ライフサイエンスコーパス: factor B

1 nction through activation of profactor D and factor B.

2 4 and the positive transcription elongation factor b.

3 wis rats treated with antibody against C4 or factor B.

4 IFN-gamma decreased in the presence of anti-factor B.

5 scription was positively influenced by sigma factor B.

6 OPQMN, but is epistatic to alternative sigma factor B.

7 ludes the binding sites of both factor H and factor B.

8 directly interact with either C3b or cleaved factor B.

9 ponent C4, and alternative pathway component factor B.

10 ent of the positive transcription elongation factor b.

11 subunit of positive transcription elongation factor b, a complex that inhibits OL maturation.

12 In free factor B, a pair of salt bridges binds the Arg(234) side

13 ups contain peptides related to antidiuretic factor-b (ADF-b), CRF-like diuretic hormone (DH37 and DH

14 -/-) and Crry(+/+)fB(-/-) mice with purified factor B (an essential protein of the alternative pathwa

15 Moreover, we found that properdin factor B, an alternative pathway complement activator th

16 Mutant C3 showed an increased affinity for factor B and a reduced binding to membrane cofactor prot

17 ility to AOM in mice deficient in complement factor B and C2 (Bf/C2(-/)(-)), C1qa (C1qa(-/)(-)), and

18 ment 3 (C3) and an HLA locus containing both factor B and C2 genes have also been implicated.

19 Activation of factor B and C3 in the middle ear lavage fluids was sign

20 y of CR2-fH in vitro was superior to mAbs to factor B and C5.

21 Mutations of the activating components factor B and complement C3 have also been reported.

22 HpSCs produced complement activation factor B and factor D which then enhanced C3 cleavage to

23 effects on positive transcription elongation factor b and HMBA inducible protein-1.

24 mutation resulted in increased C3 binding to factor B and increased net formation of the C3 convertas

25 sustained ability of CFHR4-bound C3b to bind factor B and properdin, leading to an active convertase

26 comprising positive transcription elongation factor b and RNA polymerase II.

27 aired the interaction of C3b with complement factor B and, consequently, formation of the active C3 c

28 Nuclear factor-B and MLCK signalling appear to be important down

29 on of TPN upregulated the downstream nuclear factor-B and myosin light-chain kinase (MLCK) signalling

30 d kinase/positive transcriptional elongation factor-b and NF-kappaB.

31 The combination of factors B and A increased failure by 24-fold, factors P

32 ual complement proteins revealed that C3 and factors B and D were essential for complex formation.

33 hat was inhibited by EDTA, in the absence of factor B, and by purinergic P2 receptor antagonists.

34 f Igs and the complement system proteins C3, factor B, and clusterin.

35 Using mice deficient in complement C1qa, factor B, and factor B/C2, we found that complement C3 a

36 ity of Tat to recruit positive transcription factor b, and poor processivity of RNA polymerase II (RN

37 intense staining for PLA2R, IgG4, C3, C5b-9, factor B, and properdin and very weak staining for C1q,

38 metalloproteinase 9, platelet-derived growth factor B, and S1P(1) receptor.

39 vent binding of both the activating protein, factor B, and the inhibitor, factor H, which are opposit

40 f Crry(-/-)fB(-/-) mice after injection with factor B, and the mice developed acute tubular injury.

41 or CD3epsilon, CD105, TLR4, CD14, complement factor B, and vimentin that distinguishes acute rejectio

42 al-derived factor-1, platelet-derived growth factor-b, and S100A4 in R-cells were downregulated by va

43 n Willebrand factor, platelet-derived growth factor-B, and VEGF-A.

44 Factor B- and C3-deficient mice were also studied to det

45 e of radiolabeled organisms showed that both factor B- and C3-deficient mice were less effective than

46 at levels similar to those of wild-type and factor B- and C3-deficient mice.

47 was decreased in the presence of serum from factor B- and C3-deficient versus wild-type mice.

