ライフサイエンスコーパス: FRA

1 FRA was demonstrated to be important to pathogenesis, wh

2 FRA-1 expression was localized in the differentiating ut

3 FRA-1 forms activator protein-1 complexes in association

4 FRA-1 greatly enhanced the rate of proliferation, motili

5 FRA-1 has been implicated in the development of airway s

6 FRA-1, a member of the FOS family of transcription facto

7 transcription factor FOS-related antigen 1 (FRA-1) as a central node in tumour cell plasticity netwo

8 uding the proinvasive Fos-related antigen 1 (FRA-1) oncoprotein.

9 study we report that Fos-related antigen 1 (FRA-1), a member of the Fos family of transcription fact

10 and that vimentin and fos-related antigen-1 (FRA-1) were consistently overexpressed in the more highl

11 One env mutant, which was detected in a FRA-induced thymic lymphosarcoma, had a large internal d

12 sociated with strong firing rate adaptation (FRA) and occurred preferentially in large multipolar neu

13 xpressing FRAs at 7:00 PM but did not affect FRAs expression at 7:00 AM when compared with animals re

14 Antibodies against FRAs and tyrosine hydroxylase (TH) identified activated

15 n downstream effector of PI3K, did not alter FRA-1 expression.

16 Frequency response analyzer (FRA) algorithm was used to obtain impedance spectra so a

17 nduced by the AAR, whereas JUN-D, FRA-1, and FRA-2 were not.

18 r the pathologic differences between F6A and FRA is the lower propensity for F6A to undergo de novo r

19 pershift analysis with antisera to c-Fos and FRA proteins demonstrated that 4-Fos and the 35 kDa FRA

20 rather than individual) activity of MPII and FRA is required for the overall B. fragilis virulence in

21 and proteolytic characteristics of MPII and FRA.

22 t substrate cleavage preferences of MPII and FRA.

23 ogens activate both the PI3K-Akt pathway and FRA-1 expression in human bronchial epithelial (HBE) cel

24 th respect to neurons lacking strong PRF and FRA.

25 ly localized the genes for PAPA syndrome and FRA to chromosome 15q and suggested that they are the sa

26 trials with fibrinogen receptor antagonists (FRAs) have been associated with thrombocytopenia.

27 and two-dimensional Western blots with anti-FRA and anti-FosB antibodies.

28 atum of c-Fos, a 35 kDa Fos-related antigen (FRA) and the phosphorylated form of cyclic AMP response

29 gene products Fos and its related antigens (FRA) in SS-immunoreactive (IR) neurons in the PeVN.

30 expression of Fos and its related antigens (FRA) in tuberoinfundibular dopamine (TIDA) neurons locat

31 ling and expression of Fos related antigens (FRAs) as an indicator of neuronal activation.

32 atic nucleus (SCN) and Fos-related antigens (FRAs) expression in neuroendocrine dopaminergic neurons

33 oteins, termed chronic Fos-related antigens (FRAs), that are induced in brain in a region-specific ma

34 constructing tonal frequency response areas (FRAs) in primary auditory cortex for different SNRs, ton

35 The areas of nonV frequency response areas (FRAs) were modulated, but the areas of almost all V-shap

36 AI frequency response areas (FRAs), derived from tone bursts presented to the poorer

37 M #604416) and familial recurrent arthritis (FRA) are rare inherited disorders of early onset, primar

38 ure Organization Forest Resource Assessment (FRA) in all tropical regions, especially for the 1980s.

39 sing data from Forest Resources Assessments (FRAs) of the United Nations Food and Agriculture Organiz

40 ly caused by folate receptor autoantibodies (FRAs) that interfere with folate transport across the bl

41 n 16 children, the concentration of blocking FRA significantly correlated with cerebrospinal fluid 5-

42 Both FRA-1 and PBX1 are required for the mesenchymal changes

43 Interestingly, the -283 to +32 bp FRA-1 promoter fragment containing an SRE and an ATF sit

44 We show in this study that the chronic FRAs are isoforms of deltaFosB, a truncated splice varia

45 nd 37 kDa proteins correspond to the chronic FRAs that are induced in brain by chronic treatments, wh

46 ue to antibody cross-reactivity with chronic FRAs, and that behavioral sensitization to amphetamine i

47 closely related subgroup A molecular clone, FRA, we demonstrated high pathogenicity and a strong pro

48 rats, 10-15% of all SS-IR neurons contained FRA-IR.

