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

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

10 Between April 1, 1985, and Oct 2, 1991, 589 patients were enrolled and randomly ass

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

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

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

14 688 patients were recruited between Oct 2, 2008, and July 11, 2011, of which 564 patients wh

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

16 79 patients were enrolled in the study from Oct 2, 2009, to May 31, 2012.

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

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

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

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

21 Between Oct 2, 2015, and Oct 19, 2016, 48 participants were enro

22 Between Jan 22, 2014, and Oct 2, 2016, we assessed 364 patients, of whom 69 with R

23 Between Feb 7, 2014, and Oct 2, 2017, 5937 participants were enrolled and then ra

24 Between Oct 2, 2017, and Feb 28, 2019, 19 460 participants were

25 Between Oct 2, 2017, and Sept 12, 2019, 108 participants were ra

26 Between Feb 11, 2016, and Oct 2, 2018, 95 patients were enrolled.

27 hospitals in Uganda between Jan 13, 2016 and Oct 2, 2019.

28 Between June 18, 2018, and Oct 2, 2020, 1350 patients were assessed for eligibility

29 Between Feb 18 and Oct 2, 2020, 740 individuals were screened for eligibili

30 ected as the phase 2a recommended dose; from Oct 2, 2020, to June 27, 2021, 106 patients were randoml

31 for articles published from Jan 1, 1946, to Oct 2, 2023, using specific search terms such as "Tuberc

32 articipants collected from June 12, 2020, to Oct 2, 2023.1124 participants were included in the full

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 er off-flavors (2-pentylfuran, pyridine, (E)-oct-2-enal).

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

87 50-300 degrees C, 8-exo-methoxybicyclo[4.2.0]oct-2-ene (1a) undergoes a [1,3] sigmatropic rearrangeme

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

89 .0]oct-2-ene (1) isomerizes to bicyclo[2.2.2]oct-2-ene (2) via a formal [1,3] sigmatropic carbon migr

90 .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

91 , when 1-amino-methyl-2,3-diazabicyclo[2.2.2]oct-2-ene (DBOA) is complexed by the macrocycle beta-cyc

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

93 o-methylene double bond of the bicyclo[3.2.1]oct-2-ene adduct illustrated the potential postfunctiona

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

95 preparation of functionalized bicyclo[3.2.1]oct-2-ene and bicyclo[3.3.1]nonadiene via gold-mediated

96 aminyl radicals into 2,8-diazabicyclo[3.2.1]oct-2-ene systems.

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

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

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

100 -the deazetization of 2,3-diazabicyclo[2.2.2]oct-2-ene-for which we demonstrate that momentum dominat

101 to give an array of 1,6-dioxo-2-azaspiro[3.4]oct-2-enes and related spirocycles.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

119 OCT-2 immunostaining was primarily restricted in normal

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 odules in KpsC transfer 3-deoxy-beta-d-manno-oct-2-ulosonic acid (beta-Kdo) from cytidine-5'-monophos

173 3-Deoxy-beta-d-manno-oct-2-ulosonic acid (beta-Kdo) glycosides are mainly fou

174 id terminus containing 3-deoxy-beta-d- manno-oct-2-ulosonic acid (beta-Kdo).

175 acid, pseudaminic acid, and 3-deoxy-d-manno-oct-2-ulosonic acid (KDO) affords the hypothesis that su

176 yl dibutyl phosphates in the 3-deoxy-d-manno-oct-2-ulosonic acid (KDO) and pseudaminic acid series an

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

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

179 3-Deoxy-d-manno-oct-2-ulosonic acid (Kdo) is an essential component of b

180 3-Deoxy-d-manno-oct-2-ulosonic acid (Kdo) is an essential component of L

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

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

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

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

185 e MS shows the LPS-precursor 3-deoxy-D-manno-oct-2-ulosonic acid (Kdo)(2)-lipid A (KDL) can tune the

186 cting with the LPS-precursor 3-deoxy-D-manno-oct-2-ulosonic acid (Kdo)(2)-lipid A (KDL).

187 larly for the LPS-precursor, 3-deoxy-D-manno-oct-2-ulosonic acid (Kdo)(2)-lipid A (KDL).

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

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

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

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

192 ct-2-ulosonic acid (KO), and 3-deoxy-d-manno-oct-2-ulosonic acid (KDO).

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

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

195 f), d-glycerol 1-phosphate, d-glycero-d-talo-oct-2-ulosonic acid (KO), and 3-deoxy-d-manno-oct-2-ulos

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

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

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

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

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

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

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

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

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

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

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

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

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

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

210 (4-chlorophenyl)-8-methyl-8-azabicyclo[3.2.1]oct-2- yl]methyl](2-mercaptoethyl)amino]ethyl]amino]-eth

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

212 (4-chlorophenyl)-8-methyl-8-azabicyclo[3,2,1]oct-2-yl]methyl ](2-mercaptoethyl) amino]ethyl]-amino]et

213 4-chlorophenyl)-8-methyl-8-azabicyclo [3.2.1]oct-2-yl]methyl](2-mercaptoethyl)amino]ethy] amino]ethan