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1 the spleen-focus-forming virus component of Friend virus.
2 virus envelope protein and a live attenuated Friend virus.
3 ral recovery controlled by the resistance to Friend virus 3 (rfv3) gene, the rfv3 gene has been mappe
5 ted that mouse APOBEC3 encodes Recovery from Friend virus 3 (Rfv3), a classical resistance gene in mi
7 were unable to maintain long-term control of Friend virus and developed gross splenomegaly with high
8 s of gammaretrovirus envelope proteins (from Friend virus and GALV or xenotropic viruses) assemble in
9 th various doses of a pathogenic retrovirus (Friend virus) and assessed immune parameters and disease
10 he early stages of transformation induced by Friend virus are characterized in vitro by the Epo-indep
19 role during primary immune responses against Friend virus but is dispensable during vaccine-primed se
21 odel of the splenomegaly-inducing retrovirus Friend virus complex (FVC) infection, we find that while
22 f the mice against challenge with pathogenic Friend virus complex was determined to be 10(3) focus-fo
24 that is initiated by the interaction of the Friend virus-encoded glycoprotein gp55 with the erythrop
25 ation, such as interaction with the env gene Friend virus envelope glycoprotein (F-gp55) of spleen fo
26 infected cells by forming a complex with the Friend virus envelope glycoprotein, gp55, and the erythr
27 recombinant vaccinia virus vector expressing Friend virus envelope protein and a live attenuated Frie
28 mice infected both in vitro and in vivo with Friend virus failed to give rise to erythropoietin-indep
29 sts infected with the anemia-inducing strain Friend virus (FAV cells), RPS19 mRNA and protein express
30 haracteristic progression and specificity of Friend virus for the erythroid lineage have allowed for
34 -viral activity of CD4+ T cells during acute Friend Virus (FV) infection, they were absolutely requir
39 7-deficient mice with a retroviral pathogen, Friend virus (FV), I determined that TLR7 potently inhib
40 ted with the polycythemia-inducing strain of Friend virus (FVP), p53 null mice exhibited accelerated
41 we show that the Kit+ pathogenic targets of Friend virus in the spleen are distinct from the pathoge
48 A role for p53 in the in vivo progression of Friend virus-induced erythroleukemia has been suggested
54 n this study, we used the highly immunogenic Friend virus-induced FBL-3 tumor as a model to study the
58 ld not maintain control and developed severe Friend virus-induced splenomegaly and erythroleukemia by
64 s required for the Epo-independent growth of Friend virus-infected cells and that the activation of S
65 -Stk to participate in the transformation of Friend virus-infected cells requires the kinase activity
66 h Sf-Stk in the Epo-independent expansion of Friend virus-infected cells, and suggest a pivotal role
67 iculocytes formed in vitro by enucleation of Friend virus-infected erythroblasts were purified and re
68 roerythroblasts isolated from the spleens of Friend virus-infected mice fed an amino acid-based, fola
69 Control proerythroblasts were obtained from Friend virus-infected mice fed the same diet plus 2 mg f
72 demonstrate that erythroleukemias arising in Friend virus-infected p53 null mice are biologically and
73 mutation observed in cell lines derived from Friend virus-infected p53 wild type mice, it was not a u
74 ity of responses necessary for recovery from Friend virus infection has implications for both immunot
78 onstrate that, following recovery from acute Friend virus infection, a small number of B cells evade
79 n-independent colonies at any time following Friend virus infection, suggesting that mutation of the
89 re, we extend those findings by showing that Friend virus infects two distinct populations of bone ma
92 rrelated with a 10-fold reduction of chronic Friend virus levels in the liver compared with the splee
97 ry erythroid progenitor cells in response to Friend virus.Oncogene advance online publication, 12 Dec
99 Thus, even very low levels of persistent Friend virus posed a significant threat during immunosup
100 ind that the env gene of an anemic strain of Friend virus, Rauscher virus envelope glycoprotein, does
101 ress erythropoiesis pathway in the spleen by Friend virus results in the rapid expansion of stress BF
102 receptors, and we confirmed our results in a Friend virus retroviral model of infection in mice.
105 w that in vitro expression of Sf-Stk confers Friend virus sensitivity to erythroid progenitor cells f
107 f the induced bursts with those induced with Friend virus suggested that either sarcoma virus such as
113 to control retrovirus replication, including Friend-virus-susceptibility-1, Fv1, on mouse chromosome
116 of Sf-Stk to induce colonies in response to Friend virus, while the Grb2 binding site from EGFR rest