ライフサイエンスコーパス: CRE-binding protein

1 es via the cyclic AMP-inducible factor CREB (CRE binding protein).

2 on factor CREB (cyclic AMP response element [CRE] binding protein).

3 undifferentiated PC12 cells and recombinant CRE binding protein.

4 of neurons and increased phosphorylation of CRE binding protein.

5 d that the CRE in the alpha 1B-AR gene bound CRE binding protein.

6 This approach identified EWSR1 as a CRE-binding protein.

7 hrough increased interaction between CRE and CRE-binding protein.

8 transcription factor cAMP response element (CRE)-binding protein.

9 is mobility supershift assays indicated that CRE-binding protein 1 (CREB1) and Smad3 were the major c

10 ssibility that the transcriptional activator CRE-binding protein 1 (CREB1) mediates 5-HT-induced regu

11 king region of the MuSK gene binds to CREB1 (CRE-binding protein 1).

12 d that both bradykinin and IL-1beta elicited CRE-binding protein-1 (CREB-1) binding, and IL-1beta als

13 nd thyroid-specific proteins as follows: the CRE-binding protein, a Y-box protein termed thyrotropin

14 tion factors of the cAMP-responsive element (CRE) binding protein/activating transcription factor (CR

15 Here we show that cAMP-mediated CRE-binding protein activation of the M-MITF promoter re

16 suggested that the CRE complex consisted of CRE binding protein and EGF-ERK-dependent recruitment of

17 Homo- and heterodimers composed of the CRE-binding protein and activating transcription factor-

18 AngII also induced transactivation of CRE-binding protein and transcription from the fibronect

19 In unstimulated THP-1, CRE-binding protein and, to a lesser extent, c-Jun compl

20 The TxRE binds CREB (CRE-binding protein) and Tax to form a ternary complex a

21 e show that the expression of phosphorylated CRE-binding protein, Arc, and BDNF, three genes whose in

22 le-stranded sequences when proteins, such as CRE-binding protein, are bound to an adjacent cis-regula

23 sponse element (CRE)-binding complexes, with CRE binding protein as the major active component.

24 Furthermore, the CRE-binding protein-binding protein (CBP), a histone ace

25 NA-binding protein (cAMP-responsive element (CRE)-binding protein) bound to a CRE.

26 The sequestration of CRE-binding proteins by microinjection of CRE sequence-c

27 tion of this promoter, we searched for novel CRE-binding proteins by using a 32P-labeled beta-pol CRE

28 al transducer and activator of transcription/CRE binding protein) complex to the GFAP promoter by ind

29 of these two enhancer elements requires the CRE binding protein CREB because a dominant negative CRE

30 nse element (CRE), and demonstrated that the CRE-binding protein CREB can function as a nuclear calci

31 onse to nicotine, and nicotine activated the CRE-binding protein CREB through phosphorylation at seri

32 KCREB, a dominant negative mutant of the CRE-binding protein CREB, blunted activation of chromogr

33 action with the nuclear transcription factor CRE-binding protein CREB.

34 elanogaster that is similar to the mammalian CRE-binding protein CREB.

35 onal repressor(s) to attenuate the action of CRE binding protein (CREB) and show that inducible cAMP

36 Both the total amount of phospho-CRE binding protein (CREB) and the pCREB bound to nmnat2

37 ith a plasmid encoding the dominant-negative CRE binding protein (CREB) completely abolished the indu

38 Hypoxia diminished CRE binding protein (CREB) expression.

39 mbers of the activating transcription factor/CRE binding protein (CREB) family may mediate mIg-depend

40 sion of dominant negative mutants of ERK1/2, CRE binding protein (CREB) kinase RSK2, or CREB.

41 tal neurons, but not in hippocampal neurons, CRE binding protein (CREB) phosphorylation and CRE-media

42 bility shift assays (EMSA) revealed that the CRE binding protein (CREB) was phosphorylated on serine

43 scription, as well as the phosphorylation of CRE binding protein (CREB), in several limbic brain regi

44 rain derived neurotrophic factor and phospho-CRE binding protein (CREB), predated inclusion formation

45 n correlates with the phosphorylation of the CRE binding protein (CREB); however, the mechanisms medi

46 search has shown that cAMP response element (CRE) binding protein (CREB) in the nucleus accumbens gat

47 The cAMP response element (CRE) binding protein (CREB) is emerging as a key regulat

48 inase A (PKA) and the cAMP response element (CRE) binding protein (CREB) signaling pathways mediate p

49 transcription factor cAMP-response element (CRE) binding protein (CREB), and by the complement of ac

50 r-2 (ATF-2) and cyclic AMP response element (CRE) binding protein (CREB), are intimately involved in

51 factor 1 (ATF1) and cAMP-responsive element (CRE)-binding protein (CREB) activate transcription throu

52 Overexpression of cAMP-response element (CRE)-binding protein (CREB) and activating transcription

53 transcription factor cAMP response element (CRE)-binding protein (CREB) has been shown to regulate n

54 actor-1 (ATF-1) and cAMP-responsive element (CRE)-binding protein (CREB) have been implicated in cAMP

55 The cAMP response element (CRE)-binding protein (CREB) is a key regulatory factor o

56 - and ethanol-induced cAMP response element (CRE)-binding protein (CREB) phosphorylation and CRE-medi

57 e inhibition of cyclic AMP response element (CRE)-binding protein (CREB) phosphorylation did not lead

58 transcription factor cAMP response element (CRE)-binding protein (CREB) plays an essential role in t

59 iption factors, cyclic AMP response element (CRE)-binding protein (CREB), activates transcription of

60 coupling of DYRK3 to cAMP response element (CRE)-binding protein (CREB), and 3) effects of DYRK3 on

61 tivation of the cyclic AMP response element (CRE)-binding protein (CREB), and in some cells its effec

62 and dominant-negative cAMP response element (CRE)-binding protein (CREB), we now find that UVC-induce

63 n factor Phox2a, in a cAMP response element (CRE)-binding protein (CREB)-mediated mechanism.