48 of S. pneumoniae were greatly attenuated in factor B- and factor B/C2-deficient mice.

49 Anti-C3b and anti-factor B (anti-FB) IgG have been reported in three patie

50 Anti-factor B antibody inhibited the ability of MAA-specific

51 Treatment with anti-factor B antibody resulted in suppression of ocular comp

52 all MAA-sensitized Lewis rats injected with factor B antibody.

53 l growth factor, and platelet-derived growth factor-B as well as their respective receptors in human

54 During convertase assembly, factor B associates with C3b and Mg(2+) forming a pro-co

55 d C2 (Bf/C2(-/)(-)), C1qa (C1qa(-/)(-)), and factor B (Bf(-)(/)(-)).

56 Mice lacking factor B (Bf(-/-)), the initiator of the alternative pat

57 and inversely correlated with the results of factor B binding, C3b/iC3b deposition, and neutrophil as

58 uitment of the AP by mAb 2C7, as measured by factor B binding, occurred in a properdin-dependent mann

59 heterozygous C3 mutation was identified in a factor B-binding region in exon 41, V1636A (4973 T > C).

60 specific proteins from each pathway, such as factor B, C2, and C4b.

61 deficient in complement C1qa, factor B, and factor B/C2, we found that complement C3 activation and

62 iae were greatly attenuated in factor B- and factor B/C2-deficient mice.

63 ipts encoding alternative pathway components factor B, C3 and properdin, and C3a receptor and C5a rec

64 n = 5 donor lungs) induces C' components (C' factor B, C3, and GPCR kinase isoform 5), cytokines (IL8

65 haptoglobin, serum amyloid A, and complement factors (B, C3, and C9).

66 (-/-) B cells proliferate to the prosurvival factor B cell activating factor (BAFF).

67 The B cell-restricted transcription factor, B cell regulator of Ig(H) transcription (Bright)

68 The ASC survival factors B cell-activating factor of the tumor necrosis f

69 ls express reduced levels of the prosurvival factor B-cell lymphoma 2 and the integrin lymphocyte fun

70 ailed to express the T(FH) key transcription factor B-cell lymphoma-6 and other T(FH)-related molecul

71 hat NK-22 cells released the B-cell survival factor, B-cell activating factor belonging to the TNF fa

72 th expression of vascular endothelial growth factor, B-cell lymphoma extra-large protein, and Cyclin

73 from transplantation, the B-cell activating factor/B-cell ratio was significantly higher in subjects

74 oreactive EF response elicited in rheumatoid-factor B cells by DNA-containing immune complexes.

75 ls, we transferred anti-self-IgG (rheumatoid factor) B cells and their physiologic target Ag, anti-ch

76 In the absence of either factor, B cells activated for CSR frequently generate AI

77 Recently, polymorphisms in the factor B (CFB) and complement component 2 (CC2) genes we

78 he genes encoding complement factor H (CFH), factor B (CFB) and component 3 (C3) was determined.

79 ion of complement component 2(C2)/complement factor B (CFB) gene polymorphisms with age-related macul

80 the complement factor H (CFH) and complement factor B (CFB) genes has targeted the search for additio

81 isms in the complement component 2 (CC2) and factor B (CFB) genes, as potential functional variants a

82 or alpha (TNF-alpha) induction of complement factor B (CFB) in RPE cells.

83 es of complement component C3 and complement factor B (CFB) in the growth of cSCC.

84 Complement factor B (cfB) is an essential component of the alternat

85 TLR3, and TLR4 markedly enhanced complement factor B (cfB) synthesis and release by macrophages and

86 ression of complement components C3 (C3) and factor B (CFB) was increased.

87 A1), complement component 2 (C2), complement factor B (CFB), complement component 3 (C3), collagen ty

88 1 of these proinflammatory genes, complement factor B (Cfb), in detail, because complement proteins s

89 ine CCL2, SDF-1, and complements C3, C4, and factor B (CFB), were examined by real-time PCR and, sele

90 5 and a AMD-associated variant in complement factor B (CFB, rs512559).

