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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
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                                We found that CRE-binding protein activation is regulated through the
16              Here we show that cAMP-mediated CRE-binding protein activation of the M-MITF promoter re
17  suggested that the CRE complex consisted of CRE binding protein and EGF-ERK-dependent recruitment of
18       Homo- and heterodimers composed of the CRE-binding protein and activating transcription factor-
19        AngII also induced transactivation of CRE-binding protein and transcription from the fibronect
20                       In unstimulated THP-1, CRE-binding protein and, to a lesser extent, c-Jun compl
21                         The TxRE binds CREB (CRE-binding protein) and Tax to form a ternary complex a
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
24 sponse element (CRE)-binding complexes, with CRE binding protein as the major active component.
25                             Furthermore, the CRE-binding protein-binding protein (CBP), a histone ace
26 NA-binding protein (cAMP-responsive element (CRE)-binding protein) bound to a CRE.
27                         The sequestration of CRE-binding proteins by microinjection of CRE sequence-c
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
34 action with the nuclear transcription factor CRE-binding protein CREB.
35 elanogaster that is similar to the mammalian CRE-binding protein CREB.
36 onal repressor(s) to attenuate the action of CRE binding protein (CREB) and show that inducible cAMP
37             Both the total amount of phospho-CRE binding protein (CREB) and the pCREB bound to nmnat2
38 ith a plasmid encoding the dominant-negative CRE binding protein (CREB) completely abolished the indu
39                           Hypoxia diminished CRE binding protein (CREB) expression.
40 mbers of the activating transcription factor/CRE binding protein (CREB) family may mediate mIg-depend
41 sion of dominant negative mutants of ERK1/2, CRE binding protein (CREB) kinase RSK2, or CREB.
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
48             The cyclic AMP response element (CRE) binding protein (CREB) is a transcription factor th
49                   The cAMP response element (CRE) binding protein (CREB) is emerging as a key regulat
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
57                   The cAMP response element (CRE)-binding protein (CREB) is a key regulatory factor o
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
65 n factor Phox2a, in a cAMP response element (CRE)-binding protein (CREB)-mediated mechanism.
66         Inhibition of cAMP response element (CRE)-binding protein (CREB)-mediated transcription block
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
69                             CRE site 2 bound CRE-binding protein (CREB) and activating transcription
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
76                                              CRE-binding protein (CREB) belongs to a family of transc
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
80 ens, leading to increased phosphorylation of CRE-binding protein (CREB) in the striatum.
81                                              CRE-binding protein (CREB) is the most studied activator
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
84                            Overexpression of CRE-binding protein (CREB) or activation of cAMP-depende
85  D1 transcription involved Wnt signaling and CRE-binding protein (CREB) pathways.
86 o CRE-mediated gene expression by modulating CRE-binding protein (CREB) phosphorylation.
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
93 ne transfer of a dominant negative mutant of CRE-binding protein (CREB).
94  we found can be recognized and activated by CRE-binding protein (CREB).
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
97                 Here we demonstrate that the CRE-binding protein, CREB, is specifically cleaved by th
98                  Furthermore, the Drosophila CRE-binding protein dCREB-B binds to the Ultrabithorax C
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
101 ted, corresponding to various members of the CRE-binding protein family.
102            Coexpression of dominant-negative CRE-binding protein greatly reduced ethanol induction of
103              However, none of the decamer or CRE-binding proteins identified thus far is restricted i
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
109                 The current study identifies CRE-binding proteins induced in pharmacological paradigm
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
114 ial pathway from Gs-adenylyl cyclase-cAMP to CRE binding protein phosphorylation.
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
117 ession depends on interactions with cellular CRE-binding proteins such as CREB.
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
120                                Activation of CRE binding proteins was inhibited by delta 9-THC.
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

 
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