ライフサイエンスコーパス: Oct-3

1 melanoma-cell extracts is also related to N-Oct 3.

2 ecific organic cation transporters OCT-1 and OCT-3.

3 d, including a partnership between Sox-2 and Oct-3.

4 is only observed when Sox2 is complexed with Oct-3.

5 mediated by the combined action of Sox-2 and Oct-3.

6 nd B, and octamer-binding proteins Oct-1 and Oct-3.

7 rials of multidrug chemotherapy done between Oct 3, 2000, and Aug 28, 2018, in which tyrosine-kinase

8 n Izhevsk occurring between Oct 20, 2003, to Oct 3, 2005.

9 Between Oct 3, 2009, and Jan 14, 2014, we recruited 22 patients

10 clinical trial, we enrolled patients between Oct 3, 2011, and Feb 14, 2012, at 53 sites in 11 countri

11 After the baseline period (Oct 3, 2011, to Nov 30, 2012), continuation of empirical

12 Between Sept 12, 2011, and Oct 3, 2012, 191 women were enrolled to the trial.

13 kraine, and the UK between Feb 13, 2009, and Oct 3, 2012.

14 nts were recruited between Jan 25, 2012, and Oct 3, 2012; 757 patients were assessed for eligibility

15 Between May 8, 2009, and Oct 3, 2013, 235 patients were enrolled and randomly ass

16 patients screened between June 7, 2013, and Oct 3, 2013, 81 (78%) were PD-L1-positive.

17 Between March 4, 2014, and Oct 3, 2014, 200 HIV-positive pregnant women were enroll

18 Between Oct 3, 2014, and Dec 21, 2016, we enrolled 34 patients (

19 Between Oct 3, 2014, and July 31, 2015, 740 patients were enroll

20 Between Oct 3, 2017, and July 22, 2019, 2595 women were identifi

21 From Jan 8, 2016, to Oct 3, 2018, 1345 patients were screened, of which 1012

22 Between Oct 3, 2018, and Jan 7, 2022, 551 patients were randomly

23 ence assessment of articles (Jan 1, 2008, to Oct 3, 2018; with searches of MEDLINE, Embase, and PsycI

24 Between July 19, 2017, and Oct 3, 2019, 439 patients were randomly assigned to rece

25 Between June 17 and Oct 3, 2019, 458 participants were screened and 280 were

26 The study was conducted between Oct 3, 2019, and Mar 24, 2022.

27 fferentiation marker transcripts, as well as Oct 3/4 protein distribution, supported the hypothesis t

28 uding well-known stem cell factors Nanog and Oct 3/4.

29 ing sites and confirmed the critical role of Oct-3/4 (aka Oct-4) in directing ER recruitment to TOT p

30 The POU transcription factor Oct-3/4 (encoded by Pou5f1) is a candidate regulator in

31 Our findings establish a role for Oct-3/4 as a master regulator of pluripotency that contr

32 l system, we found that the precise level of Oct-3/4 governs three distinct fates of ES cells.

33 tem (ES) cells to determine requirements for Oct-3/4 in the maintenance of developmental potency.

34 We suggest that silencing of Oct-3/4 in trophectoderm is a prerequisite for hCG up-re

35 In contrast, repression of Oct-3/4 induces loss of pluripotency and dedifferentiati

36 Thus a critical amount of Oct-3/4 is required to sustain stem-cell self-renewal, a

37 The transcription factor Oct-3/4 may be important in maintaining embryonic cells

38 studies argue that overexpression of neither Oct-3/4 nor Nanog broadly inhibits Sox2:Oct-3/4 target g

39 CGbeta fragment specifically bound synthetic Oct-3/4 protein as measured in electrophoretic mobility

40 Oct-3/4 reduced chloramphenicol acetyltransferase (CAT)

41 When stably transfected into JAr cells, Oct-3/4 reduced the amounts of both endogenous hCGbeta m

42 d mutagenesis of this binding site abolished Oct-3/4 repression.

43 Here we report that Oct-3/4 strongly inhibits the hCGbeta subunit (hCGbeta)

44 oreover, small changes in the levels of Sox2:Oct-3/4 target genes alter the fate of stem cells.

45 he diversity of mechanisms that control Sox2:Oct-3/4 target genes and argue that Sox2 functions as a

46 ther Oct-3/4 nor Nanog broadly inhibits Sox2:Oct-3/4 target genes.

47 ibits the endogenous expression of five Sox2:Oct-3/4 target genes.

48 Other studies have shown that Sox2 and Oct-3/4 work together cooperatively to stimulate the tra

49 s expressed stem cell markers ABCG2, Notch1, OCT-3/4, AnkG, and MUC1 but not TM markers AQP1, MGP, CH

50 levels of several 'stemness' genes including Oct-3/4, Bmi, beta-catenin, and SMO.

51 , a significant reduction of ALDH1, CD44 and Oct-3/4, key markers of pancreatic CSC was observed when

52 ipotent state-specific transcription factors Oct-3/4, Rex-1 and Nanog.

53 ssion of the Yamanaka reprogramming factors (Oct-3/4, Sox2, Klf4 and c-Myc [OSKM]) has been shown to

54 ectrophoretic mobility shift assays, and the Oct-3/4-binding site was localized around -270 by methyl

55 reprogramming of ECs, via overexpression of Oct-3/4-Sox-2-Klf-4 (OSK) transcription factors, we aime

56 mice were treated with LV control or LV with Oct-3/4-Sox-2-Klf-4 and evaluated 10 days post-infection

57 n) with empty vector (LV control) or LV with Oct-3/4-Sox-2-Klf-4.