91 lated by cocaine via platelet-derived growth factor B chain (PDGF-B).

92 ctor A (VEGF-A), and platelet-derived growth factor B chain (PDGF-BB), to stimulate MM cell different

93 an oncoprotein human platelet-derived growth factor B-chain (PDGF-BB) using two screened fluorescent

94 y capture and detect platelet-derived growth factor B-chain (PDGF-BB).

95 Clumping factor B (ClfB) from Staphylococcus aureus is a bifuncti

96 lysin (Hla H35L), CP5 conjugated to clumping factor B (ClfB), or CP8 conjugated to iron-surface deter

97 ponent 2, complement component 3, complement factor B, collagen type VIII alpha 1, and RAD51 paralog

98 C3 levels, and the mutant C3 interacted with factor B comparably to wild-type (WT) C3 to form a C3 co

99 mponent of positive transcription elongation factor b complex responsible for Ser2 phosphorylation.

100 ed P-TEFB (positive transcription elongation factor b) complexes in the transcriptionally inactive BR

101 use of human sera depleted of either C1q or factor B confirmed that LytA prevented activation of bot

102 he P-TEFb (positive transcription elongation factor-b) (CycT1:CDK9) C-terminal domain (CTD) kinase to

103 itionally show that the protective effect of factor B deficiency and CR2-fH treatment is sustained in

104 Factor B deficiency or pretreatment with an inhibitory a

105 er neutrophilic infiltration was observed in factor B-deficient mice compared with controls and local

106 Importantly, factor B-deficient mice developed a delayed and signific

107 Both C3- and factor B-deficient mice had increased fungal burdens in

108 While factor B-deficient mice showed an enhanced rate of death

109 of the amount of protection of that seen in factor B-deficient mice that lacked functional AP.

110 icient, mannan-binding lectin-deficient, and factor B-deficient mice with rabbit Abs against murine t

111 process (mean aortic diameter of 105+/-4% in factor B-deficient mice, P<0.001 compared with controls)

112 nulocytes restored the blistering disease in factor B-deficient mice.

113 Factor B-deficient or CR2-fH-treated mice were protected

114 Laser-induced CNV was analyzed in factor-B-deficient mice or in mice treated with CR2-fH,

115 To address this issue, we utilized a sigma factor B (DeltasigB) mutant where protease activity resu

116 human serum (NHS) was compared with that in factor B-depleted and C1q-depleted human serum.

117 Substitution of NHS with factor B-depleted sera abrogated these increases in iC3b

118 tial quenching was observed with C2, C3, and factor B-depleted sera, but was more pronounced with the

119 virions, and the mutants were neutralized by factor B-depleted serum but not by C4-depleted serum.

120 leted sera, but was more pronounced with the factor B-depleted serum.

121 re double-knockout for Crry and either C3 or factor B did not show priming, demonstrating dependence

122 mph nodes of donor animals treated with anti-factor B did not transfer EAAU to naive syngenic rats.

123 P-TEFb (positive transcriptional elongation factor b) events during elongation.

124 e generated using four purified proteins-C3, factor B, factor D, and target protein-and Mg(2+) to all

125 gG antibodies on the interaction of C3b with Factor B, Factor H, and complement receptor 1.

126 ctivated, resulting in the deposition of C3, factor B, factor H, and MAC in the area of photic lesion

127 er (CD3), and complement components C1q, C3, factor B, factor H, and membrane attack complex (MAC).

128 jor contributor to the effective temperature factor (B-factor) describing contrast loss and therefore

129 ty in crystals with high overall temperature factors (B-factors).

130 the alternative pathway complement proteases factor B (FB) and factor D (FD) and the central compleme

131 Coupling factor B (FB) is a mitochondrial inner membrane polypept

132 ulated C3 convertase have been identified in Factor B (FB) ligand binding sites.

