ライフサイエンスコーパス: CREB protein

1 showing that Notch regulates dCrebB-17A, the CREB protein.

2 ts signalling receptor pTrkB, as well as the CREB protein.

3 in the de novo appearance of phosphorylated CREB protein.

4 f ERK2 MAPK and decreased phosphorylation of CREB protein.

5 lso occurs in the context of the full-length CREB protein.

6 was markedly inhibited by dominant-negative CREB proteins.

7 ranscription factor CREB but not related ATF/CREB proteins.

8 ), GATA4, and cAMP-response element binding (CREB) protein.

9 , such as the cAMP Response Element Binding (CREB) protein.

10 orylation of c-AMP response element binding (CREB) protein.

11 ase and cyclic AMP response element-binding (CREB) protein.

12 f control) and phosphorylation (300%) of the Creb protein, a transcription factor that is downstream

13 sphorylation is accompanied by a decrease in CREB protein abundance and no change in Cre-luciferase r

14 ism that links oxidative stress to decreased CREB protein abundance is predicted to contribute to the

15 genesis studies indicate that H2O2 decreases CREB protein abundance via a mechanism that does not req

16 of Regulated cAMP response element-binding (CREB) protein activity (TORCs) in HD, since TORCs play a

17 ndance, and phosphorylation of eIF2alpha and CREB proteins) alongside perturbations in hepatokine exp

18 aracterization of the full-length, wild-type CREB protein, an altered CREB protein (CREB/SER) in whic

19 or to forskolin treatment not only decreased CREB protein and its phosphorylation at Ser-133, but als

20 to show that the drug increased levels of P-CREB protein and P-CREB binding to the CART promoter CRE

21 ng protein from up-regulating the CTNNB1 and CREB proteins and their target genes, indicating that WN

22 by inhibiting cAMP response element binding (CREB) protein and AKT phosphorylation, respectively.

23 nal activator cAMP response element binding (CREB) protein and the KIX domain of its coactivator, CRE

24 lation of the cAMP response element binding (CREB) protein and via the dephosphorylation of the laten

25 ch indicates that expression and function of CREB protein are increased along with its mRNA.

26 ferentiated cells, levels of Sp3, KSR-1, and CREB proteins are lower; the unidentified regulator prot

27 ased, and levels of total and phosphorylated CREB proteins are unchanged as well.

28 cAMP-response element binding (CREB) proteins are involved in transcriptional regulatio

29 s the levels of miR-34a target genes such as CREB protein as shown by real time PCR.

30 gram circadian transcription, and identifies CREB proteins as candidates for this reprograming.

31 These DNA-binding complexes contained CREB proteins, based on competitive EMSAs, supershift as

32 t, in contrast to c-Jun, SRF, Elk1, ATF1 and CREB proteins bind to SRE and ATF sites of the FRA-1 pro

33 ked in the silent normal bcl-2 allele, while CREB proteins bind to the site on the translocated allel

34 rmation of p-CREB/p300 complexes and the DNA-CREB protein binding.

35 Expression of a dominant negative CREB protein blocked mIg-mediated transcription from a j

36 shift assays did not detect Jun, Fos, or ATF/CREB proteins but identified Nrf2 and the small Maf prot

37 n dimerization) domain characteristic of ATF/CREB proteins, but no other functional domains or clear

38 We show that CREB protein can compete with c-Jun for the AP1 site and

39 m we show that phosphorylation of Ser-133 on CREB protein can occur in isolated dendrites independent

40 P), and cyclic AMP-response element-binding (CREB) protein (CBP).

41 phosphorylation of CREB at Ser 133, whereas CREB protein content was unaltered by either HG or GlcN.

42 l-length, wild-type CREB protein, an altered CREB protein (CREB/SER) in which the three cysteine resi

43 of CREB binding but not that of another ATF/CREB protein, CREB2, to the 21-bp repeat.