58 uch as MMP9, PAI-1, and the stem cell factor OCT-3/4.

59 dependent on the binding sites for Sox2 and Oct-3/4.

60 ated with the transcription factors Sox2 and Oct-3/4.

61 c in vitro proteolytic cleavage product of N-Oct 3 and is not directly related to melanocyte malignan

62 ding N-Oct 3 directs synthesis of both the N-Oct 3 and N-Oct 5 proteins and that the N-Oct 5 protein

63 The neural POU-domain proteins N-Oct 3 and N-Oct 5 were first identified in electrophoret

64 mental to synergistic activation by Sox2 and Oct-3 and further emphasize the critical role of enhance

65 Consistent with this hypothesis, Oct-3 and Sox2 can participate in a direct protein-prote

66 s requires a synergistic interaction between Oct-3 and Sox2 on the FGF-4 enhancer.

67 Between Oct 3, and March 30, 2012, and Oct 1, and March 29, 2013

68 eyes of each patient were analyzed using the OCT-3, and analysis showed a statistically significant c

69 which bind the transcription factors Sox-2, Oct-3, and Sp1/Sp3, respectively.

70 done in the context of its interaction with Oct-3, as well as its ability to transactivate as a fusi

71 These observations indicate that Oct-3* assembly results from protein-protein interaction

72 Sox2 and Oct-3 bind cooperatively to the enhancer DNA through the

73 Sox2 and Oct-3 bind to adjacent sites within this enhancer to for

74 Sox-2 and Oct-3 bind to the enhancer and are required for the acti

75 te weak activation by Sox2 in the absence of Oct-3 but their deletion has no effect on the Sox2 x Oct

76 In addition, analysis of Oct-1/Oct-3 chimeras indicates that the Oct-3 homeodomain also

77 role in the formation of a functional Sox2 x Oct-3 complex.

78 at play a role in the activity of the Sox2 x Oct-3 complex.

79 function was only detected within the Sox2 x Oct-3 complex.

80 hat contribute to the activity of the Sox2 x Oct-3 complex.

81 t their deletion has no effect on the Sox2 x Oct-3 complex.

82 We have analyzed a number of Sox2 and Oct-3 deletion mutants to identify the domains within ea

83 We show here that a cDNA encoding N-Oct 3 directs synthesis of both the N-Oct 3 and N-Oct 5

84 intermediate to afford tricyclo[4.2.0.0(1,5)]oct-3-ene (23).

85 e, 3, 4, 5, 6, 7, and 2-carbenabicyclo[3.2.1]oct-3-ene at the B3LYP/6-311+G(3df, 2p)//B3LYP/6-31G lev

86 ive interaction contributes to the defect in Oct-3* formation observed for the enhancer spacing mutan

87 s of Oct-1/Oct-3 chimeras indicates that the Oct-3 homeodomain also plays a critical role in the form

88 eracts with POU domains of Oct-1, Oct-2, and Oct-3 in vitro in a DNA-independent manner.

89 racts from melanocytes and melanoma cells: N-Oct 3 is present in extracts from both melanocytes and m

90 g that a direct interaction between Sox2 and Oct-3 is necessary for enhancer function.

91 Total CNV area measured using SS OCT and SD OCT 3 mm x 3 mm OCTA were 0.949 +/- 1.168 mm(2) and 0.34

92 Multivariate analysis demonstrated that the OCT 3 o'clock temporal sector, average C:D ratio, vertic

93 in which the synergistic action of Sox2 and Oct-3 results from two major processes.

94 of commercial optical coherence tomography, OCT-3 (StratusOCT, software ver.

95 the co-activator p300 as a mediator of Sox-2/Oct-3 synergistic activation of a heterologous promoter,

96 interactions between the domains of Sox2 and Oct-3 that mediate their binding to DNA, but it also req

97 d a putative role for C/EBP-beta, OCT-1, and OCT-3 transcription factor binding sites in the minimal

98 Within Oct-3, we have identified two activation domains, the N-

99 , PEA-3, ETS-2, Sp-1, c-Myc, TBP, GATA-1 and Oct-3 were conserved in the promoter sequence.

100 of two transcriptional regulators, Sox2 and Oct-3, which bind to adjacent sites on the FGF-4 enhance

101 ancer to form a ternary protein-DNA complex (Oct-3*) whose assembly correlates with enhancer activity

102 s by the synergistic interaction of Sox2 and Oct-3 with the Fgf4 EC cell-specific enhancer.

103 1,4-bis(2-tert-butyl-2,3-diazabicyclo[2.2.2]oct-3-yl)-2,3,5,6-tetramethylb enzene-1,4-diyl dication.

104 honium) or serotonin (N-(1-azabicyclo-[2.2.2]oct-3-yl)-6-chloro-4-methyl-3-oxo-3,4-dihydro-2H-1 ,4-be

105 N-(R)-1-Aza-bicyclo[2.2.2]oct-3-yl-4-(11)C-methylsulfanyl-benzamide 2 was synthesi

106 N-(R)-1-Aza-bicyclo[2.2.2]oct-3-yl-4-(125)I-iodo-benzamide 3 was synthesized by ha

107 N-[2-(Pyridin-3-ylmethyl)-1-azabicyclo[2.2.2]oct-3-yl]benzo[b]furan-2-car boxamide (7a, TC-5619), a n

108 N-[(3R)-1-Azabicyclo[2.2.2]oct-3-yl]furo[2,3-c]pyridine-5-carboxamide (14, PHA-543,