ライフサイエンスコーパス: Oct-2

1 for the octamer motif-binding protein (OCT-1/OCT-2).

2 he CD36 promoter refractory to activation by Oct-2.

3 oexpression of Oct-4 but not either Oct-1 or Oct-2.

4 than the closely related POU domain protein Oct-2.

5 wn to interact with POU domains of Oct-1 and Oct-2.

6 ple of a gene activated in neuronal cells by Oct-2.

7 groove within the binding site for Oct-1 or Oct-2.

8 s but MDA-MB-231 also express high levels of Oct-2.

9 ithin the COOH-terminal activation domain of Oct-2.

10 represses neuronal differentiation, whereas Oct-2.2 activates neuron formation.

11 ent with a role in neuronal differentiation, Oct-2.2 expression is induced during differentiation, an

12 ts and Freedoms, came into full operation on Oct 2, 2000.

13 688 patients were recruited between Oct 2, 2008, and July 11, 2011, of which 564 patients wh

14 Between Oct 2, 2009, and June 22, 2011, we recruited 15 patients

15 79 patients were enrolled in the study from Oct 2, 2009, to May 31, 2012.

16 completed all four 72 h study stays between Oct 2, 2013, and July 29, 2014, and consumed all the foo

17 Between May 15, 2012, and Oct 2, 2013, we did an open-label phase 2 trial in patie

18 Between March 13, 2012, and Oct 2, 2013, we randomly assigned 515 participants: 260

19 Between Oct 2, 2014, and Nov 30, 2015, we recruited 807 people w

20 ression experiments demonstrate that isoform Oct-2.4 represses neuronal differentiation, whereas Oct-

21 is study, we show that MiR-210 is induced by Oct-2, a key transcriptional mediator of B cell activati

22 We conclude that Oct-2 activates CD36 gene expression in mouse B cells vi

23 nce the B-cell-specific transcription factor Oct-2 also directly interacts with Z and inhibits its fu

24 Rather, Ikaros affected the expression of Oct-2 and Bcl-6, other transcription factors that direct

25 and immunoglobulin production, although both Oct-2 and Bob-1 are required for a proper immune respons

26 tigations have shown increased expression of Oct-2 and Bob-1 in lymphomas, and we observed greatly in

27 These include RFX, X2BP, NF-Y, CIITA, OCT-2 and Bob1.

28 dition, human hs4 enhancer activity required Oct-2 and correlated with expression of Oct coactivator

29 The CD86-induced increase in Oct-2 and IgG1 was less when either Phb1/2 expression wa

30 eased expression of the transcription factor Oct-2 and its coactivator OCA-B (Oct coactivator from B

31 es that the POU2 family transcription factor Oct-2 and its cofactor Bob-1 have an important function

32 uring differentiation, and cells depleted of Oct-2 and its homolog Oct-1 have a reduced capacity to d

33 hat promote NF-kappaB activation to increase Oct-2 and mature IgG1 mRNA and protein expression, as we

34 These results indicate that Oct-2 and OCA-B interact with the 3' enhancer in regulat

35 r selective Ig isotype expression defects in Oct-2 and OCA-B null mice.

36 We therefore examined the impact of Oct-2 and OCA-B on ORF50 activation.

37 We show the lack of Oct-2 and OCA-B transcription factors to be responsible,

38 le transcription factors including Oct-1 and Oct-2 and the high mobility group (HMG) protein HMGI(Y)

39 those for the transcription factors IRF and Oct-2 and was coincident with activation and differentia

40 enter B cells and plasma cells, where HoxC4, Oct-2, and Oca-B expression correlates with hs1,2 activa

41 HoxC4, Oct-1/Oct-2, and Oca-B recruitment is negligible in pro-B cell

42 at MAT1 interacts with POU domains of Oct-1, Oct-2, and Oct-3 in vitro in a DNA-independent manner.

43 When crossed to Oct-2(+/-) animals, transheterozygotes were recovered at

44 Gene-targeting studies showed that Oct-1 and Oct-2 are largely dispensable for B-cell development and

45 Oct-1 and Oct-2 are members of the POU homeodomain family of trans

46 Our results show that OCA-B and Oct-2 are regulatory partners in this process and that P

47 DNA-binding specificity mutants of Oct-1 and Oct-2 are used to examine their function from varied reg

48 cells and identify the C-terminal domain of Oct-2 as responsible for its unique function in these ce

49 his enhancer was specifically dependent upon Oct-2, as contrasted to the closely related Oct-1 transc

50 ranscription factors, Oct-1 (ubiquitous) and Oct-2 (B lineage specific), which bind the octamer motif

51 oct-2-/- B cells displayed aberrant behavior during acti

52 In MDA-MB-231 cells, both Oct-1 and Oct-2 bind the iNOS promoter, forming a higher-order com

53 equence because mutations that blocked Oct-1/Oct-2 binding also eliminated inhibition of the B29 prom

54 elements FROG, TOAD, and the A+T-rich Oct-1/Oct-2 binding motif may be essential for normal B cell d

55 Allele-specific suppression of mutant Oct-2 binding sites in this enhancer by a variant Oct-2

56 kinase A-dependent manner to cooperate with Oct-2 binding to the 3'-IgH enhancer.

