ライフサイエンスコーパス: SP-B

1 SP-B induces a reversible folding transition at monolaye

2 SP-B is a member of the saposin-like family of proteins,

3 SP-B is expressed in a cell-type specific manner by the

4 SP-B is expressed in a cell/tissue-specific manner by th

5 SP-B is the only surfactant-associated protein absolutel

6 SP-B lyses negatively charged liposomes and was previous

7 SP-B(1-25), a peptide comprised of the N-terminal 25 ami

8 SP-B(9-36), synthesized with (13)C=O-labeled Ala residue

9 SP-B, a lung-specific, hydrophobic protein essential for

10 SP-B/C also interacted specifically with DOPG in 7:1 DPP

11 SP-B/C had no significant effect on DPPC-d(62) structure

12 SP-B/C had preferential interactions with DPPG in 1:1, 2

13 tide derived from human SP-B, residues 9-36 (SP-B(9-36)).

14 of surfactant-associated proteins A (SP-A), SP-B, SP-C, and SP-D; Clara cell-associated protein CC-1

15 rfactometry), mean +/- SEM contents of SP-A, SP-B, and SP-C (3.7 kD) were 7.1 +/- 1.4%, 1.8 +/- 0.2%,

16 The major postnatal increases for SP-A, SP-B, and SP-C occurred during the 1st, 2nd, and 3rd wee

17 On the 2nd day of life, contents of SP-A, SP-B, and SP-C were 13.4%, 8.4%, and 0.1%, respectively,

18 he onset of ARDS, and the responses of SP-A, SP-B, and SP-D differ in important ways.

19 e lung, the messenger RNAs (mRNAs) for SP-A, SP-B, and SP-D were expressed in both type II cells and

20 X to up-regulate its surfactant genes (SP-A, SP-B, and SP-D).

21 factant lipids and proteins, including SP-A, SP-B, SP-C, SP-D, ABCA3 (a lamellar body associated prot

22 d, both solid and papillary, expressed SP-A, SP-B, SP-C, SP-D, and thyroid transcription factor-1, bu

23 SP-A/SP-B(N)-treated infected mice showed significant reducti

24 C genes, and the potential roles of abnormal SP-B and SP-C expression and genetic variation in these

25 pressure, leading to a reorientation of all SP-B subunits in phase with one another.

26 other surfactant proteins were not altered (SP-B) or were modestly increased (SP-A and SP-D).

27 lymers are diminished relative to that of an SP-B-derived peptide and a peptoid-based mimic.

28 r the other SP-B fragments of SP-B(8-25) and SP-B(59-80), indicating a critical role for the proline

29 und that therapeutic treatment with SP-A and SP-B(N) 6 or 24 h after bacterial challenge conferred si

30 of K. pneumoniae-infected mice with SP-A and SP-B(N) conferred more protection against K. pneumoniae

31 SP-A and SP-B(N) were able to interact in solution (Kd = 0.4 muM)

32 ral microorganisms are resistant to SP-A and SP-B(N).

33 on spans two Sp1/Sp3 binding sites (SP-A and SP-B) and is necessary and sufficient for the observed e

34 d synergistically in vitro against SP-A- and SP-B(N)-resistant capsulated Klebsiella pneumoniae (sero

35 ctant phospholipid films containing SP-B and SP-B peptides, our experiments show that KL(4) improves

36 evident from decreased cytoplasmic CCSP and SP-B protein levels, enlargement and disorganization of

37 ies indicate a specific decrease in TTF1 and SP-B expressing cells correlating with reduced epithelia

38 tide polymorphisms, rs1130866 (also known as SP-B + 1580 C/T) and rs3024793, were associated with the

39 idue of lung pulmonary surfactant protein B (SP-B(1-25)) in a phospholipid bilayer (PB) was determine

40 Inability to produce surfactant protein B (SP-B) causes fatal neonatal respiratory disease.

41 Surfactant protein B (SP-B) deficiency is an autosomal recessive disorder that

42 l changes of pulmonary surfactant protein B (SP-B) due to the heterogeneous reaction with O(3), field

43 apoptosis and reduced surfactant protein B (SP-B) expression.

