ライフサイエンスコーパス: aFGF

1 aFGF and bFGF fully accounted for the CM effect, indicat

2 aFGF appeared to play a central but insufficient role, r

3 (IC50=250 nM) and selective over EGF, IGF-1, aFGF, bFGF and HRGbeta.

4 nM) and selective for PDGF over EGF, IGF-1, aFGF, bFGF, and HRGbeta (IC50 values > 100 microM), but

5 tumor), we found elevated levels of acidic (aFGF) and basic (bFGF) fibroblast growth factors in the

6 We recently reported that acidic (aFGF) and basic (bFGF) fibroblast growth factors confer

7 hat in RA, interactions between TGFbeta1 and aFGF may contribute to angiogenesis and fibroblast proli

8 oblast growth factor 1 (FGF-1, also known as aFGF) have been previously identified in our laboratory.

9 a indicate that the binding affinity between aFGF and the C2A domain is significantly enhanced at pH

10 tibody to aFGF was used to measure bioactive aFGF levels in culture media.

11 In addition, both aFGF and the C2A domain exhibit much higher lipid bindin

12 ed equilibrium unfolding (at pH 3.4) of both aFGF and the C2A domain are non-cooperative and proceed

13 ion chromatography results suggest that both aFGF and the C2A domain exist as partially structured st

14 dentical to interactions observed for bovine aFGF with heparin analogs.

15 Activation of the chimeric receptor by aFGF induced a stronger and more persistent increase in

16 ts indicate elevated levels of extracellular aFGF/bFGF as an epigenetic mechanism by which cancer cel

17 eraction of acidic fibroblast growth factor (aFGF) and a coactivator (dopamine, protein kinase A, or

18 erface with acidic fibroblast growth factor (aFGF) and chondroitinase ABC (ChABC).

19 Acidic fibroblast growth factor (aFGF) has been reported to support cholinergic neuronal

20 Acidic fibroblast growth factor (aFGF) has shown the great potential to prevent the struc

21 Acidic fibroblast growth factor (aFGF) is a signal peptide-less protein that is secreted

22 Acidic fibroblast growth factor (aFGF) mRNA expression was determined in serial endomyoca

23 expressing acidic fibroblast growth factor (aFGF), glial cell line-derived neurotrophic factor (GDNF

24 response to acidic fibroblast growth factor (aFGF); however, its response to nerve growth factor (NGF

25 micked by co-treatment with a growth factor (aFGF, bFGF or BDNF; but not GDNF, IGF-1, EGF or TGF) and

26 Treatment with combined factors (aFGF+5-HT+IBMX+forskolin+TPA) yielded the greatest level

27 acidic and basic fibroblast growth factors (aFGF and bFGF), epidermal growth factor (EGF), and vascu

28 SPG) on binding and signaling by acidic FGF (aFGF) and KGF via the KGFR were studied using surface-bo

29 dose- and time-dependent manner, acidic FGF (aFGF) had no effect on translocation of PKCgamma, and PK

30 Exogenously added acidic FGF (aFGF), which generated a rapid tyrosine phosphorylation

31 X-ray crystal structure of human acidic FGF (aFGF), with data extending to 2.0 angstroms resolution.

32 ion and possible colocalization of mRNAs for aFGF and the cholinergic neuron marker choline acetyltra

33 index) to other aFGF treatment groups (free aFGF+/-UTMD or aFGF-NP).

34 GF treatments for 12 consecutive weeks (free aFGF or aFGF-NP+/-UTMD), with the strongest improvements

35 of the four independent structures of human aFGF.

36 (CVF) and cardiac myocyte apoptosis index in aFGF-NP+UTMD group reduced to 4.15% and 2.31% respective

37 Myocardial microvascular density (MCD) in aFGF-NP+UTMD group was up to 35n/hpf, much higher than t

38 rbed in the partially structured state(s) in aFGF are mostly located at the N- and C-terminal ends of

39 hibitor of multiple growth factors including aFGF and bFGF, enhanced the in vitro antitumor activity

40 a1 (TGFbeta1) was found to markedly increase aFGF production by cultured synovial cells.

41 and epidermal growth factor did not increase aFGF expression in vitro; in contrast, transforming grow

42 antly more severe CAV than patients with low aFGF and no late elevations.

43 hypothesis that, via an autocrine mechanism, aFGF provides local trophic support for cholinergic neur

44 e combination therapy of aFGF-nanoparticles (aFGF-NP) and ultrasound-targeted microbubble destruction

45 mbinant proteins, we found that bFGF but not aFGF induced chemoresistance whereas aFGF amplified the

46 e biphasic effect of heparin on KGF, but not aFGF, binding and signaling suggests that occupancy of t

47 eparin concentrations inhibited KGF, but not aFGF, binding and signaling.

