ライフサイエンスコーパス: SFFV

1 SFFV gp55 has been shown to interact with the Epo recept

2 Although SFFV infects many cell types, deregulation of cell growt

3 nt study, using busulfan conditioning and an SFFV retrovirus vector, achieved more than 20% marking i

4 an erythroleukemia cell line derived from an SFFV-infected mouse.

5 onverging on MAPK in both Epo-stimulated and SFFV-infected erythroid cells and that activation of onl

6 that the requirements for EpoR activation by SFFV-related viruses are dependent on sequences at the 3

7 dicate that induction of Epo independence by SFFV requires the activation of PI 3-kinase and suggest

8 ythroid cells rendered factor independent by SFFV infection for constitutive activation of signal-tra

9 This transformation by SFFV gp55 requires the kinase activity of sf-Stk and the

10 In erythroid cells, SFFV gp55 interacts with the EpoR complex and sf-Stk, le

11 Like SFFV-infected erythroid cells, SFFV gp55-sf-Stk-transformed fibroblasts express high le

12 Next, we selected a constitutive SFFV promoter and NFkappaB binding sequence for biolumin

13 In this study, we examined SFFV MEL cells to determine whether their transformed ph

14 Erythroid cells expressing SFFV gp55 proliferate in the absence of their normal reg

15 mary erythroleukemic splenocytes from Friend SFFV-infected mice and in erythroleukemia cell lines fro

16 of primary erythroleukemic cells from Friend SFFV-infected mice, with little induction of apoptosis,

17 ng in erythroleukemia cell lines from Friend SFFV-infected mice.

18 thway was constitutively activated in Friend SFFV-infected erythroid cells, and in this study JNK is

19 In an effort to understand how SFFV causes Epo independence, we have been examining ery

20 on pathways activated by Epo to determine if SFFV exerts its biological effects by constitutively act

21 ly for the activation of MAPK, not Raf-1, in SFFV-infected cells.

22 ermine if this pathway was also activated in SFFV-infected cells in the absence of Epo.

23 tat pathway, are constitutively activated in SFFV-infected cells.

24 ase pathway, are constitutively activated in SFFV-infected erythroid cells in the absence of Epo.

25 uce STAT1 phosphorylation and DNA binding in SFFV MEL cells.

26 f STAT1/3 DNA binding activity is blocked in SFFV MEL cells.

27 -Jun and JunB, but not c-Fos, was induced in SFFV-infected cells in the absence of Epo, suggesting th

28 at constitutive activation of this kinase in SFFV-infected cells may occur primarily through interact

29 -kinase, are both tyrosine phosphorylated in SFFV-infected cells grown in the absence of Epo.

30 re constitutively tyrosine phosphorylated in SFFV-infected cells.

31 We further show that in SFFV-infected erythroid cells grown in the absence of Ep

32 odent fibroblasts and providing insight into SFFV-induced disease.

33 Like SFFV-infected erythroid cells, SFFV gp55-sf-Stk-transfor

34 When injected into adult mice, SFFV induces a rapid erythroleukemia, with susceptibilit

35 s indicated that the ultimate virus is a new SFFV that encodes a glycoprotein of 410 amino acids with

36 that culminated in the formation of a novel SFFV.

37 t, neither Epo stimulation in the absence of SFFV gp55 expression nor expression of a mutant of SFFV

38 Recently, we discovered that coexpression of SFFV gp55 and sf-Stk is sufficient to transform NIH 3T3

39 er studies demonstrated that coexpression of SFFV gp55 with sf-Stk significantly extends the half-lif

40 which may mediate the biological effects of SFFV infection.

41 MAPK pathway, we investigated the effects of SFFV on upstream components of this pathway, and our res

42 Thus, expression of SFFV gp55 in nonerythroid cells coexpressing sf-Stk resu

43 Expression of SFFV gp55 in rodent fibroblasts engineered to express sf

44 To determine whether expression of SFFV gp55 leads to the activation of sf-Stk, we expresse

45 ythroid cells, the Epo-independent growth of SFFV-infected cells can still occur in the absence of Ra

46 p55 expression nor expression of a mutant of SFFV that cannot interact with sf-Stk was able to induce

47 ent for the Epo-independent proliferation of SFFV-infected cells.

48 red for the Epo-independent proliferation of SFFV-infected cells.