133 deficient in the alternative pathway protein factor B (fB) were protected from traumatic SCI in terms

134 nt components or receptors including C3, C4, factor B (fB), factor properdin (fP), mannose-binding le

135 escued on a partial as well as on a complete factor B (fB)- or C3-deficient maternal background.

136 he generation of a novel mAb targeting human factor B (FB).

137 t growth factor-a (FGF-a), fibroblast growth factor-b (FGF-b), and fibroblast growth factor-8b (FGF-8

138 and VEGF, vIL-6, and basic-fibroblast growth factor (b-FGF) in mouse xenografts.

139 We propose that when factor B first associates with C3b, it bears two intact

140 ng that FH does not efficiently compete with factor B for C3b binding.

141 athway regulator factor H (FH) competes with factor B for C3b binding; however, the capability of FH

142 Direct competition of SCIN with factor B for C3b slightly decreased the formation of sur

143 The activated fragment of C3 (C3b) and factor B form the C3 proconvertase (C3bB), which is clea

144 Examination of mice deficient in factor B further indicated that the alternative pathway

145 lycoprotein, alpha-1 antitrypsin, complement factor B, haptoglobin, transthyretin, plasma retinol bin

146 kines interleukin-10 and transforming growth factor-b have been suggested, respectively, to play impo

147 Human platelet-derived growth factor B (hPDGFB) has been characterized in vitro and sh

148 cleavage of mouse complement component 3 and factor B in plasma and in retinal pigment epithelium/cho

149 derived factor 1 and platelet-derived growth factor B in the wound bed.

150 bunits of RNA pol III-specific transcription factor B, in adult myocardium under basal conditions.

151 treatment most significantly by 23-fold, and factor B increased it by 11-fold.

152 This activation was dependent on factor B, indicating involvement of the alternative path

153 to oligodendroglial platelet-derived growth factor B-induced tumors in Ctv-a mice with targeted dele

154 P-TEFb (positive transcription elongation factor b) inhibitors such as flavopiridol or 4-amino-6-h

155 s cleaved to C3b which, after recruitment of factor B, initiates formation of the alternative pathway

156 tumor necrosis factor-a, transforming growth factor-b, interleukin-1b, interleukin-6, endothelin-1, m

157 Factor B is a zymogen that carries the catalytic site of

158 onstitutes positive transcription elongation factor b, is a well-validated target for treatment of se

159 ein-protein interactions among transcription factors, (b) it captures combinatorial control of transc

160 eukaryotic-like gene C2)/YlfB (yeast lethal factor B), LegC3, and LegC7/YlfA] functionally mimic glu

161 of P-TEFb (positive transcription elongation factor b) levels caused by NF90 depletion.

162 ulated the expression of Tfh cell suppressor factor B lymphocyte-induced maturation protein 1 (Blimp-

163 egulation by IFN-gamma and the transcription factor B lymphocyte-induced maturation protein-1 (also k

164 The transcription factor B lymphocyte-induced maturation protein-1 (Blimp-

165 in response to IgM, CD40, B cell-activating factor/B lymphocyte stimulator, CpG, and LPS.

166 ntibody that neutralizes the B-cell survival factor, B-lymphocyte stimulator (BLyS).

167 -like protein 1 (CHI3L1), CHI3L2, complement factor B, matrix metalloproteinase 3, ECM-1, haptoglobin

168 o intraocular inflammation in EAAU, and anti-factor B-mediated inhibition of EAAU is due to diminishe

169 y period, and, surprisingly, all C3(-/-) and factor B(-/-) mice died by day 5.

170 Unexpectedly, we observed that C4(-/-) and factor B(-/-) mice were fully susceptible to disease, in

171 e with wild-type disease; however, C5-/- and factor B-/- mice developed no disease.

172 The transcription factor B-Myb plays a critical role in regulating gene ex

173 sitive transcription factors such as nuclear factor B (NFB), activator protein-1 (AP1) and heat shock

174 or-binding protein 2 (IGFBP-2), nerve growth factor (b-NGF), platelet-derived growth factor receptor

175 nesis within 10 min in wild-type (WT) and C2/factor B-null mice.

