ライフサイエンスコーパス: bile salt

1 suggested residual enterohepatic cycling of bile salts.

2 flexneri strain 2457T following exposure to bile salts.

3 using hydropropyl-cyclodextrins (HP-CDs) and bile salts.

4 tance of enteric bacteria to acetic acid and bile salts.

5 biliary tree from the detergent activity of bile salts.

6 mal plasma levels ( approximately 10 muM) of bile salts.

7 engaged in the enterohepatic circulation of bile salts.

8 cterial outer membrane following exposure to bile salts.

9 ce to pepsin and pancreatin and tolerance to bile salts.

10 both all exhibited increased sensitivity to bile salts.

11 ering response of Salmonella and Shigella to bile salts.

12 ociated with increased circulating levels of bile salts.

13 R upregulated leuO expression in response to bile salts.

14 e type III secretion system 2 in response to bile salts.

15 regulated carRS transcription in response to bile salts.

16 rC complex activates VtrB in the presence of bile salts.

17 ention of toxic bile constituents, including bile salts.

18 M, and its activity requires the presence of bile salts, a class of physiological anionic detergents.

19 eres with basolateral uptake of unconjugated bile salts, a process mediated by organic anion-transpor

20 together with kinetic analysis, reveals that bile salts act as partial non-competitive inhibitors of

21 Bile salts act as steroidal detergents in the gut, and c

22 In rat liver, excess levels of bile salts activate a GAPDH-mediated transnitrosylation

23 ings of this study indicate that hydrophobic bile salts activate GPBAR1 on GBSM, and this leads to ac

24 Bile salts activate the Shigella T3SS but repress the Sa

25 s, cucurbit[n]urils, DNA, serum albumins and bile salt aggregates are presented that describe the typ

26 A co-crystal structure of VtrA/VtrC with bile salt, along with biophysical and mutational analysi

27 We recently reported that CamSA, a bile salt analog, inhibits C. difficile spore germinatio

28 ed by increases in concentrations of biliary bile salt and a reduced cholesterol saturation index.

29 The kinetics of passage of a model bile salt and complete porcine bile across a dialysis me

30 For both, a model bile salt and complete porcine bile, rate coefficients d

31 strategies to accelerate renal excretion of bile salt and other toxins should be beneficial for pati

32 but not of wcaG, decreased susceptibility to bile salts and abrogated invasion of intestinal cells.

33 onstrates that the hydrophobic chamber binds bile salts and activates the virulence network.

34 nsive to various environmental cues, such as bile salts and alkaline pH, but how these factors influe

35 study, we define mechanisms of resistance to bile salts and build on previous research highlighting i

36 FRAP) analysis demonstrated that exposure to bile salts and Ca(2+) together decreases the recovery ra

37 ry transporters, which expose hepatocytes to bile salts and cause chronic inflammation that develops

38 n sugar composition, promoting resistance to bile salts and cell wall integrity.

39 y important roles in H. pylori resistance to bile salts and ceragenins.

40 ining envZP41L also became more resistant to bile salts and colicin V and grew 50% slower in vitro in

41 E. coli MG1655 mot-1 is more resistant to bile salts and colicin V than E. coli MG1655 DeltaflhD a

42 an important physiological route to recycle bile salts and ensure intestinal absorption of dietary l

43 not placebo, effectively reduced total serum bile salts and fibroblast growth factor 19 levels, but o

44 cubations with serial 2-fold dilutions of 10 bile salts and four ceragenins, which are novel bile sal

45 flexneri 2457T biofilms determined that both bile salts and glucose were required for formation, disp

46 ype, resulting in a reduction of circulating bile salts and liver injury.

47 ed by decreases in biliary concentrations of bile salts and phospholipids and an increases in the cho

48 permeability barrier and hypersensitivity to bile salts and sodium dodecyl sulfate.

