb binding site for lymphomagenesis by the retrovirus SL3-3.
@nl
P2093
P2860
P1433
P1476
Importance of a c-Myb binding site for lymphomagenesis by the retrovirus SL3-3.
@en
P2093
P2860
P304
P407
P577
1997-02-01T00:00:00Z