44 omoter activity of the surfactant protein B (SP-B) gene in respiratory epithelial cells.

45 Surfactant protein B (SP-B) is a 79-amino acid peptide critical to postnatal r

46 Surfactant protein B (SP-B) is a 79-residue essential component of lung surfac

47 Surfactant protein B (SP-B) is a hydrophobic, 79 amino acid peptide that regul

48 Surfactant protein B (SP-B) is a small, hydrophobic protein that is an essenti

49 Pulmonary surfactant protein B (SP-B) is an essential protein for lowering surface tensi

50 Surfactant protein B (SP-B) is detected in the airways as a sulfhydryl-depende

51 Surfactant protein B (SP-B) is essential to the function of pulmonary surfacta

52 Surfactant protein B (SP-B) is essential to the function of pulmonary surfacta

53 Surfactant protein B (SP-B) is one of two helical, amphipathic proteins critic

54 Surfactant protein B (SP-B) is required for the maintenance of biophysical pro

55 Surfactant protein B (SP-B) is secreted into the airspaces with surfactant pho

56 Surfactant protein B (SP-B) mRNA and protein are restricted to alveolar Type I

57 Surfactant protein B (SP-B) proprotein contains three saposin-like protein (SA

58 Surfactant protein B (SP-B), a hydrophobic protein of lung surfactant, is esse

59 RD (ESRD-HDL) included surfactant protein B (SP-B), apolipoprotein C-II, serum amyloid A (SAA), and a

60 ophobic amino acids in surfactant protein B (SP-B), on the structure and collapse of dipalmitoylphosp

61 ysterious but requires surfactant protein B (SP-B), which is synthesized as a precursor (pre-proSP-B)

62 rminal region of human surfactant protein-B (SP-B(1-25)) in dipalmitoylphosphatidylcholine (DPPC) and

63 t function and reduced surfactant protein-B (SP-B) expression.

64 nherited deficiency of surfactant protein-B (SP-B) is a fatal autosomal recessive disorder of lung ce

65 easure the turnover of surfactant protein-B (SP-B).

66 Surfactant B (SP-B) is a 79-amino acid peptide critical to postnatal r

67 The overlap of function between SP-B and SP-C helps explain why replacement surfactants

68 Both SP-B and SP-C eliminate squeeze-out of POPG from mixed D

69 For both SP-B and SP-C, a statistical windowed autocorrelation me

70 ibility of the hydrophobic domain created by SP-B folding may explain the key functional properties o

71 alogues of lung surfactant proteins B and C (SP-B and SP-C), two helical and amphiphilic proteins tha

72 alone; with 3% surfactant proteins B and C (SP-B/C); with SP-B/C and 5% surfactant protein A (SP-A);

73 on of the lung epithelial marker genes SP-C, SP-B and SP-A.

74 ung surfactant phospholipid films containing SP-B and SP-B peptides, our experiments show that KL(4)

75 However, whereas (DAPL + SP-B/C) and (DAPL + SP-B/C + SP-A) mixtures were similar to corresponding PL

76 nearly normal dynamic properties to (DAPL + SP-B/C + SP-A + NL), whereas phosphatidylcholine (PC) (5

77 The addition of NL to (DAPL + SP-B/C + SP-A) produced an increase in gamma(min) to 15

78 However, whereas (DAPL + SP-B/C) and (DAPL + SP-B/C + SP-A) mixtures were similar

79 dependent of cytokine stimulation, decreased SP-B promoter activity and mRNA expression in mouse lung

80 The different SP-B secondary structures reacted identically to increas

81 This cleavage event distinguishes SP-B production in type 2 cells from less complete proce

82 The non-specific nature of DPPC-SP-B(1-25) interactions allows for significant flexibili

83 Mutations in the gene encoding SP-B result in severe, fatal neonatal lung disease, and

84 f human monomer in the absence of endogenous SP-B dimer (hSP-B(mon), mSP-B-/-).