49 1.5 h) in the percentage of TH-IR containing FRA-IR nuclei.

50 d the percentage of TH-IR neurons containing FRA-IR nuclei in the DM-ARC, but this effect was of long

51 (TH)-immunoreactive (IR) neurons containing FRA-IR nuclei in the DM-ARC.

52 eased the number of SS-IR neurons containing FRA-IR, without affecting the total number of SS-IR neur

53 ns or the number of SS-IR neurons containing FRA-IR.

54 In contrast, FRA-1 failed to promote tumor formation by BEAS-2B.

55 FOS-B was induced by the AAR, whereas JUN-D, FRA-1, and FRA-2 were not.

56 Deletion of either FRA gene has the same effect on transcription as deletio

57 ated in high iron medium, deletion of either FRA gene results in the translocation of the low iron-se

58 d the percentage of TH-IR neurons expressing FRA in the DM-ARC, but had no effect on haloperidol-indu

59 rease in the number of SS neurons expressing FRA-IR.

60 uroendocrine dopaminergic neurons expressing FRAs at 7:00 PM but did not affect FRAs expression at 7:

61 uroendocrine dopaminergic neurons expressing FRAs was significantly lower than all other time points.

62 ergic neurons in the ARN and PeVN expressing FRAs was greatest and equivalent at 7:00 AM, 9:00 AM, 12

63 NF), Food and Agricultural Organization (FAO FRA), and University of Maryland (Landsat forests), but

64 expanded bandwidths, as is usually seen for FRAs obtained without background noise.

65 ese results suggest that alterations in Fos, FRA and CREB transcription factors are common neuronal r

66 imum threshold parameters are extracted from FRAs, and they are used to quantify interaural response

67 of the newly identified IR-responsive genes, FRA-1 and ATF3, showed a p53-associated component to the

68 be a reasonable and non-invasive approach in FRA-positive children with ASD.

69 Prolactin causes a short-lived increase in FRA expression in TIDA neurons in the VL-ARC which is fo

70 ce of FRAs and the response to leucovorin in FRA-positive children has not been systematically invest

71 ed animals had decreased c-Fos and increased FRA proteins in striatum.

72 oxicants and carcinogens persistently induce FRA-1 expression in vitro and in vivo.

73 Akt had no significant effect on CS-induced FRA-1 expression.

74 K-Akt pathway, completely blocked CS-induced FRA-1 expression.

75 Interestingly, FRA-1 controls the expression of matrix metalloproteinas

76 teins demonstrated that 4-Fos and the 35 kDa FRA are components of the striatal AP-1 binding complex

77 ed epidermal growth factor receptor-mediated FRA-1 induction in non-oncogenic HBE cells.

78 In athymic nude mice, FRA-1, but not the control vector, rapidly enhanced tumo

79 ise levels reduced firing rates and narrowed FRA bandwidths; at higher SNRs, however, increasing the

80 s followed by a more prolonged activation of FRA expression in TIDA neurons in the DM-ARC.

81 erstood, it is poorly defined in the case of FRA-1.

82 ining neurons in the PeVN, but expression of FRA in SS neurons is not tonically inhibited by dopamine

83 hown a high level of persistent induction of FRA-1 by lung carcinogens, such as cigarette smoke and a

84 owever, is insufficient for the induction of FRA-1 promoter.

85 effect on haloperidol-induced inhibition of FRA expression in TH-IR neurons in the VL-ARC.

86 n convertases, whereas the cleavage motif of FRA (Pro-X-X-Leu-(Arg/Ala/Leu) downward arrow) resembles

87 cessary and sufficient for the regulation of FRA-1 in response to mitogens.