49 tion of the Epo-independent proliferation of SFFV-infected cells.

50 ted with the polycythemia-inducing strain of SFFV, which induces both proliferation and differentiati

51 at are common among the classical strains of SFFV.

52 es contained 3' regions identical to that of SFFV, including a 6-bp duplication and a single-base ins

53 Our studies indicate that Epo- or SFFV-induced activation of STAT1/3 DNA binding activity

54 or maintenance of the transformed phenotype, SFFV gp55-sf-Stk-transformed fibroblasts are negative fo

55 th transcription cassettes carrying promoter SFFV instead of CMV and the addition of beta-globin Repl

56 The viral envelope protein, SFFV gp55, forms a complex with the erythropoietin recep

57 In this study, we demonstrate that SFFV also activates Raf-1, MEK and mitogen-activated pro

58 In this study, we demonstrate that SFFV gp55 can also deregulate the growth of nonerythroid

59 this pathway, and our results indicate that SFFV activates Shc and Grb2 and that this leads to Ras a

60 We previously reported that SFFV induces Epo independence by constitutively activati

61 Our results suggest that SFFV gp55 may mediate its biological effects in vivo by

62 Our studies suggest that SFFV-infected erythroid cells become transformed when di

63 Our results suggest that SFFV-related viruses can form in mice by recombination o

64 The SFFV-transformed cells were shown to express elevated le

65 In the first stage, the SFFV envelope glycoprotein interacts with the erythropoi

66 Susceptibility to SFFV-induced erythroleukemia is conferred by the Fv-2 ge

67 r (EpoR), but those from mice susceptible to SFFV-induced erythroleukemia also express a short form o

68 Unlike SFFV-derived erythroleukemia cells, which depend on PU.1

69 Friend spleen focus-forming virus (SFFV) causes rapid erythroleukemia in mice due to expres

70 -inducing Friend spleen focus-forming virus (SFFV) encodes a unique envelope glycoprotein which allow

71 The Friend spleen focus-forming virus (SFFV) encodes a unique envelope glycoprotein, gp55, whic

72 -inducing Friend spleen focus-forming virus (SFFV) encodes a unique envelope protein, gp55, which int

73 The Friend spleen focus-forming virus (SFFV) env gene encodes a 409-amino-acid glycoprotein wit

74 The Friend spleen focus-forming virus (SFFV) env gene encodes a glycoprotein with apparent Mr o

75 The spleen focus forming virus (SFFV) gp55-P envelope glycoprotein specifically binds to

76 cells by Friend spleen focus-forming virus (SFFV) leads to acute erythroid hyperplasia and eventuall

77 with the Friend spleen focus-forming virus (SFFV) leads to the interaction of the viral envelope gly

78 with the Friend spleen focus-forming virus (SFFV) proliferate in the absence of Epo and show constit

79 ression of Sfpi1 spleen focus-forming virus (SFFV) proviral integration 1 (PU.1) in marrow lin(-) c-k

80 ncogene (c-fos), Spleen focus-forming virus (SFFV) proviral integration 1 (PU.1), microphthalmia-asso

81 mice with Friend spleen focus-forming virus (SFFV) results in a multistage erythroleukemia.

82 ed by the murine Spleen Focus Forming virus (SFFV), while fli-1 proved to be the target of Friend mur

83 deregulation of cell growth occurs only when SFFV infects erythroid cells, suggesting that these cell

84 To further evaluate the mechanism by which SFFV activates the Raf-1/MAPK pathway, we investigated t

85 linical signs not previously associated with SFFV-induced disease.

86 udies that infection of erythroid cells with SFFV leads to the constitutive activation of signal tran

87 endered factor independent by infection with SFFV and that PI 3-kinase activity, but not Epo receptor

88 by either point mutation or interaction with SFFV gp55, is sufficient to induce Epo-independent eryth

89 tivated by forming a strong interaction with SFFV gp55.

90 on, as well as noncovalent interactions with SFFV gp55, results in constitutive tyrosine phosphorylat

91 Our data indicate that sf-Stk interacts with SFFV gp55 as well as gp55(P), the biologically active fo

92 Covalent interaction of sf-Stk with SFFV gp55 and constitutive tyrosine phosphorylation of s

93 sf-Stk, we expressed sf-Stk, with or without SFFV gp55, in hematopoietic cells expressing the Epo rec