176 differences in S2238 cleavage between WT, C2/factor B-null, MBL-A(-/-), or MBL-C(-/-) sera; however,

177 umoniae induced increased gene expression of factor B of the alternative complement pathway and C3 in

178 trated that multiple components (C3, C4, and factor B) of the classical and alternative pathways are

179 However, using mice genetically deficient in factor B or C4, we have shown that the collagen Ab-induc

180 l and complement factors C1q, C4/C3, C2, C3, factor B or C5-depleted human sera, using anti-mouse imm

181 deficient in the alternative pathway protein factor B or mice treated with the alternative pathway in

182 or H, membrane cofactor protein, factor I or factor B, or by autoantibodies against factor H.

183 Genetic deficiencies in C1q, C4, factor B, or factor D all resulted in increased mortalit

184 The positive transcription elongation factor b (P-TEFb) (CDK9/cyclin T (CycT)) promotes mRNA t

185 pecialized positive transcription elongation factor b (P-TEFb) activation mechanism that is known to

186 4) and the positive transcription elongation factor b (P-TEFb) and facilitated transcriptional elonga

187 ctions between Runx1 and positive elongation factor b (P-TEFb) appose the silencer and enhancer in CD

188 rabidopsis positive transcription elongation factor b (P-TEFb) complex and influences global RNA poly

189 ent of the positive transcription elongation factor b (P-TEFb) complex, as a pivotal regulator of ske

190 Positive transcription elongation factor b (P-TEFb) complexes, composed of cyclin-dependen

191 ong to the positive transcription elongation factor b (P-TEFb) complexes, which phosphorylate the CTD

192 hown to be positive transcription elongation factor b (P-TEFb) dependent.

193 ease, that positive transcription elongation factor b (P-TEFb) directly regulates the initial recruit

194 The positive transcription elongation factor b (P-TEFb) exists in two forms in cells as follow

195 eased free positive transcription elongation factor b (P-TEFb) from its inhibitory 7SK snRNP.

196 ase of the positive transcription elongation factor b (P-TEFb) from the 7SK snRNP in a manner that is

197 gulated by positive transcription elongation factor b (P-TEFb) in association with bromodomain-contai

198 a role of positive transcription elongation factor b (P-TEFb) in the establishment of latent infecti

199 scription)-positive transcription elongation factor b (P-TEFb) interaction allowed for localization o

200 ers of the positive transcription elongation factor b (P-TEFb) involved in the release of "paused" RN

201 The positive transcription elongation factor b (P-TEFb) is a cyclin-dependent kinase that cont

202 The positive transcription elongation factor b (P-TEFb) is a key cellular transcription factor

203 The positive transcription elongation factor b (P-TEFb) is involved in physiological and patho

204 se II, the positive transcription elongation factor b (P-TEFb) is the critical kinase for transcripti

205 Positive transcription elongation factor b (P-TEFb) is the major metazoan RNA polymerase I

206 regulator of Pol II transcription elongation factor b (P-TEFb) kinase and, in complex with MLL fusion

207 ing of the positive transcription elongation factor b (P-TEFb) kinase was not increased.

208 ted by the positive transcription elongation factor b (P-TEFb) kinase, which is suppressed within the

209 nit of the positive transcription elongation factor b (P-TEFb) of RNA polymerase II (RNAPII).

210 Human positive transcription elongation factor b (P-TEFb) phosphorylates RNA polymerase II and r

211 ngation by positive transcription elongation factor b (P-TEFb) plays a central role in determining th

212 Positive transcription elongation factor b (P-TEFb) plays an important role in stimulating

213 The positive transcription elongation factor b (P-TEFb) promotes transcription elongation thro

214 gation and positive transcription elongation factor b (P-TEFb) recruitment are detected immediately a

215 The positive transcription elongation factor b (P-TEFb) regulates RNA polymerase II elongation

216 t recruits positive transcription elongation factor b (P-TEFb) to MHC class II promoters.