57 Oct-1/Oct-2 binding was required for the inhibitory activity o

58 The cellular protein Oct-1, but not Oct-2, binds to the K-bZIP element in a sequence-specifi

59 d stable-transfection assays bound Oct-1 and Oct-2, both of which are expressed constitutively in mac

60 ictates the relative potency of Oct-1 versus Oct-2 bound to a promoter.

61 amer element can be bound by either Oct-1 or Oct-2 but requires the expression of Oct-2 to activate t

62 ding pattern formed by NF-kappaB, Oct-1, and Oct-2 (but not by Pax5).

63 Inactivation of Oct-2 by gene targeting results in normal B cell develop

64 Oct-1 and Oct-2 can bind specifically to a site at base pair -55 i

65 ependent expression of genes like the B cell Oct 2 coactivator (OCA-B).

66 nstrate that CD36 is the first example of an Oct-2-dependent gene whose expression in B cells is inde

67 ing activity in vitro and the suppression of Oct-2-directed transcription in vivo.

68 ecursor B cells led to the loss of inducible Oct-2 DNA binding activity in vitro and the suppression

69 in, we have mutated specific residues in the Oct-2 domain in an attempt to probe their importance in

70 Our data suggest that Oct-2 downregulation in infected cells would be favorabl

71 As Ig promoter-binding factors, Oct-1 and Oct-2 each work together with a B lymphocyte-specific co

72 At 300 degrees C, bicyclo[4.2.0]oct-2-ene (1) isomerizes to bicyclo[2.2.2]oct-2-ene (2)

73 50-300 degrees C, 8-exo-methoxybicyclo[4.2.0]oct-2-ene (1a) undergoes a [1,3] sigmatropic rearrangeme

74 At 275 degrees C, 8-exo-methylbicyclo[4.2.0]oct-2-ene (1a) undergoes a [1,3] sigmatropic rearrangeme

75 .0]oct-2-ene (1) isomerizes to bicyclo[2.2.2]oct-2-ene (2) via a formal [1,3] sigmatropic carbon migr

76 .1]octa-2,6-diene (7), tricyclo[3.2.1.0(4,6)]oct-2-ene (8), and tetracyclo[3.3.0.0(2,8)0(4,6)]octane

77 yl)-1-phenylamino-2-phenyl-cis-bicyclo[3.3.0]oct-2-ene 5 is described.

78 thermal reactions exhibited by bicyclo[4.2.0]oct-2-ene and 7-d and 8-d analogues at 300 degrees C hav

79 ner exploited a rigid 6,8-dioxabicyclo[3.2.1]oct-2-ene template.

80 r than [1,3] shifts leading to bicyclo[2.2.2]oct-2-ene, and the ratio of rate constants for [1,3] car

81 identified 8-benzyl-4-oxo-8-azabicyclo[3.2.1]oct-2-ene-6,7-dicarboxylic acid (SD-1008) as a micromola

82 series of substituted 2,3-diazabicyclo[2.2.2]oct-2-enes and some simpler model systems have been stud

83 tification of substituted cis-bicyclo[3.3.0]-oct-2-enes as small molecule agonists of subfamily V orp

84 nt to 5-exo- and 5-endo-methoxybicyclo[2.2.2]oct-2-enes, 2a and 2b, respectively, with a clear prefer

85 ropic rearrangement to 5-methylbicyclo[2.2.2]oct-2-enes, of which the orbital symmetry-allowed si pro

86 to diaryl substituted tricyclo[3.2.1.0(4,6)]oct-2-enes.

87 and phosphorylated RelA (p65) and increased Oct-2 expression and binding to the 3'-IgH enhancer, in

88 he level of NF-kappaB activation, as well as Oct-2 expression and binding to the 3'-IgH enhancer.

89 Remarkably, if we sustain Oct-2 expression during cell fusion, all the other tissu

90 In the present study, we monitored Oct-2 expression in cells arrested for the activation of

91 Manipulation of Oct-2 expression in these cell lines demonstrates that i

92 constitutively expressed in many cell types, Oct-2 expression is restricted primarily to B lymphocyte

93 nNOS gene regulatory region is activated by Oct-2 expression vectors upon cotransfection into both n

94 se two signaling pathways leads to increased Oct-2 expression, increased gene activity mediated by NF

95 phoma hybrids can be prevented by preserving Oct-2 expression.