85 results suggest that the role of endogenous SP-B in host defense may be limited; however, synthetic

86 nt phospholipids, suggesting that endogenous SP-B may not play a significant role in alveolar host de

87 ther than in a synergistic manner to enhance SP-B promoter activity.

88 P-B +/- mice in order to selectively express SP-B in Type II cells or Clara cells of SP-B -/- mice.

89 that formation of homodimers is critical for SP-B function, the cysteine residue reported to be invol

90 tation of cis-DNA elements are necessary for SP-B promoter function.

91 mine the range of mechanisms responsible for SP-B deficiency, both alleles from 32 affected infants w

92 ken together, these data indicate a role for SP-B dimer in surface tension reduction in the alveolus.

93 ed; however, synthetic peptides derived from SP-B may be useful in the treatment of bacterial pneumon

94 mediary factor 2 (TIF2) stimulated human (h) SP-B promoter activity in a dose-dependent fashion in pu

95 Hereditary SP-B deficiency is caused by a variety of distinct mutat

96 y increasing membrane permeability; however, SP-B also lysed RBC, indicating that the membranolytic a

97 Human SP-B is the 79-amino acid product of extensive post-tran

98 e two transgenic lines which expressed human SP-B in Clara cells (mCCSP/hSP-B).

99 ate 3 transgenic lines which expressed human SP-B in Type II cells (mSP-C/hSP-B).

100 on in a synthetic peptide derived from human SP-B, residues 9-36 (SP-B(9-36)).

101 processing, sorting, and secretion of human SP-B monomer were crossed with SP-B +/- mice to achieve

102 of SP-B(1-25) (a shortened version of human SP-B) at the air-liquid interface.

103 d for retinoic acid stimulation of the human SP-B (hSP-B) promoter.

104 h cysteine residues 235 and 246 of the human SP-B proprotein were mutated to serine and cloned under

105 culture using polyclonal antibodies to human SP-B(8) (Phe(201)-Met(279)) and specific epitopes within

106 To determine if SP-B and SP-C might promote adsorption by inducing negat

107 To test the role of this bridge in SP-B function in vivo, a construct was generated in whic

108 a support a primary role for pepsinogen C in SP-B proteolytic processing in alveolar type 2 cells.

109 h two separate populations of alpha-helix in SP-B-a hydrophobic fraction associated with the lipid ch

110 cysteine residue reported to be involved in SP-B dimerization was mutated to serine (Cys(248) --> Se

111 oic acids (RA) and their receptors (RARs) in SP-B gene transcription.

112 ressed in peripheral lung tubules, including SP-B and pro-SP-C, was inhibited.

113 eas overexpression of pepsinogen C increased SP-B production.

114 xpression of CREB, ATF-2 and c-Jun inhibited SP-B promoter activity in NCI-H441 cells.

115 elivering murine or human proSFTPB cDNA into SP-B deficient mice restores surfactant homeostasis, pre

116 s also indicated that interactions involving SP-B/C and lipids led to exclusion of PC and PG lipids f

117 onensin; 3) the final cleavage of 9 to 8 kDa SP-B is a monensin-sensitive, post-Golgi event occurring

118 al N-terminal processing event of 9 to 8 kDa SP-B.

119 olytic cleavages to produce the mature 8-kDa SP-B.

120 Like SP-B(1-25), the peptoids were designed to adopt helical

121 ydrophobic proteins of lung surfactant (LS), SP-B and SP-C, are critical constituents of an effective

122 The 79-amino acid, mature SP-B peptide contains three intramolecular disulfide bon

123 nsgenic mice overexpressing SP-BN and mature SP-B peptide had significantly decreased bacterial burde

124 Absence of proSP-B and mature SP-B was associated with nonsense and frame-shift mutati

125 of saturated phosphatidylcholine and mature SP-B.

126 The bioactive, mature SP-B is derived from multistep post-translational proteo

127 ions or insertions, and low levels of mature SP-B expression were associated with four mutations.