49 Bile salts and steroid hormones are biosynthesized from

50 he protonation of biliary glycine-conjugated bile salts and uncontrolled cell entry of the correspond

51 rs have not been identified, taurocholate (a bile salt) and glycine (an amino acid) have been shown t

52 Taurocholate (a bile salt) and glycine (an amino acid) have been shown t

53 C. difficile spores require taurocholate (a bile salt) and glycine (an amino acid) to germinate.

54 of deoxycholate, a pro-lithogenic secondary bile salt, and increasing the fraction of intestinal cho

55 genous organic anions, including biliverdin, bile salts, and BSP, were predominantly excreted by way

56 increased intrahepatic and biliary levels of bile salts, and deficiency in repression of CYP7A1 (at t

57 displayed higher levels of plasma AST, ALT, bile salts, and hepatic necrosis after 3 days of BDL tha

58 chemical signals examined included glucose, bile salts, and preconditioned media from E. coli/Shigel

59 defense against detergents such as EDTA and bile salts, and resistance to antimicrobial peptides pol

60 RS was significantly more sensitive to acid, bile salts, and sodium dodecyl sulfate stresses.

61 in 2457T was subcultured in media containing bile salts, and the ability of the bacteria to adhere to

62 und two key microbial pathways for degrading bile salts, and the impact of bile acid composition in t

63 results show that both steroid hormones and bile salts are able to increase C. sordellii spore germi

64 Furthermore, our work confirms that bile salts are important physiological signals to activa

65 Hydrophobic bile salts are thought to contribute to the disruption o

66 mainly from the reduced level of enzymes and bile salts, as well as the higher gastric pH in the infa

67 f the Lab4 probiotic consortium to hydrolyse bile salts, assimilate cholesterol and regulate choleste

68 , reduction of hepatic cholesterol and serum bile salts, bilirubin, and transaminase levels.

69 The difference in bile salt (BS) composition between rodents and humans is

70 a-D-glucan (betaG) and arabinoxylan (AX) and bile salt (BS) or diluted porcine bile, were identified

71 tually leads to cholestasis, and this causes bile salt (BS)-mediated toxic injury of the "upstream" l

72 mprovement, we studied the biliary output of bile salts (BS) and the functional expression of the can

73 dylcholine aqueous dispersions stabilized by bile salts (BS) under simulated intestinal conditions (p

74 osed of soybean phosphatidylcholine with the bile salts (BSs) cholate (Ch), glycocholate (GC), chenod

75 langiocytes from the proapoptotic effects of bile salts by maintaining them deprotonated.

76 We then show that a set of bile salts cause dimerization of the transmembrane trans

77 Here, we show that bile salts cause widespread protein unfolding and aggreg

78 re, using NMR and DSF, it was shown that the bile salts cholate and chenodeoxycholate interact with p

79 eys tolerate cholestasis by altering hepatic bile salt composition, while maintaining normal plasma b

80 ch, which is attributed to the high acid and bile salt concentrations present.

81 protect periportal hepatocytes from harmful bile salt concentrations.

82 sion site, conferring full resistance to the bile salt deoxycholate, improving the efficiency of cell

83 growth and tolerance during stress from the bile salt deoxycholate.

84 ues are affected by the interaction with the bile salts deoxycholate, chenodeoxycholate, and taurodeo

85 We then found bile salt-dependent effects of these cysteine mutations

86 sed against a pathological onco-glycoform of bile salt-dependent lipase isolated from the pancreatic

87 e does not affect virulence, Ca(2+) enhances bile salt-dependent virulence activation for V. cholerae

88 for formation, dispersion was dependent upon bile salts depletion, and recovered bacteria displayed i

89 minated hydrophobic tail was combined with a bile salt derivative, divinyl benzene (DVB), and a photo

90 e salts and four ceragenins, which are novel bile salt derivatives that mimic membrane-disrupting act

91 Strong and selective binding of bile salt derivatives was obtained, depending on the cro

92 Surprisingly, bile salt destabilization of ToxRp enhanced the interact

93 challenged with a high fat/high cholesterol/bile salt diet, T39(-/-) mice or mice with hepatocyte-sp

94 SEC length fractionation can be achieved for bile salt dispersed SWCNTs by using porous silica-based

95 Thus, both cholesterol and the putative bile salt efflux pump HefC play important roles in H. py

96 induced by environmental signals, including bile salts, encountered in the small intestine prior to

97 (-/-) mice, along with a decrease in urinary bile salt excretion.