217 in hijacks positive transcription elongation factor b (P-TEFb) to phosphorylate and activate this pau

218 4 recruits positive transcription elongation factor b (P-TEFb) to stimulate RNA polymerase II phospho

219 (PCAF) and positive transcription elongation factor b (P-TEFb) to Tat/transactivation response-RNA co

220 cruits the positive transcription elongation factor b (P-TEFb) to the viral promoter.

221 binds the positive transcription elongation factor b (P-TEFb), a complex containing the cyclin-depen

222 Positive transcription elongation factor b (P-TEFb), a complex of Cdk9 and cyclin T1, prom

223 ivates the positive transcription elongation factor b (P-TEFb), an essential eukaryotic mRNA transcri

224 ing to the positive transcription elongation factor b (P-TEFb), and potentiates its transcriptional a

225 The positive transcription elongation factor b (P-TEFb), composed of cyclin-dependent kinase 9

226 Positive transcription elongation factor b (P-TEFb), composed of cyclin-dependent kinase 9

227 The positive transcription elongation factor b (P-TEFb), comprised of cyclin-dependent kinase

228 ion factor positive transcription elongation factor b (P-TEFb), the complex of cyclin T1 and CDK9.

229 mponent of positive transcription elongation factor b (P-TEFb), to target gene promoters, enhancing t

230 (RNAPII), positive transcription elongation factor b (P-TEFb), which is composed of CycT1 or CycT2 a

231 hibitor of positive transcription elongation factor b (P-TEFb), which regulates the transcription elo

232 lymerase II (Pol II) and positive elongation factor b (P-TEFb), which releases paused Pol II to produ

233 e DOT1 and positive transcription elongation factor b (P-TEFb).

234 F) IIH and positive transcription elongation factor b (P-TEFb).

235 ent on the positive transcription elongation factor b (P-TEFb).

236 r known as positive transcription elongation factor b (P-TEFb).

237 Ralpha and positive transcription elongation factor b (P-TEFb).

238 lex of the positive transcription elongation factor b (P-TEFb).

239 ction with positive transcription elongation factor b (P-TEFb).

240 CDK11 and positive transcription elongation factor b (P-TEFb).

241 ctivity of positive transcription elongation factor b (P-TEFb).

242 biting the positive transcription elongation factor b (P-TEFb, a complex of CDK9 and cyclin T), we ex

243 l cellular cofactor transcription elongation factor-b (P-TEFb) by binding simultaneously at the RNA b

244 C2 (complement component 2)-CFB (complement factor B) (P =5.2 x 10(-9)), C3 (complement component 3)

245 Positive transcription factor b, P-TEFb, is composed of cyclin-dependent kinase

246 me that pneumococcal adherence and virulence factor B (PavB) and pneumococcal surface protein C (PspC

247 tion of pneumococcal adherence and virulence factor B (PavB), a bacterial surface protein with orthol

248 ven by expression of platelet-derived growth factor B (PDGF-B) in lymphatic endothelial cells and sig

249 (HS) is required for platelet-derived growth factor B (PDGF-B) retention and platelet-derived growth

250 Because platelet-derived growth factor B (PDGF-B) signaling has a pivotal role in mesang

251 helial expression of platelet-derived growth factor B (PDGF-B), leading to mural cell recruitment the

252 of the gene encoding platelet-derived growth factor B (PDGF-B), which has proliferative and chemotact

253 g (Shh) is driven by platelet-derived growth factor B (PDGF-BB) in vascular smooth muscle cells, cont

254 bound to its target, platelet-derived growth factor B (PDGF-BB).

