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

6 e coverage involving platelet-derived growth factor B.

7 directly interact with either C3b or cleaved factor B.

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

9 scription was positively influenced by sigma factor B.

10 At onset, autoantibodies targeting factor B (a component of the alternative pathway C3 conv

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 We demonstrated that anti-factor B antibodies enhance alternative pathway converta

47 ndrome with low C3 level, screening for anti-factor B antibodies might help guide indications for kid

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

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

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

51 SK RNA and positive transcription elongation factor b are critical for HEXIM1 subdiffusion and thus p

52 Bacterial alternative rescue factor B (ArfB) releases nascent peptides from ribosomes

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 acute postinfectious GN by identifying anti-factor B autoantibodies as contributing factors in alter

56 In acute postinfectious GN, anti-factor B autoantibodies were transient and correlated wi

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

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

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

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

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

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

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

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

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

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

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

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

69 The transcription factor B cell CLL/lymphoma 11B (BCL11B) is indispensable

70 Instead, the transcription factor B cell leukemia/lymphoma 6 (BCL6) acts in a cell-

71 identified overexpression of the prosurvival factor B cell lymphoma 2 (BCL-2) as a distinguishing fea

72 (BTB) domain of the oncogenic transcription factor B cell lymphoma 6 (BCL6) and leads to the proteas

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

74 g analysis, we report that the transcription factor B-cell leukemia/lymphoma 11A (BCL11A) is highly e

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 igate the possible association of Complement Factor B (CFB) rs4151667 (L9H) variants and their possib

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

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

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

94 1 of these proinflammatory genes, complement factor B (Cfb), in detail, because complement proteins s

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

96 5 and a AMD-associated variant in complement factor B (CFB, rs512559).

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

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

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

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

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

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

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

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

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

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

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

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

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

110 Factor B deficiency or pretreatment with an inhibitory a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 Over multiple cycles of flowing factor B, factor D, and C3 over the SPR chip, we amplifi

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

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

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

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

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

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

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

134 The serine protease factor B (FB) is a key node in the AP and is integral to

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

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

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

138 esized that circulating levels of complement factor B (FB), an important component of the alternative

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

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

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

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

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

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

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

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

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

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

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

150 ith elevated AH50 had increased levels of AP factors B, H, and properdin, and fewer showed a "hyperin

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

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

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

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

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

156 identified crucial antibody binding sites on factor B, including one correlated to disease severity.

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

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

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

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

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

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

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

164 he P-TEFb (positive transcription elongation factor b) kinase complex and for its recruitment to chro

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

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

167 y receptor for receptor activator of nuclear factor B ligand (RANKL), plays an essential role in regu

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

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

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

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

172 ports have identified MAF BZIP Transcription Factor B (MAFB) to be present in human beta-cells postna

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

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

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

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

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

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

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

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

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

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

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

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

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

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

187 ng RCAS/tv-a-induced platelet-derived growth factor B-overexpressing glioblastoma results in reduced

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

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

190 al loss of positive transcription elongation factor b (P-TEFb) activity, a key factor in promoting tr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

210 The Positive Transcription Elongation Factor b (P-TEFb) phosphorylates Ser2 residues of the C-

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

217 4 recruits positive transcription elongation factor b (P-TEFb) to stimulate RNA polymerase II phospho

218 vating the positive transcription elongation factor b (P-TEFb) via its release from the inhibitory 7S

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

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

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

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

223 The positive transcription elongation factor b (P-TEFb), composed of CDK9 and cyclin T, stimul

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

256 glycosidase (MYORG), platelet-derived growth factor B (PDGFB) and platelet-derived growth factor rece

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

258 Platelet-derived growth factor B (PDGFB) plays a crucial role in recruitment of

259 nfluence of a 1.5 kb platelet derived growth factor B (PDGFB) promoter.

260 tein homologous to human scaffold attachment factor B. phm-2(lf) mutant worms have an abnormal pharyn

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

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

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

264 t the host positive transcription elongation factor b (pTEFb) complex onto the viral trans-activation

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

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

267 using, and positive transcription elongation factor b releases (P-TEFb) paused complex after phosphor

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

269 0199), and complement component 2/complement factor B (rs4151667) were examined using multiplicative

270 ndothelial cadherin, platelet-derived growth factor B, S1P(1), and CCN1 (molecules associated with an

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

272 eoprotein K (HNRNPK) and scaffold-attachment factor B (SAFB), we demonstrate that these proteins inte

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

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

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

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

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

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

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

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

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

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

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

284 he Notch ligand DLL4 and transforming growth factor-b (TGF-beta) family ligands produced by sinusoida

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

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

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

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

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

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

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

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

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

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

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

296 Factor B was the most important single negative predicti

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