ライフサイエンスコーパス: DRB

1 DRB induced the appearance of short 0.4 to 0.8 kb TCRbet

2 DRB reduced the TNF-alpha-induced increase in MMP-9 mRNA

3 DRB sensitivity-inducing factor (DSIF or Spt4/5) is a co

4 DRB sequences isolated from three exotic cats demonstrat

5 DRB-induced apoptosis was independent of the cell cycle

6 7 of the 14 DRB molecules (DRB1*0401, 0101, 0404, 0405, DRB5*0101, D

7 tro binding of the OspA163-175 peptide to 14 DRB molecules.

8 ced the peptide binding regions (PBRs) of 41 DRB (= E beta) genes and eight DRA (= E alpha) genes fro

9 dentified, together with 19 DRB1*0406 and 43 DRB*w201 selective binders.

10 tored inhibition of microtubule sliding in a DRB- and CK1-7-sensitive manner.

11 We have isolated a DRB- and heparin-sensitive protein kinase activity that

12 tion at higher levels of DRB suggests that a DRB-resistant/stress-activated pathway may target serine

13 After DRB removal, cells are collected at several time points,

14 ition, p53 accumulating in the nucleus after DRB treatment was able to interact with MDM2 and was ubi

15 tested this hypothesis and found that after DRB treatment, p53 accumulated despite the fact that MDM

16 n sequencing (NGS) was used to determine all DRB alleles in consecutively diagnosed patients ages 1-1

17 The new alleles DRB*23 and DRB*24, were closely related to two other Ovc

18 with recombinant retroviruses for allogeneic DRB followed by BM transplantation.

19 Also, DRB abolished the inhibitory effect of the NMDAR antagon

20 ARC than to the well-known nucleoside analog DRB (5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole),

21 ces imply extensive maintenance of ancestral DRB alleles across species.

22 The new alleles DRB*23 and DRB*24, were closely related to two other Ovca-DRB exon

23 t with HMBA (hexamethylene bisacetamide) and DRB (5,6-dichlorobenzimidazole 1-beta-ribofuranoside), w

24 nd restores sensitivity to actinomycin D and DRB.

25 f apoptosis by M protein, actinomycin D, and DRB was inhibited in stably transfected HeLa cell lines

26 Transcripts of the MHC class II DRA and DRB gene homologues of the domestic cat (Felis catus) we

27 man and mouse MHCs, the domestic cat DRA and DRB genes have undergone multiple duplications and the D

28 absolute and relative rate tests on DRA and DRB genes imply increased substitution rates at two- and

29 , X2BP, NF-Y, and X-Y box DNA of the DRA and DRB genes were formed.

30 To test this hypothesis, DRA and DRB transcripts from 24 captive BHS (Ovca-DRA and Ovca-D

31 merly, casein kinase II), such as emodin and DRB, were able to duplicate the effects of H7 and H89.

32 ence of the cdk9 inhibitors Flavopiridol and DRB (5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole) a

33 we compared the ability of flavopiridol and DRB to inhibit transcription in vivo using nuclear run-o

34 is activity depends on both its RNaseIII and DRB domains.

35 The Mamu-DRB1*0406 and -DRB*w201 binding capacity of a set of 311 overlapping pe

36 ors rescued IFN-gamma-inducible HLA-DRA and -DRB mRNA and cell surface protein expression, demonstrat

37 l domain (CTD) of RNA polymerase II, such as DRB and H7, induced rapid nuclear accumulation of p53 pr

38 loro-1-beta- D -ribofuranosyl benzimidazole (DRB), a potent inhibitor of CDK9, the protein kinase sub

39 chloro-1-beta-D-ribofuranosyl benzimidazole (DRB), did not affect the enhancement of exocytosis produ

40 chloro-1-beta-d-ribofuranosyl-benzimidazole (DRB) and heparin.

41 chloro-1-beta-D-ribofuranosyl-benzimidazole (DRB) as well as by the kinase inhibitor H8 at concentrat

42 6-dichloro-1-D-ribofuranosyl-benzimidazole (DRB) or actinomycin D.

43 chloro-1-beta-d-ribofuranosyl-benzimidazole (DRB) suppressed CTD phosphorylation (especially serine 2

44 carries one RNaseIII and two dsRNA binding (DRB) domains, is a unique Arabidopsis RNaseIII enzyme re

45 is encodes five double-stranded RNA binding (DRB) proteins.

46 f p70 S6 kinase, which was inhibited by both DRB and flavopiridol.

47 topo I activity were unaltered by the brief DRB treatment.