48 tors [BDNF, neurotrophin (NT) 4/5, NGF, NT3, aFGF, and bFGF) were measured at varying time points dur

49 undant production of cytoplasmic and nuclear aFGF.

50 Of aFGF+ cells, 20% and 41% were NGF+ and 67% and 83% were

51 Conversely, about 32% of aFGF+ and 24% of GDNF+ cells in dorsal striatum and 55%

52 nd GDNF+ cells in dorsal striatum and 46% of aFGF+ and 61% of GDNF+ cells in ventral striatum were ch

53 of GDNF+ cells in dorsal striatum and 55% of aFGF+ and 27% of GDNF+ cells in ventral striatum were GA

54 Approximately 75% of aFGF+ and GDNF+ cells in dorsal striatum and 46% of aFGF

55 high levels of colocalization (over 85%) of aFGF and ChAT mRNAs were observed in the medial septum,

56 In the absence of aFGF+ChABC fewer catecholaminergic axons entered the gra

57 and S phase entrance, while the addition of aFGF or bFGF alone was insufficient to induce these resp

58 nvestigate the structural characteristics of aFGF and the C2A domain of p40 Syt1 under acidic conditi

59 multiprotein release complex, consisting of aFGF, S100A13 (a calcium binding protein), and a 40 kDa

60 Using CM that had been depleted of aFGF and/or bFGF and subsequently reconstituted with res

61 ction were used to examine the expression of aFGF by synovial cells in vitro.

62 flammatory cytokines, is a potent inducer of aFGF production by synoviocytes in vitro.

63 We further showed that an inhibitor of aFGF/bFGF (suramin) enhanced the in vitro and in vivo ac

64 lease complex mediated by the interaction of aFGF and p40 Syt1with the phospholipids of the cell memb

65 Patients with high levels of aFGF mRNA and elevations after the early posttransplant

66 A portion of aFGF+ and NGF+ cells was of the parvalbumin GABAergic su

67 emoresistance, whereas inhibition/removal of aFGF resulted in partial reversal.

68 ased in the partially structured state(s) of aFGF.

69 formation of partially structured states of aFGF and the C2A domain of p40 Syt1.

70 and mechanism of the combination therapy of aFGF-nanoparticles (aFGF-NP) and ultrasound-targeted mic

71 Fibroblast growth factor 1 (FGF-1 or aFGF), is a mitogen for a variety of mesoderm- and neuro

72 Fibroblast growth factor 1 (FGF-1 or aFGF), is the prototype member of the heparin-binding gr

73 ments for 12 consecutive weeks (free aFGF or aFGF-NP+/-UTMD), with the strongest improvements observe

74 group and other groups treated with aFGF or aFGF-NP.

75 r aFGF treatment groups (free aFGF+/-UTMD or aFGF-NP).

76 nd cardiac myocyte apoptosis index) to other aFGF treatment groups (free aFGF+/-UTMD or aFGF-NP).

77 Parenchymal aFGF expression varies between patients and in the same

78 These results indicate that PNG+aFGF+ChABC treatment of the chronically contused spinal

79 In single-labeling preparations, aFGF mRNA-containing neurons were found to be codistribu

80 ory synovial cells were competent to release aFGF into the media, even though aFGF lacks a signal pep

81 R-1 into fnr-PC12 cells efficiently restored aFGF-induced neurite outgrowth, whereas transfection of

82 f FGFR-1, termed FR31b, efficiently restored aFGF-induced neurite outgrowth.

83 From Mason staining and TUNEL staining, aFGF-NP+UTMD group showed significant differences from t

84 These findings demonstrate that aFGF, GDNF, and NGF are synthesized by discrete but over

85 Although these data indicate that aFGF is present in regions containing cholinergic cell b

86 riatum and olfactory tubercle labeled by the aFGF cRNA.

87 h the strongest improvements observed in the aFGF-NP+UTMD group.

88 r role in the non-classical secretion of the aFGF release complex mediated by the interaction of aFGF

89 to release aFGF into the media, even though aFGF lacks a signal peptide.

90 sence or absence of neutralizing antibody to aFGF was used to measure bioactive aFGF levels in cultur

91 sed by the different extents of twice weekly aFGF treatments for 12 consecutive weeks (free aFGF or a

92 rgic and never by cholinergic cells, whereas aFGF and GDNF mRNAs were expressed by both cell types.

93 but not aFGF induced chemoresistance whereas aFGF amplified the bFGF effect.

94 diabetes group and other groups treated with aFGF or aFGF-NP.