128 no lamellar bodies, and expression of mature SP-B protein was disrupted when compared with the normal

129 reduced, as well as absent, levels of mature SP-B, likely caused by impaired processing of proSP-B.

130 pepsinogen C inhibited production of mature SP-B, whereas overexpression of pepsinogen C increased S

131 a SAPLIP domain corresponding to the mature SP-B peptide is essential for lung function and postnata

132 similar features and all functionally mimic SP-B(1-25) to some degree, it is notable that small diff

133 those of discrete peptides intended to mimic SP-B.

134 one and in the presence of 0.5-10 wt % mixed SP-B/C purified chromatographically from calf lung surfa

135 For 1-3 mol% SP-B(1-25), a return to a single lamellar phase above th

136 pid mixture T(m) is observed, but for 5 mol% SP-B(1-25) a significant isotropic component is observed

137 nts are conserved in human, rabbit and mouse SP-B genes.

138 t expressed hSP-B(C235S/C246S) in the murine SP-B-/- background survived the neonatal period.

139 f the mutant peptide in the wild-type murine SP-B background was invariably lethal in the neonatal pe

140 -B and suggest that overexpression of mutant SP-B in the wild-type background may be lethal.

141 Native SP-B aggregated and killed clinical isolates of Klebsiel

142 Synthetic peptides derived from native SP-B were effective at killing both Gram-positive and Gr

143 ssess the antimicrobial properties of native SP-B and synthetic peptides derived from the native pept

144 microbial and hemolytic activities of native SP-B were inhibited by surfactant phospholipids, suggest

145 Thirteen novel SP-B gene mutations were identified, which were not foun

146 The ability of SP-B(1-25) to fuse lipid lamellae via this mechanism, pa

147 In the absence of SP-B or SP-C, the unsaturated lipids are irreversibly lo

148 peptide based on the first 25 amino acids of SP-B also induces a similar folding transition at monola

149 at in the LS context, the combined action of SP-B and SP-C appears to facilitate cholesterol dynamics

150 stulated to result in diminished activity of SP-B.

151 to retain much of the biological activity of SP-B.

152 Addition of SP-B to liposomes composed of DPPC/PG (7:3) leads to mem

153 ensities reveal the preferential affinity of SP-B(1-25) for anionic phospholipids.

154 Simulations of a few mutated analogs of SP-B(1-25) also suggest that the charged amino acids are

155 Although the peptoid analogues of SP-B(1-25) studied here share many similar features and

156 f six different helical peptoid analogues of SP-B(1-25) to investigate the importance of mimicking it

157 f SP-B in some, but not all Type II cells of SP-B -/- mice, allowed postnatal survival, but resulted

158 ress SP-B in Type II cells or Clara cells of SP-B -/- mice.

159 restored in Type II cells or Clara cells of SP-B -/- mice.

160 t structurally specific oxidative changes of SP-B(1-25) (a shortened version of human SP-B) at the ai

161 plasia and increased the cellular content of SP-B.

162 Complete deficiency of SP-B in mice and humans results in lethal, neonatal resp

163 as to map the fusogenic and lytic domains of SP-B and assess the effects of altered fusion and lysis

164 The effect of SP-B(1-25) on lipid organization and polymorphisms was i

165 ing measurements to determine the effects of SP-B(1-25), the N-terminus peptide of lung surfactant-sp

166 Expression of SP-B by respiratory epithelial cells is regulated by dev

167 Expression of SP-B in some, but not all Type II cells of SP-B -/- mice

168 ot been seen for the other SP-B fragments of SP-B(8-25) and SP-B(59-80), indicating a critical role f

169 The fractional synthetic rate (FSR) of SP-B measured using the most abundant proteolytic fragme

170 In order to investigate the function of SP-B in these distinct cell types, transgenic mice were

171 protein) is essential for proper function of SP-B.

172 ature of the peptide in the functionality of SP-B(1-25) are established.

