ライフサイエンスコーパス: GRF

1 ing type switch-activating protein Sap1 is a GRF in S. pombe, demonstrating the general applicability

2 One line, bearing a single copy of a GRF-hGH transgene, has been characterized in detail, and

3 y, the IQ motif of GRF1 determines whether a GRF protein can induce LTD.

4 e or alter its spatial relationship abrogate GRF binding.

5 Systematic analysis of additional GRFs suggests a network architecture that rationalizes t

6 eractions identified here between miR396 and GRF and PLT transcription factors are necessary to estab

7 retrogradation was observed in both NRF and GRF with MPP added of all levels.

8 r different coding regions of human SOS1 and GRF genes were used to screen expression of these genes

9 tion of Ras by the mammalian GEFs, Sos1, and GRF/CDC25Mm.

10 dephosphorylation pathway, and MAF3-like and GRFs genes, may be considered as markers of growth compe

11 ng tissues, a process mediated by miR396 and GRFs.

12 ns of 8.3 and 6.1 kb, whereas an Arabidopsis GRF gene occupies a single domain of 27 kb.

13 nding, loci exhibiting Pol II readthrough at GRF binding sites are depleted for upstream NNS signals.

14 Although both GRF proteins transduce calcium signals emanating from NM

15 GRF1 are key to the induction of HFS-LTP by GRF proteins.

16 CDC25 domain in the induction of TBS-LTP by GRF proteins.

17 of synaptic plasticity that are regulated by GRF proteins in the CA1 hippocampus, specificity is enco

18 We identified a pathway regulated by GRF transcription factors that represses stem cell-promo

19 reveals that the specific sequences bound by GRFs have diverged substantially across evolution, corre

20 actors determine mRNA output and then derive GRFs for target genes in the CLB2 gene cluster that are

21 Each GRF protein contains a Dbl homology (DH) domain.

22 ecrease of starch retrogradation, especially GRF.

23 examine the contribution of these essential GRFs to transcription genome-wide, by using ts mutants t

24 y, FG skewed the direction of the GVS-evoked GRF vector towards the axis of baseline postural instabi

25 PLC domains, contains a GTP exchange factor (GRF CDC25) domain and two C-terminal Ras-binding (RA) do

26 hat members of the GROWTH-REGULATING FACTOR (GRF) family act as players in this network.

27 of miR396 and its Growth-Regulating Factor (GRF) target genes resulted in reduced syncytium size and

28 abidopsis thaliana growth-regulating factor (GRF)] gene family, which encodes putative transcription

29 ring trans-acting general regulatory factor (GRF) binding sites.

30 keratinocytes, termed gamma response factor (GRF).

31 gated the role of Growth-Regulating Factors (GRFs) and of microRNA miR396 in UV-B-mediated inhibition

32 genes, including growth-regulating factors (GRFs) and transcripts for proteins participating in diff

33 since copurified GROWTH-REGULATING FACTORs (GRFs) varied throughout the growing leaf.

34 interacting with GROWTH-REGULATING FACTORs (GRFs).

35 lators, including GROWTH REGULATING FACTORs (GRFs).

36 s, including the general regulatory factors (GRFs) Reb1p, Rap1p, and Abf1p, and Pol III transcription

37 bf1 and Rap1 are general regulatory factors (GRFs) that contribute to transcriptional activation of a

38 for one or more General Regulatory Factors (GRFs), most frequently Abf1 and Reb1, and that these fac

39 for GRF1, we identified another gene family, GRF-interacting factor (GIF), which comprises three memb

40 l rice flour (NRF) and glutinous rice flour (GRF) at three levels (400, 800 and 1200 ppm) and their e

41 nd Stat1alpha homodimers fail to compete for GRF binding in EMSA, and pIgammaRE does not cross-compet

42 ltaneous reduction in ground reaction force (GRF) through the feet.

43 lues of peak vertical ground reaction force (GRF), stance time, contact length and vertical centre of

44 Such a 'gene regulation function' (GRF) generally cannot be measured because the experiment

45 n of ERF/AP2, C2H2 zinc finger, homeodomain, GRF, TCP, zinc finger homeodomain, BES, and STERILE APET

46 Peak horizontal GRF and mechanical work per step were lower when POFT oc

47 be expected to overestimate peak horizontal GRF and mechanical work per step.

48 Tgr rats had reduced hypothalamic GRF and mRNA, in contrast to the increased GRF expressio

49 c GRF and mRNA, in contrast to the increased GRF expression which accompanies GH deficiency in other

50 evolutionary transition from Cbf1 as a major GRF in pre-whole-genome duplication (WGD) yeasts to Reb1

51 xpression profiling revealed that the miR396-GRF regulatory system can alter the expression of 44% of

52 Binding of GRF is tyrosine phosphorylation-dependent, and mutations

53 ant dwarfism by local feedback inhibition of GRF.

54 nd Rap1 or Abf1, but not affected by loss of GRF binding.

55 monstrate here that the C-terminal region of GRF proteins has transactivation activity.

56 volutionary transitions in the repertoire of GRFs.

57 her Ras exchange factor, CDC25Mm, or p140Ras-GRF.