98 h retrieval of the canalicular transporters, bile salt export pump (Abcb11) and multidrug resistance-

99 rum alpha-fetoprotein and undetectable liver bile salt export pump (ABCB11) expression.

100 the two main canalicular bile transporters, bile salt export pump (BSEP) and multidrug resistance pr

101 age induces a Fyn-dependent retrieval of the bile salt export pump (Bsep) and multidrug resistance-as

102 l intrahepatic cholestasis-1 (FIC1), 18 with bile salt export pump (BSEP) disease, and 4 others with

103 tasis type 2 patients and how they relate to bile salt export pump (BSEP) expression and its (re)targ

104 The bile salt export pump (BSEP) is an ATP-binding cassette

105 The liver-specific bile salt export pump (BSEP) is crucial for bile acid-de

106 Bile salt export pump (BSEP) is responsible for biliary

107 ced cholestasis due to the inhibition of the bile salt export pump (BSEP) is well investigated, only

108 As a canalicular bile acid effluxer, the bile salt export pump (BSEP) plays a vital role in maint

109 esistance-associated protein 2 (MRP2) and of bile salt export pump (BSEP) variants and mutants.

110 encies in the gene ABCB11, which encodes the bile salt export pump (BSEP), a liver-specific adenosine

111 salt secretion is mediated primarily by the bile salt export pump (Bsep), a transporter on the canal

112 expression; small heterodimer partner (SHP), bile salt export pump (BSEP), and increased Cyp7A1.

113 reactive metabolite formation, inhibition of bile salt export pump (BSEP), and mitochondrial dysfunct

114 is a result of mutations in ABCB11 encoding bile salt export pump (BSEP), the canalicular bile salt

115 lysis showed that Sumo1 was recruited to the bile salt export pump (BSEP), the small heterodimer part

116 by WIF-B9/R cells, which do not express the bile salt export pump (BSEP).

117 r (FXR), small heterodimer partner (SHP) and bile salt export pump (BSEP).

118 e [organic solute transporter alpha/beta and bile salt export pump (BSEP)] promoter reporter activity

119 The bile salt export pump (BSEP/ABCB11) transports bile salt

120 sed the hyperosmolarity-induced retrieval of bile salt export pump from the canalicular membrane.

121 ile salt export pump (BSEP), the canalicular bile salt export pump of hepatocyte.

122 holestasis, namely ABCB11, which encodes the bile salt export pump, and ABCB4, which encodes hepatoca

123 amily B, member 11 (ABCB11) gene encodes the bile salt export pump, which is exclusively expressed at

124 in HE-iPSCs, resulting in the expression of bile salt export pump.

125 Despite the elevation in toxic bile salts, expression of genes involved in bile salt ho

126 lability by forming insoluble complexes with bile salts/fatty acids, inhibiting micelle formation.

127 /-)(low) mice, were sensitive to hydrophobic bile salt feeding (0.3% glycochenodeoxycholate); they ra

128 le salt export pump (BSEP/ABCB11) transports bile salts from hepatocytes into bile canaliculi.

129 at serves as the primary system for removing bile salts from the liver.

130 dent bile acid transporter (ASBT) transports bile salts from the lumen of the gastrointestinal (GI) t

131 ocess as the major transporter of conjugated bile salts from the plasma compartment into the hepatocy

132 We found that the toxic bile salt glycochenodeoxycholate (GCDC) rapidly fragment

133 as previously shown that the presence of the bile salts glycocholate and taurocholate in the small in

134 e primary and secondary binding sites of the bile salt glycodeoxycholate.