173 e a better understanding of the functions of SP-B and SP-C and the structural basis for their actions

174 The N-terminal half of SP-B (residues 1-37), which includes the nonhelical N-te

175 The C-terminal half of SP-B (residues 43-79), which includes helices 3, 4, and

176 ides corresponding to the N-terminal half of SP-B indicated that, in general, decreased fusion or lyt

177 map predominantly to the N-terminal half of SP-B.

178 Inhibition of SP-B production recapitulated the SP-B-deficient phenoty

179 e measured both the quantity and kinetics of SP-B tryptic peptides in tracheal aspirate samples of sy

180 rate study indicated that elevated levels of SP-B in the airspaces of transgenic mice did not confer

181 edicted helices and/or interhelical loops of SP-B and tested for fusion, lytic, and surface activitie

182 ess physiologic lung dysfunction and loss of SP-B expression than did WT animals.

183 The detailed topographical mapping of SP-B(1-25) and its dimer in PB provides new insights int

184 The generation of non-natural mimics of SP-B and SP-C has previously been restricted to step-by-

185 k, we created helical, non-natural mimics of SP-B(1-25) based on sequence-specific peptoid 17mers and

186 Mutation of SP-B CRE into a scrambled sequence reduced promoter acti

187 sent studies of the interfacial oxidation of SP-B(1-25) in a nonionizable 1-palmitoyl-2-oleoyl-sn-gly

188 the nearly complete homogeneous oxidation of SP-B(1-25), only a subset of the amino acids known to re

189 e structures are detected in the presence of SP-B, SP-C, or the native mixture of both proteins.

190 may explain the key functional properties of SP-B including their impact on phospholipid transport be

191 for the surface tension reducing property of SP-B.

192 indicate that the heterogeneous reaction of SP-B(1-25) at the interface is quite different from that

193 Structure-function relationships of SP-B are currently under investigation as the protein an

194 of the N-terminal 25 amino-acid residues of SP-B, is known to retain much of the biological activity

195 e the simulation results to the sequences of SP-B(1-25) in other organisms.

196 pe II epithelial cells, the cellular site of SP-B synthesis.

197 To examine the intracellular sites of SP-B processing, we carried out immunofluorescence cytoc

198 The asynchronous 2D IR spectrum of SP-B showed the presence of two alpha-helix components,

199 Knowledge of the structure of SP-B and its related peptides in bulk and monolayer phas

200 ontaining 1-5 mol% peptide, the structure of SP-B(1-25) remains constant, but (2)H and (31)P NMR spec

201 sm results and the solution NMR structure of SP-B(11-25) (CRALIKRIQAMIPKG) dissolved in CD(3)OH at 5

202 his disease, as de novo protein synthesis of SP-B in alveolar type 2 epithelial cells is required for

203 role for the highly conserved N-terminus of SP-B in the packing of lipid lamellae into surfactant la

204 quence of KL 4 is based on the C-terminus of SP-B, a naturally occurring helical protein that binds t

205 is critical for intracellular trafficking of SP-B and suggest that overexpression of mutant SP-B in t

206 t-Golgi event occurring prior to transfer of SP-B to lamellar bodies.

207 urfactant protein SP-B and peptides based on SP-B induce a reversible folding transition at monolayer

208 ion site shows a dominant negative effect on SP-B gene transcription.

209 acing and orientation of cis-DNA elements on SP-B promoter function in NCI-H441 cells, a human cell l

210 ated the effects of transcription factors on SP-B promoter expression by co-transfection experiments.

211 their binding to bacteria with which SP-A or SP-B(N) alone could not interact.

212 his behavior has not been seen for the other SP-B fragments of SP-B(8-25) and SP-B(59-80), indicating

213 s enhanced in transgenic mice overexpressing SP-B(N).

214 The anionic antimicrobial peptide SP-B(N), derived from the N-terminal saposin-like domain

215 mulations of the interactions of the peptide SP-B(1-25), which is a truncated version of the full pul

216 cid (PA) and a surfactant protein B peptide, SP-B(1-25).

217 significant impact on the behavior of (PL + SP-B/C + SP-A).