44 firmed that mice lacking the alpha and Delta CREB proteins (CREBalphaDelta-) have abnormal long-term,

45 tutive neuronal COX-2 expression via Sp1 and CREB protein-dependent transcriptional mechanisms.

46 The total amount of CREB protein did not change at the time points examined.

47 to the ATM-dependent phosphorylation of the CREB protein, extrusion of neuritic processes, and diffe

48 appears to be due to up-regulation of other CREB protein family members, i.e. ATF1 and CREM.

49 ne monophosphate responsive element-binding (CREB) protein family.

50 A in isolated dendrites is feasible and that CREB protein found in dendrites can interact with the ci

51 s in chromatin condensation and exclusion of CREB proteins from the IFN-gamma promoter.

52 cyclic AMP (cAMP) response element binding (CREB) protein gene, or overexpressing a dominant-negativ

53 sine monophosphate response element binding (CREB) protein has been implicated in both antidepressant

54 CIITA and does not interact detectably with CREB proteins implicated in CIITA recruitment, but the s

55 enic mice that express the dominant-negative CREB protein in B lymphocytes were developed as a means

56 Further, CREB protein in dendrites is not transported to this sit

57 lated cAMP-response element-binding protein (CREB) protein in Caco2-BBE cells, whereas our deletion,

58 kinase A and cAMP response element binding (CREB) protein in Wt mice, but CREB only was activated in

59 tion with KIX, the disordered pKID region of CREB protein is central in the transcription of cAMP res

60 The increased phosphorylation of CREB protein is preceded by an increase in the amount of

61 We expanded upon these results showing that CREB protein is present in dendrites, that translation o

62 Rather, the H2O2-dependent decrease in CREB protein is prevented by the proteasome inhibitor la

63 t CREB mRNA were used to disrupt hippocampal CREB protein levels in adult rats.

64 a specific PKC-theta inhibitor, diminished p-CREB protein levels when normal T cells were treated wit

65 CTNNB1) and cAMP responsive element binding (CREB) protein levels to decreaseviaa glycogen synthase k

66 Therefore, a CREB protein may act as a nuclear target, or as a partne

67 In addition, CREB protein microperfused into dendrites was rapidly tr

68 horylation of cAMP response element-binding (CREB) protein on the IL-10 promoter.

69 ulated by the cAMP response element-binding (CREB) protein pathway.

70 Ca(2+) in the role of CaM KIV activation and CREB protein phosphorylation associated with hypoxia.

71 xia-induced increase in CaM KIV activity and CREB protein phosphorylation.

72 lcium/cyclic AMP responsive element-binding (CREB) protein phosphorylation, leading to temporally gat

73 proximal promoter regions and activation of CREB proteins play a crucial role in transcriptional reg

74 Phosphorylation of CREB protein prevents its interaction with a coactivator

75 utant CBP (S436A) is aberrantly recruited to CREB protein, resulting in inappropriate activation of g

76 horylation of cAMP response element-binding (CREB) protein, resulting in recruitment of the coactivat

77 mplicated the cAMP Response Element Binding (CREB) protein signaling pathway in long-term memory.

78 mutants reveals a much broader function for CREB proteins than previously thought.

79 nant-negative (DN) CREB mutants, KCREB and A-CREB, proteins that dimerize with CREB family members an

80 yed the cyclic AMP-response element-binding (CREB) protein to provide evidence for substrate discrimi

81 ns, including cAMP response element binding (CREB) protein, translation-initiation factor eIF2B, and

82 auto- and cross-regulation of expression of CREB proteins, via CRE elements in or near their genes.

83 CREB protein was elevated in TRAF3(-/-) B cells, without

84 antibody that detects Ser133-phosphorylated CREB protein, we show that CREB phosphorylation is maxim

85 onditions, no changes in relative amounts of CREB protein were observed by Western blot.

86 EB, although no significant changes in total CREB proteins were observed.

87 ascade, the cAMP-regulatory element binding (CREB) protein, were affected also.

88 Furthermore, when dominant negative CREB proteins with mutations in either the CREB phosphor