135 rs were severely cholestatic, with levels of bile salts >1 mM, but no evidence of necrosis, fibrosis,

136 he capacity of MdtM to catalyse electrogenic bile salt/H(+) antiport.

137 -term feedback regulation of Ntcp by primary bile salts has not yet been investigated in vivo.

138 explanation for the antimicrobial effects of bile salts, help explain the beneficial effects of bile

139 bile salts, expression of genes involved in bile salt homeostasis and detoxification were not affect

140 out the ability to secrete bile, we examined bile salt homeostasis in larval and adult lampreys.

141 rotein nitrosylation (via dithiothreitol) on bile salt homeostasis in male Wistar rats placed on a ch

142 Adaptive control of cholestasis, including bile salt homeostasis, is necessary for recovery and sur

143 a ligand for nuclear receptors that modulate bile salt homeostasis.

144 e observed within the physiological range of bile salts; however, growth was inhibited at higher conc

145 lly reducing the genus Lactobacillus and its bile salt hydrolase (BSH) activity leading to the accumu

146 Using this approach we show that bacterial bile salt hydrolase (BSH) mediates a microbe-host dialog

147 lpha-hydroxylase mRNA expression, implicates bile salt hydrolase activity as a potential mechanism of

148 asmic function-sigma factors, a urease and a bile salt hydrolase.

149 conjugated bile acids-generated by bacterial bile salt hydrolases (BSH)-correlated with faster transi

150 g for genes encoding glyosyltransferases and bile salt hydrolases.

151 the predominant bile salt, whereas the major bile salts in adult liver were sulfated C27 bile alcohol

152 lt synthesis, indicating that elevated serum bile salts in Fut2(-/-)(high) mice were not explained by

153 hanism of de novo synthesis and secretion of bile salts in intestine after developmental biliary atre

154 Total bile salts in plasma were extremely elevated (up to 1,50

155 Importantly, the presence of secondary bile salts in the circulation suggested residual enteroh

156 s from a biochemical imbalance of lipids and bile salts in the gallbladder bile.

157 Resistance to high concentrations of bile salts in the human intestinal tract is vital for th

158 ulation of the biosynthesis and transport of bile salts in the liver and intestine.

159 -Gln-Trp, and Leu-Gln-Lys-Trp, and different bile salts in the submicellar or micellar state was inve

160 ivers reflecting increased concentrations of bile salts in these conditions.

161 y include elevated biomarkers of aspiration (bile salts) in bronchoalveolar lavage fluid (BALF).

162 owed by a 2 h incubation with pancreatin and bile salts including a cellulose dialysis tubing (molecu

163 It has been shown that a set of bile salts, including taurocholate, serve as host signal

164 In an in vitro setting, we demonstrate that bile salts increase SPI-6 antibacterial activity and tha

165 Acid and bile salts increased CDX2 messenger RNA (mRNA), protein,

166 ide new insights into the mechanism by which bile salts induce V. cholerae virulence but also suggest

167 talized H69 human cholangiocytes to not only bile salt-induced apoptosis (BSIA) but also etoposide-in

168 drolysis of egg white proteins and abrogated bile salt-induced precipitation of LYS in the duodenal m

169 gical levels of Ca(2+) may result in altered bile salt-induced TcpP protein movement and activity, ul

170 that Ca(2+) enhances virulence by promoting bile salt-induced TcpP-TcpP interaction.

171 that exposure of esophageal cells to acidic bile salts induces phosphorylation of the p47(phox) subu

172 Bile salts inhibit their own production by inducing the

173 was undertaken to determine how hydrophobic bile salts interact with GBSM, and how they reduce GBSM

174 Our NMR results indicate that that bile salt interaction of SipD will be different from wha

175 BALF was assessed for pepsin, bile salts, interleukin-8 and neutrophils.

176 ter is the main import system for conjugated bile salts into the liver but also indicates that auxili

177 of weak physiological allosteric inhibitors (bile salts) into potent competitive Autotaxin inhibitors

178 The enterohepatic circulation of bile salts is an important physiological route to recycl

179 Further, how SipD binds to bile salts is currently unknown.

180 the mechanism of this differing response to bile salts is poorly understood.