218 A genetic polymorphism (SP-B + 1580) is postulated to result in diminished activ

219 rations using SP-B(9-36) in place of porcine SP-B indicating that the peptide has the potential to mi

220 or (TTF)-1 and pro-surfactant protein-B (pro-SP-B), and mesenchymal (alpha-smooth muscle actin (alpha

221 eldin A blocked all processing of 42-kDa pro-SP-B whereas similar studies using monensin blocked the

222 that: 1) the first enzymatic cleavage of pro-SP-B to the 25-kDa intermediate is in the brefeldin A-se

223 ecific antisera showed colocalization of pro-SP-B with the endoplasmic reticulum resident protein BiP

224 Flank, Gly(284)-Ser(304)) propeptides of pro-SP-B.

225 The surfactant-specific protein SP-B decreases the mean domain size and polydispersity a

226 peptide of lung surfactant-specific protein SP-B, on the structure of palmitic acid (PA) monolayers.

227 aspects of the pulmonary surfactant protein SP-B and has been tested clinically as a therapeutic age

228 Lung surfactant protein SP-B and peptides based on SP-B induce a reversible fold

229 ion of the full pulmonary surfactant protein SP-B, with dipalmitoylphosphatidylcholine monolayers, wh

230 to the other hydrophobic surfactant protein SP-B.

231 st report of NMR data related to the protein SP-B, whose structure promises to help elucidate the mec

232 The hydrophobic proteins SP-B and SP-C promote rapid adsorption of pulmonary surf

233 proteins, including the hydrophobic proteins SP-B and SP-C, in charge of stabilizing the respiratory

234 d to study lung surfactant specific proteins SP-B and SP-C in monolayers of dipalmitoylphosphatidylgl

235 es based on the surfactant-specific proteins SP-B and SP-C on the morphology and function of surfacta

236 e cationic lung surfactant specific proteins SP-B and SP-C that induce structural changes in the mono

237 The hydrophobic surfactant proteins SP-B and SP-C greatly accelerate the adsorption of vesic

238 pectroscopy of pulmonary surfactant proteins SP-B and SP-C in lipid-protein monolayers at the air-wat

239 assess the effect of the surfactant proteins SP-B and SP-C on cholesterol distribution in membranes.

240 The hydrophobic surfactant proteins SP-B and SP-C promote rapid adsorption of pulmonary surf

241 contains the hydrophobic surfactant proteins SP-B and SP-C.

242 dy, we explore the possibility that proteins SP-B and SP-C induce the permeabilization of phospholipi

243 e influence of the two hydrophobic proteins, SP-B and SP-C, on the thermodynamic barriers that limit

244 The hydrophobic surfactant proteins, SP-B and SP-C, greatly accelerate the adsorption of the

245 gues of two hydrophobic surfactant proteins, SP-B and SP-C, have been incorporated into therapeutic a

246 The hydrophobic surfactant proteins, SP-B and SP-C, have important roles in surfactant functi

247 of the two hydrophobic surfactant proteins, SP-B and SP-C, which are thought to play pivotal roles i

248 ontaining -236/+39 base pairs (bp) of rabbit SP-B gene that is necessary and sufficient for high leve

249 udies showed that the activity of the rabbit SP-B minimal promoter (-236/+39 bp) is dependent on the

250 and orientation of cis-DNA elements reduced SP-B promoter activity indicating that proper alignment

251 id transcription factor 1 (TTF-1) stimulated SP-B gene expression in respiratory epithelial cells.

252 s similar to those of full-length, synthetic SP-B.

253 -3 mol% peptide and physiologic temperature, SP-B(1-25) partitions at the interface of negatively cha

254 ce of a novel DNA regulatory element, termed SP-B CRE, with the sequence TGAGGTCA in the SP-B minimal

255 , amphipathic 25mer from the amino terminus (SP-B(1-25)) exhibits surface-active properties similar t

256 activity, by comparison to natural LS, than SP-B(1-25).

