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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
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
17 suggested that the CRE complex consisted of CRE binding protein and EGF-ERK-dependent recruitment of
22 e show that the expression of phosphorylated CRE-binding protein, Arc, and BDNF, three genes whose in
23 le-stranded sequences when proteins, such as CRE-binding protein, are bound to an adjacent cis-regula
28 tion of this promoter, we searched for novel CRE-binding proteins by using a 32P-labeled beta-pol CRE
29 al transducer and activator of transcription/CRE binding protein) complex to the GFAP promoter by ind
30 of these two enhancer elements requires the CRE binding protein CREB because a dominant negative CRE
31 nse element (CRE), and demonstrated that the CRE-binding protein CREB can function as a nuclear calci
32 onse to nicotine, and nicotine activated the CRE-binding protein CREB through phosphorylation at seri
33 KCREB, a dominant negative mutant of the CRE-binding protein CREB, blunted activation of chromogr
36 onal repressor(s) to attenuate the action of CRE binding protein (CREB) and show that inducible cAMP
38 ith a plasmid encoding the dominant-negative CRE binding protein (CREB) completely abolished the indu
40 mbers of the activating transcription factor/CRE binding protein (CREB) family may mediate mIg-depend
42 tal neurons, but not in hippocampal neurons, CRE binding protein (CREB) phosphorylation and CRE-media
43 bility shift assays (EMSA) revealed that the CRE binding protein (CREB) was phosphorylated on serine
44 scription, as well as the phosphorylation of CRE binding protein (CREB), in several limbic brain regi
45 rain derived neurotrophic factor and phospho-CRE binding protein (CREB), predated inclusion formation
46 n correlates with the phosphorylation of the CRE binding protein (CREB); however, the mechanisms medi
47 search has shown that cAMP response element (CRE) binding protein (CREB) in the nucleus accumbens gat
50 inase A (PKA) and the cAMP response element (CRE) binding protein (CREB) signaling pathways mediate p
51 transcription factor cAMP-response element (CRE) binding protein (CREB), and by the complement of ac
52 r-2 (ATF-2) and cyclic AMP response element (CRE) binding protein (CREB), are intimately involved in
53 factor 1 (ATF1) and cAMP-responsive element (CRE)-binding protein (CREB) activate transcription throu
54 Overexpression of cAMP-response element (CRE)-binding protein (CREB) and activating transcription
55 transcription factor cAMP response element (CRE)-binding protein (CREB) has been shown to regulate n
56 actor-1 (ATF-1) and cAMP-responsive element (CRE)-binding protein (CREB) have been implicated in cAMP
58 - and ethanol-induced cAMP response element (CRE)-binding protein (CREB) phosphorylation and CRE-medi
59 e inhibition of cyclic AMP response element (CRE)-binding protein (CREB) phosphorylation did not lead
60 transcription factor cAMP response element (CRE)-binding protein (CREB) plays an essential role in t
61 iption factors, cyclic AMP response element (CRE)-binding protein (CREB), activates transcription of
62 coupling of DYRK3 to cAMP response element (CRE)-binding protein (CREB), and 3) effects of DYRK3 on
63 tivation of the cyclic AMP response element (CRE)-binding protein (CREB), and in some cells its effec
64 and dominant-negative cAMP response element (CRE)-binding protein (CREB), we now find that UVC-induce
67 ity of E1A to block cAMP-regulated enhancer (CRE)-binding protein (CREB)-stimulated gene expression.
68 cAMP agonists stimulated phosphorylation of CRE-binding protein (CREB) and activated expression of c
70 fection with dominant negative (dn) forms of CRE-binding protein (CREB) and CCAAT/enhancer-binding pr
71 ond, VIP/PACAP induce phosphorylation of the CRE-binding protein (CREB) and its binding to the CREB-b
72 eins known to bind the PEPCK CRE include the CRE-binding protein (CREB) and members of the CCAAT/enha
73 s, that the CRE is primarily occupied by the CRE-binding protein (CREB) and phospho-CREB, and that ci
74 ts with multiple nuclear proteins, including CRE-binding protein (CREB) and transcription factor YY1
75 ein kinase A (PKA), which phosphorylated the CRE-binding protein (CREB) at serine 133, which probably
77 retic mobility shift assays demonstrate that CRE-binding protein (CREB) binds to the CFTR CRE with hi
78 nd Western blotting techniques revealed that CRE-binding protein (CREB) constitutively binds the majo
79 he beta-pol promoter in vitro and found that CRE-binding protein (CREB) from MNNG-treated cells diffe
82 s in its promoter and the phosphorylation of CRE-binding protein (CREB) may regulate its expression.
83 duced the FSK-induced phosphorylation of the CRE-binding protein (CREB) measured on Western blots (co
87 pershift assay using an antibody against the CRE-binding protein (CREB) shows specific affinity to th
88 rosine kinase induces phosphorylation of the CRE-binding protein (CREB) transcription factor on serin
89 kDa that bound to the putative AP2/SP1 site, CRE-binding protein (CREB), and CREB-binding protein/p30
90 cal studies showed that c-Fos, Fos-B, Jun-D, CRE-binding protein (CREB), and phosphorylated CREB (pCR
91 HepG2 nuclear extracts, including HNF3gamma, CRE-binding protein (CREB), C/EBPalpha, and C/EBPbeta.
92 vate CRE (cAMP responsive element), activate CRE-binding protein (CREB)-binding protein (CBP) and gen
95 -1-like element that binds both the AP-1 and CRE-binding protein (CREB)/ATF proteins (c-Jun, ATF-1, A
96 tivation of the cyclic AMP-response element (CRE)-binding protein, CREB, an event that likely plays a
99 he cloning of a cyclic AMP response-element (CRE)-binding protein, dCREB-A, in Drosophila melanogaste
100 r-2 (ATF-2) mRNA encodes a member of the ATF/CRE-binding protein family of transcription factors and
104 ugh tandem CRE sequences in the promoter and CRE binding proteins; IL-2 stimulates CREB phosphorylati
105 ment (CRE), which binds to ATF-1, ATF-2, and CRE-binding protein in PC12 nuclear extracts, a novel CC
106 ation, and AC8 KO mice also fail to activate CRE-binding protein in the CA1 region after restraint st
107 Aplysia motor neurons to examine the role of CRE-binding proteins in axonal regeneration after injury
108 e first evidence for a differential role for CRE-binding proteins in multiple stages of B cell develo
110 -mediated transcription by dominant-negative CRE binding protein inhibited cardiac hypertrophy, where
111 rotein promoter activities via increased CRE/CRE-binding protein interaction in a cell background-dep
112 betadelta9 results in the phosphorylation of CRE-binding protein on serine 129 and enhancement of CRE
113 arget of PKG, we examined changes in phospho-CRE-binding protein (phospho-CREB) immunofluorescence in
115 ide evidence that G-protein coupled receptor/CRE-binding protein signaling can potentially act on HFS
116 provide direct evidence that canonical cAMP/CRE-binding protein signaling through adrenergic recepto
118 s demonstrates a nonredundant function for a CRE-binding protein that will be useful in studying the
119 monstrated binding of cAMP response element (CRE)-binding protein to a CART promoter CRE site in isch
121 r protein-1 and cyclic AMP-response element (CRE)-binding protein were analyzed as targets of GSK-3be
122 le trans-acting factors besides the USF- and CRE-binding proteins were required for full promoter act