96 d the relative binding affinity of Oct-1 and Oct-2 for the variant octamer motif and determined the f

97 A 40 amino acid region of Oct-2 from amino acids 142 to 181 functions as an active

98 l defect correlated with a specific block to Oct-2 gene expression at the level of transcription, whe

99 OCT-2 immunostaining was primarily restricted in normal

100 s the expression of the transcription factor Oct-2 in a protein kinase C- and NF-kappaB1-dependent ma

101 e further evidence for an essential role for Oct-2 in Ig-secreting cells and identify the C-terminal

102 and we observed greatly increased levels of Oct-2 in lymphoma cells with the t(14;18) translocation.

103 ment and a stringent gene dosage effect with Oct-2 in mediating postnatal survival.

104 discussed in terms of the potential role of Oct-2 in regulating nNOS expression in the nervous syste

105 gh the variant octamer motif binds Oct-1 and Oct-2 in vitro with 5-fold lower affinity than the conse

106 Furthermore, Oct-2 induced bcl-2 promoter activity and mediated this

107 These findings indicate that Oct-2 induction of MiR-210 provides a novel inhibitory m

108 e POU domain transcription factors Oct-1 and Oct-2 interact with the octamer element, a motif conserv

109 We conclude that Oct-2 is required for B-1 cell maintenance and for norma

110 Here we show that Oct-2 is required for normal humoral responses upon immu

111 itous and regulates a variety of genes while Oct-2 is restricted to B-cells and neurones.

112 The finding that Oct-2 is under NF-kappaB control highlights an important

113 The POU domain transcription factor, Oct-2, is essential for the B cell-specific expression o

114 atly reduced in neuronal cell lines in which Oct-2 levels have been reduced by an antisense method, a

115 not detected in animals with a reconstituted oct-2-/- lymphoid system.

116 neuronal differentiation, and indicate that Oct-2 may serve as a binary switch to repress differenti

117 In order to determine how Oct-2 mediates expression of CD36 in B cells, we cloned

118 homa hybrids established a critical role for Oct-2 not only in maintaining Ig gene expression, but in

119 oct-2-null T cell behavior was normal, implying a B cell

120 nhancer-binding proteins tested (E2-2, Pu.1, Oct-2, OCA-B, TFE3 and USF) were able to activate I(mu)

121 We found that Oct-2, on the other hand, inhibited ORF50 expression and

122 of the B cell-specific transcription factors Oct-2 or OCA-B/BOB-1/OBF-1 dramatically affects B cell t

123 Decreased expression of Oct-1, Oct-2, or Bob-1 by RNA interference resulted in apoptosi

124 This suggests that Oct-2 plays a central role in maintaining the gene expre

125 Oct-1 (POU2f1) and Oct-2 (POU2f2) are members of the POU family of transcri

126 Oct-1 and the related but tissue-restricted Oct-2 protein bind to a DNA sequence termed the octamer

127 binding sites in this enhancer by a variant Oct-2 protein revealed that in a mature B cell line this

128 Phosphorylation of the Oct-2 protein was important for this activation and was

129 between Oct-1 and Oct-2 using chimeric Oct-1/Oct-2 proteins in cell fusion assays.

130 g Ig, J chain, and the transcription factors Oct-2, PU.1, and the coactivator OCA-B.

131 The POU transcription factors Oct-1 and Oct-2 regulate the activity of octamer-dependent promote

132 These findings support the notion that Oct-2 regulates gene transcription by both OBF-1-depende

133 Oct-1 and Oct-2 represent the prototypical example of related tran

134 amer-binding transcription factors Oct-1 and Oct-2, respectively.

135 transcription as induced by HoxC4 and Oct-1/Oct-2 suggests an important role of these homeodomain pr

136 ing sites for transcriptional factors Oct-1, Oct-2, T cell factor 1alpha, and GATA1.

137 Oct-2, therefore, acts as a cell survival factor in t(14

138 tation analysis we found that the ability of Oct-2 to activate bcl-2 required C/EBP, Cdx, and TATA-bi

139 ct-1 or Oct-2 but requires the expression of Oct-2 to activate transcription in B cells.

140 ly expressed Oct-1 and the B cell-restricted Oct-2 to activate transcription via the octamer site (5'

141 ctivator that functions with either Oct-1 or Oct-2 to mediate efficient cell type-specific transcript

142 directly, but interacts with either Oct-1 or Oct-2 to potentiate transcriptional activation.

143 ssociated with increased binding of PU.1 and Oct-2 to the CD20 promoter sequences.

144 ressed POU-homeodomain proteins Oct-1 and/or Oct-2 to these octamer-like sequences plays a central ro

145 mer binding transcription factors (Oct-1 and Oct-2) to mediate efficient cell type-specific transcrip

146 Here we report that overexpression of the Oct-2 transcription factor and octamer coactivator BOB.1

147 The Oct-2 transcription factor has been shown previously to

148 Targeted mutation of the gene for the Oct-2 transcription factor in mice caused neonatal letha

149 has been shown previously to bind Oct-1 and Oct-2 transcription factors in vitro.