257 required for lung function in vivo and that SP-B expression in Clara cells cannot substitute for thi

258 We find that SP-B increases the line tension, dipole density differen

259 These results indicate that SP-B fusion, lytic and surface activities map predominan

260 nd C-H/C-D band height ratios indicated that SP-B/C affected PC and PG lipids differently within the

261 and peak wavenumber analysis indicated that SP-B/C had no significant effect on the structure of DPP

262 Our results suggest that SP-B and SP-C accelerate adsorption through a mechanism

263 All those results suggest that SP-B and SP-C proteins promote the formation of proteoli

264 tion of micellar structures and suggest that SP-B(1-25) promotes the formation of a fluid isotropic p

265 The SP-B CRE sequence shared homology to cyclic AMP responsi

266 The SP-B derivatives selectively lysed bacterial membranes a

267 The SP-B minimal promoter sequence as well as the spacing an

268 Carriage of the C allele at the SP-B + 1580 site is associated with ARDS, septic shock,

269 Genotypic frequencies at the SP-B + 1580 site were T/T 183 of 402 (0.45), T/C 160 of

270 Of the 59 patients who were C/C at the SP-B + 1580 site, 21 (0.356) required mechanical ventila

271 ng diseases associated with mutations in the SP-B and SP-C genes, and the potential roles of abnormal

272 ed by a variety of distinct mutations in the SP-B gene and may be associated with reduced, as well as

273 SP-B CRE, with the sequence TGAGGTCA in the SP-B minimal promoter.

274 termolecular disulfide bond formation in the SP-B(1-25) dimer were also investigated.

275 otein, transgenic mice were crossed into the SP-B null background.

276 by a frameshift mutation in codon 121 of the SP-B gene (121ins2) and is characterized by rapidly prog

277 ere identified in the enhancer region of the SP-B gene and were required for retinoic acid stimulatio

278 iating the transcriptional regulation of the SP-B gene.

279 dicate that expression and processing of the SP-B proprotein to the mature peptide in Type II cells i

280 idues 35 and 46 (residues 235 and 246 of the SP-B proprotein) is essential for proper function of SP-

281 ibition of SP-B production recapitulated the SP-B-deficient phenotype evident by aberrant lamellar bo

282 tivate STAT3 synergistically, stimulated the SP-B promoter activity with retinoic acid, which is at l

283 The experiments suggest that the SP-B helix A has to rotate at an angle to form a disulfi

284 The objective was to determine whether the SP-B + 1580 CC genotype is associated with an increased

285 ay not be critical for the function of these SP-B mimics.

286 Here we present an alternative approach to SP-B mimicry that is based on sequence-random copolymers

287 -B transgenic mice were subsequently bred to SP-B +/- mice in order to selectively express SP-B in Ty

288 The increase in line tension due to SP-B indicates the protein avoids domain boundaries due

289 Untreated SP-B deficient mice develop fatal respiratory distress w

290 structures from in vitro preparations using SP-B(9-36) in place of porcine SP-B indicating that the

291 Circular dichroism has shown that when SP-B(1-25) interacts with negatively charged lipid vesic

292 ouse alveolar type II epithelial cells where SP-B is synthesized and processed.

293 d in alveolar type II epithelial cells where SP-B is synthesized and secreted.

294 pes, transgenic mice were generated in which SP-B expression was selectively restored in Type II cell

295 and 5% surfactant protein A (SP-A); and with SP-B/C, SP-A, and 8% neutral lipids (NL).

296 % surfactant proteins B and C (SP-B/C); with SP-B/C and 5% surfactant protein A (SP-A); and with SP-B

297 tion of human SP-B monomer were crossed with SP-B +/- mice to achieve expression of human monomer in

298 -C was observed in lungs of all infants with SP-B gene mutations.

299 affinity purified proteins interacting with SP-B CRE showed that it is a target for binding of membe

300 hology of lipid monolayers containing 1 wt % SP-B/C.

301 all, near-physiological contents of 1-2 wt % SP-B/C typically produced the maximum observed spectrosc