64 Inhibition of cAMP response element (CRE)-binding protein (CREB)-mediated transcription block

65 ity of E1A to block cAMP-regulated enhancer (CRE)-binding protein (CREB)-stimulated gene expression.

66 cAMP agonists stimulated phosphorylation of CRE-binding protein (CREB) and activated expression of c

67 CRE site 2 bound CRE-binding protein (CREB) and activating transcription

68 fection with dominant negative (dn) forms of CRE-binding protein (CREB) and CCAAT/enhancer-binding pr

69 ond, VIP/PACAP induce phosphorylation of the CRE-binding protein (CREB) and its binding to the CREB-b

70 eins known to bind the PEPCK CRE include the CRE-binding protein (CREB) and members of the CCAAT/enha

71 s, that the CRE is primarily occupied by the CRE-binding protein (CREB) and phospho-CREB, and that ci

72 ts with multiple nuclear proteins, including CRE-binding protein (CREB) and transcription factor YY1

73 ein kinase A (PKA), which phosphorylated the CRE-binding protein (CREB) at serine 133, which probably

74 CRE-binding protein (CREB) belongs to a family of transc

75 retic mobility shift assays demonstrate that CRE-binding protein (CREB) binds to the CFTR CRE with hi

76 nd Western blotting techniques revealed that CRE-binding protein (CREB) constitutively binds the majo

77 he beta-pol promoter in vitro and found that CRE-binding protein (CREB) from MNNG-treated cells diffe

78 ens, leading to increased phosphorylation of CRE-binding protein (CREB) in the striatum.

79 CRE-binding protein (CREB) is the most studied activator

80 s in its promoter and the phosphorylation of CRE-binding protein (CREB) may regulate its expression.

81 duced the FSK-induced phosphorylation of the CRE-binding protein (CREB) measured on Western blots (co

82 Overexpression of CRE-binding protein (CREB) or activation of cAMP-depende

83 D1 transcription involved Wnt signaling and CRE-binding protein (CREB) pathways.

84 o CRE-mediated gene expression by modulating CRE-binding protein (CREB) phosphorylation.

85 pershift assay using an antibody against the CRE-binding protein (CREB) shows specific affinity to th

86 rosine kinase induces phosphorylation of the CRE-binding protein (CREB) transcription factor on serin

87 kDa that bound to the putative AP2/SP1 site, CRE-binding protein (CREB), and CREB-binding protein/p30

88 cal studies showed that c-Fos, Fos-B, Jun-D, CRE-binding protein (CREB), and phosphorylated CREB (pCR

89 HepG2 nuclear extracts, including HNF3gamma, CRE-binding protein (CREB), C/EBPalpha, and C/EBPbeta.

90 vate CRE (cAMP responsive element), activate CRE-binding protein (CREB)-binding protein (CBP) and gen

91 ne transfer of a dominant negative mutant of CRE-binding protein (CREB).

92 we found can be recognized and activated by CRE-binding protein (CREB).

93 -1-like element that binds both the AP-1 and CRE-binding protein (CREB)/ATF proteins (c-Jun, ATF-1, A

94 tivation of the cyclic AMP-response element (CRE)-binding protein, CREB, an event that likely plays a

95 Here we demonstrate that the CRE-binding protein, CREB, is specifically cleaved by th

96 Furthermore, the Drosophila CRE-binding protein dCREB-B binds to the Ultrabithorax C

97 he cloning of a cyclic AMP response-element (CRE)-binding protein, dCREB-A, in Drosophila melanogaste

98 r-2 (ATF-2) mRNA encodes a member of the ATF/CRE-binding protein family of transcription factors and

99 ted, corresponding to various members of the CRE-binding protein family.

100 Coexpression of dominant-negative CRE-binding protein greatly reduced ethanol induction of

101 However, none of the decamer or CRE-binding proteins identified thus far is restricted i

102 ugh tandem CRE sequences in the promoter and CRE binding proteins; IL-2 stimulates CREB phosphorylati

103 ment (CRE), which binds to ATF-1, ATF-2, and CRE-binding protein in PC12 nuclear extracts, a novel CC

104 ation, and AC8 KO mice also fail to activate CRE-binding protein in the CA1 region after restraint st

105 Aplysia motor neurons to examine the role of CRE-binding proteins in axonal regeneration after injury

106 e first evidence for a differential role for CRE-binding proteins in multiple stages of B cell develo

107 The current study identifies CRE-binding proteins induced in pharmacological paradigm

108 -mediated transcription by dominant-negative CRE binding protein inhibited cardiac hypertrophy, where

109 rotein promoter activities via increased CRE/CRE-binding protein interaction in a cell background-dep

110 betadelta9 results in the phosphorylation of CRE-binding protein on serine 129 and enhancement of CRE

111 arget of PKG, we examined changes in phospho-CRE-binding protein (phospho-CREB) immunofluorescence in

112 ial pathway from Gs-adenylyl cyclase-cAMP to CRE binding protein phosphorylation.

113 ession depends on interactions with cellular CRE-binding proteins such as CREB.

114 s demonstrates a nonredundant function for a CRE-binding protein that will be useful in studying the

115 monstrated binding of cAMP response element (CRE)-binding protein to a CART promoter CRE site in isch

116 Activation of CRE binding proteins was inhibited by delta 9-THC.

117 r protein-1 and cyclic AMP-response element (CRE)-binding protein were analyzed as targets of GSK-3be

118 le trans-acting factors besides the USF- and CRE-binding proteins were required for full promoter act