48 ts Cdk9, we found that inhibition of Cdk9 by DRB or by siRNA could recapitulate the flavopiridol effe

49 PAIR-Emu interactions are not disrupted by DRB, which blocks transcription elongation without disru

50 inhibition of CK2 phosphorylation events by DRB (5,6-dichlorobenzimidazole) resulted in dramatic sen

51 found that long transcripts were induced by DRB from both the tet-responsive and beta-actin promoter

52 r release from transcriptional inhibition by DRB treatment, was suppressed in MEN epsilon/beta-deplet

53 l for in vitro transcriptional repression by DRB and activation by the Tat protein.

54 uced accumulation of MMP-2 was unaffected by DRB.

55 nd recipient are matched for HLA-A, -B, -C, -DRB, -DQB1 and -DPB1 alleles.

56 e association with a particular domestic cat DRB lineage, suggesting that these allelic lineages are

57 g of a single spirochetal peptide to certain DRB molecules is a marker for antibiotic-refractory Lyme

58 identified a second new and highly conserved DRB family (we named DRB7) whose members possess a singl

59 Consistently DRB and dominant-negative CDK9 completely abrogated TNF-

60 the RNA synthesis inhibitors actinomycin D, DRB, H7 and alpha-amanitin.

61 Treatment of cells with actinomycin D, DRB, or alpha-amanitin, specific inhibitors of Pol II, d

62 o blocked by dichlorofuranosylbenzimidazole (DRB), an inhibitor of transcription.

63 eca-DRB gene was seen comprising 61 distinct DRB alleles.

64 ividual cats contained three to six distinct DRB sequences, indicating that feline MHC maintains two

65 lineages), mouse (H-2Ebeta b, u, f), and dog DRB alleles.

66 urs after treatment, depending on the dose), DRB dramatically increased the levels of IVS1(Cbeta1)-co

67 olymerase II (Pol II) elongation by the drug DRB, suggesting also a negative role in vivo.

68 -NELF (negative elongation factor) and DSIF (DRB sensitivity-inducing factor)--and P-TEFb (positive e

69 Pol IIo(ser5)), and the pausing factor DSIF (DRB sensitivity-inducing factor) are still present at th

70 recruitment of the elongation factors DSIF (DRB Sensitivity-Inducing Factor), P-TEFb (Positive Trans

71 ants, four distinct clades of multiple dsRBM DRBs are always present with the exception of Brassicace

72 enetic approach, we show that multiple dsRBM DRBs are systematically composed of two different types

73 ptional elongation in the presence of either DRB or the HIV-1 Tat protein.

74 mical inhibitor of transcription elongation, DRB, had no effect on ASH1 recruitment or H3K27 methylat

75 mplicating segmental exchange of MHC-encoded DRB gene fragments as one of the evolutionary mechanisms

76 tive location and directionality of the Eqca-DRB, -DQA, -DQB and -DOB loci.

77 observed, but abundant variation in the Feca-DRB gene was seen comprising 61 distinct DRB alleles.

78 s resolved at least five monophyletic feline DRB allelic lineages (DRB*1 to *5), which are clearly di

79 urrence of recent gene duplication of feline DRB genes.

80 selection for nonrecognition sites of feline DRB sequences--in the process of evolution of DR molecul

81 ot prevent the accumulation of p53 following DRB treatment.

82 Furthermore, DRB significantly decreased the firing activity of PVN n

83 501) and Class II alleles (HLA-DRB*0401, HLA-DRB*0401 and HLA-DRB*0701).

84 02 and HLA-B*3501) and Class II alleles (HLA-DRB*0401, HLA-DRB*0401 and HLA-DRB*0701).

85 llele level for HLA-A, HLA-B, HLA-C, and HLA-DRB (n=116), or mismatched (n=166).

86 alleles (HLA-DRB*0401, HLA-DRB*0401 and HLA-DRB*0701).

87 These data suggest that certain HLA-DRB and DQB1 alleles, also associated with other T-cell-

88 When the other expressed HLA-DRB loci were examined, homozygosity for HLA-DRB4*01, en

89 n of collagen-induced arthritis (CIA) in HLA-DRB*0101+/+ (HLA-DR1+/+) mice, we investigated the immun

90 replicating a PheWAS on rs3135388 (near HLA-DRB, associated with multiple sclerosis) and performing

91 point analysis identified low levels of HLA-DRB (< 20%) and high levels of MYC (> 80%) as independen

92 GAD65 274-286 epitope in the context of HLA-DRB 1*0401, was incubated with antigen-presenting cells

93 The data suggest that HLA-DRB*11 may offer protection from trichiasis in trachoma

94 allele-specific amplification within the HLA-DRB locus.