150 s studies suggested that the 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) homopolymeric capsular p

151 8)Kdo(2-->4)Kdo (Kdo = 3-deoxy-alpha-d-manno-oct-2-ulopyranosonic acid), displays a germ-line-coded p

152 3-Deoxy-beta-d-manno-oct-2-ulosonic acid (beta-Kdo) glycosides are mainly fou

153 first committed step in the 3-deoxy-D-manno-oct-2-ulosonic acid (Kdo) biosynthesis pathway.

154 In plants, 3-deoxy-d-manno-oct-2-ulosonic acid (Kdo) is a monosaccharide that is on

155 3-Deoxy-d-manno-oct-2-ulosonic acid (Kdo) is an essential component of b

156 3-Deoxy-d-manno-oct-2-ulosonic acid (Kdo) is an essential component of L

157 educing end by a beta-linked 3-deoxy-d-manno-oct-2-ulosonic acid (Kdo) residue.

158 ulted in increased levels of 3-deoxy-d-manno-oct-2-ulosonic acid (Kdo) sugar in membrane extracts, wh

159 aA catalyzes the transfer of 3-deoxy-d-manno-oct-2-ulosonic acid (Kdo) to the lipid A precursor of LP

160 recombinants expressing the 3-deoxy-D-manno-oct-2-ulosonic acid (Kdo) transferase gene kdtA of C. tr

161 annose (Man) and one each of 3-deoxy-d-manno-oct-2-ulosonic acid (Kdo), Gal, GalN, and l-rhamnose res

162 esize an isosteric analog of 3-deoxy-D-manno-oct-2-ulosonic acid (Kdo), known as D-glycero-D-talo-oct

163 CPS via multiple residues of 3-deoxy-D-manno-oct-2-ulosonic acid (Kdo), referred to as a poly-Kdo lin

164 anno-heptose (Hep) and 3-deoxy-alpha-D-manno-oct-2-ulosonic acid (Kdo)-containing inner core oligosac

165 d-heptose), but not by 3-deoxy-alpha-d-manno-oct-2-ulosonic acid (Kdo).

166 hemical reporter 8-azido-3,8-dideoxy-d-manno-oct-2-ulosonic acid (Kdo-N3) has been reported, its inco

167 osonic acid (Kdo), known as D-glycero-D-talo-oct-2-ulosonic acid (Ko), in which the axial hydrogen at

168 Substrates containing the 3-deoxy-d-manno-oct-2-ulosonic acid disaccharide are dephosphorylated at

169 ety with a beta-linked poly-(3-deoxy-d-manno-oct-2-ulosonic acid) (poly-Kdo) linker attached to the r

170 Kdo (3-deoxy-d-manno-oct-2-ulosonic acid) is an eight-carbon sugar mostly con

171 inated by a beta-linked Kdo (3-deoxy-d-manno-oct-2-ulosonic acid) residue added by a third GT module

172 of anhydro-Kdo (4,7-anhydro-3-deoxy-d-manno-oct-2-ulosonic acid) with Arg343 and Asp325.

173 the functional differences between Oct-1 and Oct-2 using chimeric Oct-1/Oct-2 proteins in cell fusion

174 One transcription factor, Oct-2, was studied in detail and found to be a bifunctio

175 Oct-1 and Oct-2 were recruited to the enhancer upon macrophage sti

176 the downstream 5.1 promoter is activated by Oct-2, whereas the 5.2 promoter is unaffected.

177 These two sites recruit HoxC4 and Oct-1/Oct-2, which act synergistically with the Oca-B coactiva

178 otifs, we observed the direct interaction of Oct-2 with all three sites both in vitro by EMSA and in

179 Interaction of Oct-1 and Oct-2 with the B29 A+T-rich sequence was confirmed using

180 ain containing transcription factor Oct-1 or Oct-2, with the B-cell-specific coactivator OCA-B (Bob-1

181 (4-chlorophenyl)-8-methyl-8-azabicyclo[3.2.1]oct-2- yl]methyl](2-mercaptoethyl)amino]ethyl]amino]-eth

182 -chlorophenyl)-8-methyl-8-azabicyclo [3.2.1] oct-2-yl]-methyl] (2-mercaptoethyl) amino] ethyl] amino]

183 (4-chlorophenyl)-8-methyl-8-azabicyclo[3,2,1]oct-2-yl]methyl ](2-mercaptoethyl) amino]ethyl]-amino]et

184 4-chlorophenyl)-8-methyl-8-azabicyclo [3.2.1]oct-2-yl]methyl](2-mercaptoethyl)amino]ethy] amino]ethan