88 However, the exact roles of FRA-1 in regulating lung epithelial cell growth and inva

89 short interfering RNA-mediated silencing of FRA-1 enhances TNF-alpha-induced IL-8 expression, wherea

90 n amino acids of the N-terminal mature SU of FRA env gene, followed by eight amino acids from the fra

91 wn to have an infectivity similar to that of FRA when delivered as a provirus.

92 en with ASD and a high prevalence (75.3%) of FRAs was found.

93 euronal activity, indicated by expression of FRAs, was observed in the same neuron populations after

94 determine the time course of the presence of FRAs and STAT5 in the nuclei of hypothalamic dopaminergi

95 In children with ASD, the prevalence of FRAs and the response to leucovorin in FRA-positive chil

96 stimates of 1.9 (0.6-2.5) Pg.yr(-1) based on FRA national statistics of changes in forest area, this

97 of JNK activity had no significant effect on FRA-1 induction.

98 s (FeLV), which we named FeLV-A (Rickard) or FRA, was characterized with respect to viral interferenc

99 More than 20 other FRAs, including those that induced thrombocytopenia in c

100 ne this aspect, we have stably overexpressed FRA-1 in human type-II-like alveolar malignant cell line

101 enous administration of two different potent FRAs, L-738, 167 and L-739,758.

102 rhesus monkey upon administration of potent FRAs.

103 ression of the immediate early gene products FRA in SS-containing neurons in the PeVN, but expression

104 ression of an ERK1 mutant strikingly reduced FRA-1 transcription.

105 I3K through p21-activated kinase 1 regulates FRA-1 proto-oncogene induction by CS and the subsequent

106 he env gene in the ecotropic FeLV-A Rickard (FRA) provirus.

107 In this study, serum FRA concentrations were measured in 93 children with ASD

108 ulated, but the areas of almost all V-shaped FRAs were not.

109 tegrate-and-fire-type model, which simulated FRA and PRF, reproduced the phase lead observed in large

110 imilarity to known chromosomal fragile site (FRA) sequences, this polymorphic 1p21.2 sequence may rep

111 ression significantly reduced TPA-stimulated FRA-1 promoter activity.

112 new molecular clone, FeLV-A, Rickard strain (FRA).

113 in primary uterine stromal cells suppressed FRA-1 expression.

114 nd showed slower progression to disease than FRA-infected cats.

115 consistently carried higher virus loads than FRA-infected cats.

116 s that FRAs may be important in ASD and that FRA-positive children with ASD may benefit from leucovor

117 We propose that FRA-1-overexpressing clones featuring high plasticity un

118 We suggest that FRA-1 can promote motility, invasion, and anchorage-inde

119 Collectively, these results suggest that FRA-1, induced in response to estrogen signaling via ESR

120 This study suggests that FRAs may be important in ASD and that FRA-positive child

121 The FRA-1 proto-oncogene is overexpressed in a variety of hu

122 contrast to an 11% reduction reported by the FRA.

123 , and an ATF site, is also necessary for the FRA-1 induction by TPA and EGF.

124 We also discuss evidence from the FRA-1 perspective supporting the notion that clonal sele

125 omparison with FRA3, a representative of the FRA isoforms.

126 ted by direct intradermal inoculation of the FRA plasmid DNA so as to eliminate the possibility of co

127 Our recent analysis of the FRA-1 promoter has shown a critical role for a TRE locat

128 EB proteins bind to SRE and ATF sites of the FRA-1 promoter, constitutively.

129 t TNF-alpha stimulates the expression of the FRA-1 protooncogene in human pulmonary epithelial cells

130 These observations suggest that the FRA proteins are in the same signal transduction pathway

131 d the subsequent recruitment of c-Jun to the FRA-1 promoter in response to TNF-alpha in pulmonary epi

132 , and ATF1, which constitutively bind to the FRA-1 promoter, but also suppressed the recruitment of c

133 Scientists who use FRA data should check how the accuracy of their findings

134 tassium currents contributed to PRF, whereas FRA was predominantly mediated by slow potassium current

135 ease in the percentage of TH-IR neurons with FRA-IR nuclei in the VL-ARC.

136 Children with FRAs were treated with oral leucovorin calcium (2 mg kg(