95 nt studies have shifted the focus to the HLA-DRB locus.

96 nalyze sequence variation at these three HLA-DRB loci.

97 lovirus glycoprotein B presented through HLA-DRB*0701.

98 st class II beta chains, more similar to HLA-DRB, clawed frog Xela-F3, and nurse shark Gici-B.

99 ation analyses were performed on the two HLA-DRB loci haplotypes (DRB1-DRB3, -DRB4, or -DRB5).

100 Homologous DRB exon 2 sequences from 36 feral domestic cats through

101 number variation (CNV) at the hypervariable DRB locus within the MHC region to HPV seropositivity at

102 or histocompatibility complex (Mhc) class II DRB alleles, spanning 237 codons, were analyzed for phyl

103 allogeneic (n=4) or syngeneic (n=1) class II DRB genes and a drug-resistance marker.

104 ing animals, we found six different class II DRB major histocompatibility sequences.

105 cells with CTD kinase inhibitors, including DRB (5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole),

106 8 kb TCRbeta transcripts in vivo, indicating DRB enhances premature transcriptional termination.

107 that the kinase and mRNA synthesis inhibitor DRB (5,6-dichloro-1-b-D-ribofuranosylbenzimidazole) indu

108 ption elongation factor-b (P-TEFb) inhibitor DRB (5,6-dichloro 1-beta-d-ribofuranosylbenzinida-sole).

109 sensitivity to the transcriptional inhibitor DRB and to stimulate transcription at limiting nucleotid

110 phorylation or the transcriptional inhibitor DRB, prevented the reduced arteriolar tone and the enhan

111 0-fold excess of the commonly used inhibitor DRB, suggesting that the immobilized P-TEFb could be use

112 ion of P-TEFb function by the Cdk-inhibitor, DRB, or by small interfering RNA selectively blocked TNF

113 The CK1 inhibitors (DRB and CK1-7) and solubilization of CK1 restored microt

114 Instead, DRB reduces accumulation of gamma2 late mRNA in the cyto

115 Interestingly, DRB and siRNA reduced the levels of ICP22 but not those

116 ve monophyletic feline DRB allelic lineages (DRB*1 to *5), which are clearly distinct from those of h

117 t depleted of P-TEFb failed to generate long DRB-sensitive transcripts, but this activity was restore

118 ted extract lost the ability to produce long DRB-sensitive transcripts and this loss was reversed by

119 e describe five macaque MHC-II alleles (Mamu-DRB*w606, -DRB*w2104, -DRB1*0306, -DRB1*1003, and -DPB1*

120 esus macaque alleles Mamu-DRB1*0406 and Mamu-DRB*w201 have been purified, and quantitative binding as

121 ope in C5 was found to be restricted by Mamu-DRB*W201.

122 u-DRB1*0406 restricted) and HIV Env482 (Mamu-DRB*w201 restricted).

123 five offspring were identical at their Mamu-DRB loci, MHC class II differences are unlikely to accou

124 icted HA 307-319 epitope for binding to Mamu-DRB*w201 and HLA-DRB1*0101.

125 hosen for testing included both nuclear (MHC DRB) and mitochondrial DNA (cytochrome b) genes.

126 enic exchange generates repeated sets of MHC DRB polymorphisms.

127 We analyzed over 50 primate MHC DRB sequences, and identified nucleotide elements within

128 Moreover, DRB potently inhibited HIV-1 expression in chronically i

129 Patterns of ancestral polymorphism in mouse DRB alleles were also used to examine the tempo of synon

130 rations of topotecan or camptothecin but not DRB.

131 eta1)), consistent with the known ability of DRB to inhibit transcription.

132 Finally, addition of DRB reduces co-immunoprecipitation of ICP27 using an ant

133 The effect of DRB could not be explained by inhibition of DNA replicat

134 addition, we establish two novel effects of DRB not previously reported: intron stabilization and th

135 increased CK2alpha level and the effects of DRB on mEPSCs and NMDA-EPSCs.

136 We identified three other effects of DRB.

137 To examine the evolution of DRB alleles in related species, a phylogenetic analysis

138 dition, intracerebroventricular injection of DRB not only significantly reduced blood pressure and lu

139 Selective injection of DRB or emetine into the presynaptic or postsynaptic neur

140 transactivation function at higher levels of DRB suggests that a DRB-resistant/stress-activated pathw

141 Within 30 min of DRB removal, topo I relocalized to the nucleoli in the a

142 t kinase 9 (CDK9) for the phosphorylation of DRB sensitivity-inducing factor, negative elongation fac

143 lony-forming progenitors and the presence of DRB retrovirus transcripts in peripheral cells.