255 s also observed when platelet-derived growth factor-B (PDGF) controlled migration is studied in murin

256 rofibrotic peptides, platelet-derived growth factor-B (PDGF-B) and connective tissue growth factor (C

257 Inhibition of platelet-derived growth factor-B (PDGF-B) has multiple effects on tumors, includ

258 s TEAD binding, with platelet-derived growth factor-B (PDGF-B) resulted in high-grade tumors with MES

259 known tip cell genes platelet-derived growth factor B (PDGFB) and vascular endothelial cell growth fa

260 serum from MASP-1/3(-/-) mice as a source of factor B, pro-FD in 3T3 supernatants was cleaved into ma

261 pretreatment with an inhibitory antibody to factor B protected mice against Stx2/LPS-induced podocyt

262 in mice and a mutant form of the complement factor B protein that produces a stable, properdin-free

263 IgH gene and impacted positive transcription factor b (pTEFb), Ser-2 carboxyl-terminal phosphorylatio

264 categories: (a) cleavage of key RNA granule factors, (b) regulation of PKR activation, and (c) co-op

265 ctors TATA-binding protein and transcription factor B, respectively, which in turn are responsible fo

266 0199), and complement component 2/complement factor B (rs4151667) were examined using multiplicative

267 via modification of the Scaffold Associated Factor B (SAFB) protein, and the SUMOylated SAFB stimula

268 myces cerevisiae mitochondrial transcription factor B (sc-mtTFB).

269 biofilm phenotype was due to a lack of sigma factor B (SigB) activity.

270 an indication of decreased IB kinase-nuclear factor B signalling) in both obese and T2DM subjects, bu

271 Inhibition of the alternative pathway by factor B siRNA resulted in decreased levels of membrane

272 ase C3bB(Mg(2+)) that is cleaved at a single factor B site by factor D.

273 ental growth factor, platelet-derived growth factor B, stem cell factor (kit ligand), stromal-derived

274 less severe blistering disease compared with factor B-sufficient mice.

275 Transcription initiation factor B (TFB) is conserved in eukaryotes and archaea an

276 yrococcus furiosus encodes two transcription factor B (TFB) paralogs, one of which (TFB1) was previou

277 Eukaryotic transcription factor B (TFB) proteins are homologous to KsgA/Dim1 ribo

278 TATA-binding protein (TBP) and transcription factor B (TFB) to perform a genome-wide search for promo

279 Subsequent association of transcription factor B (TFB) with the TBP-DNA complex is followed by t

280 ATA box-binding protein (TBP), transcription factor B (TFB), transcription factor E (TFE) and the 12-

281 ch adjacent upstream sequence (transcription factor B (TFB)-responsive element (BRE)), which are boun

282 resistance by activating transforming growth factor b (TGF-b) signaling.

283 unization experiment using mice deficient in factor B that lack a functional alternative pathway of c

284 troduce single amino acid substitutions into factor B that preclude one or both of the Arg(234) salt

285 binding site on C3 for the Ba domain within factor B, thereby blocking an interaction essential for

286 complement factor 3 within the complex with factor B, thereby locking in the convertase in an inacti

287 S77 blocks binding of factor B to C3b inhibiting the first step in the formati

288 an factor H and, to a lesser degree, that of factor B to C3b.

289 uitment of positive transcription elongation factor b to the LTR promoter.

290 recruiting Positive Transcription Elongation Factor b to the promoter region.

291 A simple combination of standard CVD risk factors, B-type natriuretic peptide, and ankle-brachial

292 Vascular endothelial growth factor-B (VEGF-B) is a member of the VEGF family of grow

293 considered that vascular endothelial growth factor-B (VEGF-B), which promotes coronary arteriogenesi

294 Factor B was defined as a presence of chronic upper airw

295 Factor B was the most important single negative predicti

296 mmunoglobulin E, and platelet-derived growth factor B were modified with fluorescent nucleotide analo

297 d to wild-type mice, mice deficient in C3 or factor B were protected from acute dextran sulfate sodiu

298 ing factor)--and P-TEFb (positive elongation factor b), which is the key player in pause release.

299 x with the positive transcription elongation factor b, which controls phosphorylation of RNA polymera

300 As x value increases from 0.1, the quality factor B, which informs about how large a ZT can be expe