58 A Ras-GRF mutant containing the PH domain from Ras-GTPase-acti

59 es defective LTP induction in adolescent Ras-GRF knockout mice, consists of NMDA glutamate receptor a

60 vation is reduced in the brains of adult Ras-GRF knockout mice and neuronal damage is enhanced.

61 tion of cells is not sufficient to allow Ras-GRF activation by calcium.

62 domains function cooperatively to allow Ras-GRF activation.

63 calcium channels, an event that is also Ras-GRF-independent.

64 Sos and Ras-GRF are two families of guanine nucleotide exchange fact

65 cleotide exchange factors (GEFs) such as Ras-GRF; however, there is no Ca(2+)-dependent mechanism for

66 activation of a single Ras homologue by Ras-GRF/Cdc25Mm or other Ras guanine nucleotide exchange fac

67 of Ras-GRF function together to connect Ras-GRF to multiple components in the particulate fractions

68 In contrast, Ras-GRF proteins are expressed primarily in central nervous

69 the phosphorylation state of endogenous Ras-GRF.

70 inst specific domains of hSOS1 and human Ras-GRF gene products.

71 In contrast, neither Ras-GRF protein influences synaptic plasticity in prepubesce

72 main redistributes a large percentage of Ras-GRF from the particulate to the cytosolic fraction of ce

73 minal PH, coiled-coil, and IQ domains of Ras-GRF function together to connect Ras-GRF to multiple com

74 Remarkably, this form of Ras-GRF is constitutively activated.

75 Here, using a set of Ras-GRF knock-out mice, we show that Ras-GRF2 contributes pr

76 necessary for particulate association of Ras-GRF, it is not sufficient for targeting the core catalyt

77 Moreover, the postnatal appearance of Ras-GRF-dependent LTP and LTD coincides with the emergence o

78 g to an IQ domain near the N terminus of Ras-GRF.

79 te, at least in part, the specificity of Ras-GRF/CDC25Mm for Ha-Ras protein.

80 n that the neuronal exchange factor p140 Ras-GRF becomes activated in vivo in response to elevated ca

81 ism for Ras activation, mediated by p140 Ras-GRF.

82 ce; however, at this developmental stage Ras-GRF (guanine nucleotide-releasing factor) proteins are n

83 phosphorylation state of epitope-tagged Ras-GRF.

84 ls NMDARs signal through Sos rather than Ras-GRF exchange factors, implying that Ras-GRFs endow NMDAR

85 campal-dependent behavior, implying that Ras-GRF proteins contribute to forms of synaptic plasticity

86 We found that Ras-GRF/Cdc25Mm activates Ha-Ras, but does not activate N-Ra

87 ransfection of hm1 or hm2 receptors with Ras-GRF conferred carbachol-dependent increases in exchange-

88 Consistent with this function for Ras-GRFs and the known neuroprotective effect of CREB activi

89 Similar phenotypes are seen with mutant Ras-GRFs containing point mutations in either the PH or coil

90 Ras-GRF exchange factors, implying that Ras-GRFs endow NMDARs with functions unique to mature neuron

91 H) was targeted to growth hormone-releasing (GRF) neurons in the hypothalamus of transgenic rats.

92 xpressing miR396-resistant copies of several GRFs are less sensitive to this inhibition.

93 e chromatin remodeling complex with specific GRFs tightly regulate the transition between cell divisi

94 to characterized STAT proteins suggest that GRF contains a Stat1alpha-like protein; however, non-ICA

95 Here we show that GRFs may instead be inferred from natural changes in cel

96 monstrate conserved interactions between the GRF and KNOX families of transcription factors in both m

97 We now describe the GRF gene family of Arabidopsis thaliana (AtGRF), which c

98 possibly other transcription factors of the GRF family.

99 Likewise, we found that the GRF protein BGRF1 from barley (Hordeum vulgare) could ac

100 It has been known that the GRF-INTERACTING FACTOR (GIF) transcription co-activator

101 The GRFs are expressed in transit-amplifying cells but are e

102 The GRFs repress PLETHORA (PLT) genes, regulating their spat

103 If unchecked, the expression of the GRFs in the stem cell niche suppresses formative cell di

104 Inactivation of the GRFs increases the meristem size and induces periclinal

105 ates MIR396 in the stem cells to repress the GRFs.

106 Our observations point to GRFs as new multifaceted players in Ribi gene regulation

107 providing good predictions of peak vertical GRF, stance time, contact length and vertical centre of

108 The pIgammaRE x GRF complex also displays a distinctly different electro

109 Collectively, our data unveil the APE2 Zf-GRF domain as a nucleic acid interaction module in the r

110 Moreover, an APE2 Zf-GRF X-ray structure and small-angle X-ray scattering ana

111 Structure-guided Zf-GRF mutations impact APE2 DNA binding and 3'-5' exonucle

112 y is regulated by DNA interactions in its Zf-GRF domain, a region sharing high homology with DDR prot

113 the nucleic acid-binding activity of the Zf-GRF domain.

114 e X-ray scattering analyses show that the Zf-GRF fold is typified by a crescent-shaped ssDNA binding

115 d also reveal topologic similarity of the Zf-GRF to the zinc ribbon domains of TFIIS and RPB9.