144 fficiency but is reversed by the presence of DRB sensitivity-inducing factor (DSIF).

145 ase-8 and cleavage of Bid in the presence of DRB, thereby facilitating the release of proapoptotic fa

146 e to efficiently elongate in the presence of DRB.

147 xamined the role of four DCLs, two AGOs, one DRB, and one RDR in controlling viral RNA accumulation i

148 Only DRB, the CK2 inhibitor, greatly reduced the amount of (3

149 ymes, as did treatment with actinomycin D or DRB.

150 of apoptosis by M protein, actinomycin D, or DRB.

151 Posttraining infusion of either U0126 or DRB significantly impaired long-term retention of fear c

152 y is DRB4-independent, and may involve other DRB proteins that compensate for loss of DRB4.

153 Nineteen out of 24 BHS (79%) Ovca-DRB exon 3 (beta2 domain) sequences were 100% identical

154 ripts from 24 captive BHS (Ovca-DRA and Ovca-DRB) were sequenced.

155 ca leukotoxin peptides to T(h) cells by Ovca-DRB alleles is equivalent to that of Ovar-DRB1 alleles.

156 eta1 domain) sequences, eight different Ovca-DRB cDNA sequences were identified in BHS.

157 ned genetic polymorphism at a MHC gene (Ovca-DRB) in a large sample, both numerically and geographica

158 sequences, this BHS herd yielded higher Ovca-DRB allelic diversity than that reported in the previous

159 B*24, were closely related to two other Ovca-DRB exon 2 genomic DNA sequences.

160 e 100% identical to previously reported Ovca-DRB genomic DNA sequences.

161 In the first phase, DRB caused a rapid decrease (within five minutes) of pre

162 9/cyclin T2b produced in Sf9 cells possessed DRB-sensitive kinase activity and functioned in transcri

163 e five double-stranded RNA binding proteins (DRBs) related to Drosophila R2D2 and mammalian TRBP and

164 plant double-stranded RNA binding proteins (DRBs), a group of non-catalytic factors containing one o

165 ute proteins (AGOs), dsRNA-binding proteins (DRBs), and RNA-dependent RNA polymerases (RDRs).

166 Remarkably, DRB inhibition sensitized cells to TNF-alpha-induced apo

167 le explanation for why RB expression rescues DRB inducibility in H2009.

168 and 5,6-dichloro-1-beta-D-ribobenzimidazole (DRB) and an siRNA targeting p300 on the presence of RNAP

169 th 5, 6-dichloro-1-beta-D-ribobenzimidazole (DRB), an RNA Pol II-dependent transcription elongation i

170 hlorobenzimidazole 1-beta-d-ribofurandoside (DRB), a reversible RNA synthesis inhibitor, also prevent

171 chlorobenzimidazole 1-beta-D-ribofuranoside (DRB) to estimate the elongation rates of over 2000 indiv

172 chlorobenzimidazone-1-beta-d-ribofuranoside (DRB).

173 ichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) and 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (

174 ichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) and alpha-amanitin, which inhibit RNAP II function

175 ichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) and alpha-amanitin.

176 ichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) and H-8.

177 ichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) at concentrations that inhibited [3H]uridine incorp

178 ichloro-1-beta-d-ribofuranosylbenzimidazole (DRB) blocked the splicing alteration induced by CPT, whi

179 ichloro-1-beta-d-ribofuranosylbenzimidazole (DRB) is an adenosine analog that has been shown to cause

180 ichloro-1-beta-d-ribofuranosylbenzimidazole (DRB) or 4,5,6,7-tetrabromobenzotriazole (TBB) significan

181 ichloro-1-beta-d-ribofuranosylbenzimidazole (DRB) sensitivity inducing factors (DSIF) and the negativ

182 ichloro-1-beta-d-ribofuranosylbenzimidazole (DRB) sensitivity-inducing factor (DSIF).

183 ichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) sensitivity-inducing factor and found that the IC(5

184 ichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), a compound that causes premature termination.

185 ichloro-1-beta-d-ribofuranosylbenzimidazole (DRB), a CTD kinase inhibitor.

186 ichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), a dominant-negative CDK9, and a CDK9-specific smal

187 ichloro-1-beta-d-ribofuranosylbenzimidazole (DRB), a specific inhibitor of cdk9.

188 ichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), an inhibitor of CDK7 TFIIH-associated kinase, CKI

189 ichloro-1-beta-d-ribofuranosylbenzimidazole (DRB), an inhibitor of CDK9, suppresses expression of gam

190 ichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), and actinomycin.

191 ichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), can partially inhibit the UV-induced phosphorylati

192 ichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), combined with a pulse of 4-thiouridine (4sU), to t

193 ichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), or infusion of the protein synthesis inhibitor ani

194 ichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), which inhibits the Tat-associated kinase, TAK (CDK

195 ichloro-1-beta-D-ribofuranosylbenzimidazole (DRB)-mediated transcriptional inhibition and the activat

196 ichloro-1-beta-D-ribofuranosylbenzimidazole (DRB).

197 ichloro-1-beta-D-ribofuranosylbenzimidazole (DRB, a CK2 inhibitor).

198 ichloro-1-beta-D-ribofuranosylbenzimidazole [DRB]-sensitivity-inducing factor) and the negative elong

199 cin D or 5,6-dichlorobenzimidazole riboside (DRB) causes VHL to be redistributed to the nucleus.

200 cin D or 5,6-dichlorobenzimidazole riboside (DRB).

201 Second, DRB upregulated full-length normal-sized c-myc mRNA, whi

202 cell cycle or ongoing DNA replication, since DRB induced similar levels of apoptosis in asynchronous

203 e establish an efficient system for studying DRB-sensitive steps of transcriptional elongation.

204 A control animal, which received a syngeneic DRB gene, rejected its kidney allograft in 120 days afte

205 c mRNA, which provided further evidence that DRB has effects besides regulation of premature terminat

206 The fact that DRB kills tumour-derived cells without employment of DNA

207 We found that DRB had a biphasic effect on T-cell receptor-beta (TCRbe

208 of the intron IVS1(Cbeta1), indicating that DRB exerts post-transcriptional actions.

209 First, we observed that DRB induced the appearance of heterodisperse TCRbeta tra

210 models of codon substitution to analyze the DRB genes of six mammalian species: human, chimpanzee, m

211 ive to primates, and decreased rates for the DRB genes of primates relative to ungulate and carnivore

212 analysis detected positive selection in the DRB genes in each of the six mammals examined.

213 ferences based upon the exon 2 region of the DRB loci are complicated by selection and recombination,

214 study was to determine which, if any, of the DRB proteins might also participate in a nuclear siRNA p

215 However, the inability of the DRB*0101 molecule to bind hLFA-1alpha(L330-342) suggests

216 with kidney allografts solely matched to the DRB transgene.

217 330-342) showed only an association with the DRB*04 alleles.

218 Third, DRB stabilized lariat forms of the intron IVS1(Cbeta1),

219 Five cats had three DRB sequences in a single allelic lineage, indicating th

220 ating that feline MHC maintains two to three DRB loci.

221 units in common, P-TEFb is more sensitive to DRB than is TFIIH, and most importantly, TFIIH cannot su

222 dramatically increased their sensitivity to DRB, directly demonstrating that apoptosis following inh

223 nitin without affecting their sensitivity to DRB, indicating that alpha-amanitin induces apoptosis so

224 tract desensitizes transcription in vitro to DRB.

225 afts, but with DRB matched to the transduced DRB, the one with the highest gene transduction rate sho

226 Two DRB chains, DRB5*0101 and DRB1*1501, are co-expressed in

227 15 shared two DRB DQB haplotypes.

228 nitiation complex (PIC) remained unaffected, DRB, an inhibitor of P-TEFb, prevented RNAPII from elong

229 A plot of LHRH mRNA level per cell versus DRB treatment time showed a rapid initial decay of LHRH

230 five macaque MHC-II alleles (Mamu-DRB*w606, -DRB*w2104, -DRB1*0306, -DRB1*1003, and -DPB1*06) that re

231 While DRB proteins have defined roles in miRNA and cytoplasmic

232 fully mismatched kidney allografts, but with DRB matched to the transduced DRB, the one with the high

233 The results obtained with DRB were duplicated in cells transfected with small inte

234 ho-p70 S6 kinase, and neurons protected with DRB and flavopiridol showed accumulation of the kinase i

235 In cells treated with DRB, the major effect was in the accumulation of viral R

236 Treatment with DRB had little effect on the presence of RNAPII or p300

237 inhibition can be rescued by treatment with DRB or H7.

238 Treatment with DRB or TBB significantly reduced the amplitude of evoked