181 terestingly, extended periods of exposure to bile salts led to biofilm formation, a conserved phenoty

182 Half of the Fut2(-/-) mice showed serum bile salt levels 40 times higher than wt (Fut2(-/-)(high

183 d ribavirin, suggesting a potential role for bile salt levels in HCV treatment outcomes and in the fi

184 444A, has been associated with altered serum bile salt levels in healthy individuals and predisposes

185 composition, while maintaining normal plasma bile salt levels predominantly through renal excretion o

186 Recently, elevated bile salt levels were shown to be significantly associat

187 The mechanism by which bile salts limit bacterial growth is still largely unkno

188 During increased portal bile salt load this mechanism may adjust bile salt uptak

189 ile flow, biliary bile salt secretion, fecal bile salt loss, and expression of major hepatocellular b

190 altered intestinal permeability; disordered bile salt metabolism (in 10-20% of cases with diarrhoea)

191 clear hormone receptors in the regulation of bile salt metabolism, which has led to novel therapies u

192 released products (i.e. contained within the bile salt micellar phase).

193 In the presence of bile salt micelles and colipase, human PLRP2 hydrolyzed

194 adsorption site for pyrene and quercetin in bile salt micelles is more hydrophobic than that for SDS

195 loop-that are essential for accessing SM in bile salt micelles.

196 id quercetin we studied its interaction with bile salt micelles.

197 id skeleton, and the acidic function of some bile salts, might promote the interaction with the pepti

198 products are very rapidly solubilized in the bile salt mixed micelles with no fractionation according

199 alts, help explain the beneficial effects of bile salt mixtures, and suggest that we have identified

200 cyte integrity in the presence of millimolar bile salt monomers is dependent on (1) pH, (2) adequate

201 exposed to millimolar levels of hydrophobic bile salt monomers.

202 samples were determined, and the effects of bile salts on fu were investigated in vitro.

203 The effect of hydrophobic bile salts on the activity of GBSM was measured by intra

204 together, these data suggest a model whereby bile salts or other detergents destabilize ToxR, increas

205 by catalysing secondary active transport of bile salts out of the cell cytoplasm.

206 d may act as a gatekeeper to prevent hepatic bile salt overload.

207 olera and for V. cholerae resistance against bile salts, perhaps due to environmental regulation of A

208 rough the GIT due to accumulation of anionic bile salts, phospholipids, and free fatty acids at their

209 Bile salts play diverse roles in digestion and signaling

210 Strategies that alter bile salt pool composition might be developed for the pr

211 iet (0.1%) resulted in a completely restored bile salt pool in Hrn mice, with 50% +/- 9% TDC and 42%

212 that the addition of RA to UDCA reduces the bile salt pool size and liver fibrosis and might be an e

213 Reductions in the bile salt pool size and liver hydroxyproline content wer

214 The altered bile salt pool stimulated robust secretion of cholestero

215 to ameliorate liver injury and stabilize the bile salt pool through adaptation of renal transporters

216 Alterations of the bile salt pool were mediated by increased expression of

217 Hydrophilicity of the bile salt pool, controlled by FXR and FGF15/19, is an im

218 in the composition and hydrophobicity of the bile salt pool.

219 cholate in bile, inducing a more hydrophilic bile salt pool.

220 Concurrently, bile salt pools changed in similar patterns and magnitud

221 Bile salts produced by the liver and secreted into the i

222 nalling and select steroids, notably natural bile salts, provides a molecular basis for the emerging

223 s CYP27A1 and CYP3A11 as well as canalicular bile salt pump ABCB11.

224 In contrast, the bile salt reabsorption transporters Ostalpha and Ostbeta

225 anced Claudin-2 expression in colon and that bile salt receptors VDR and Takeda G-protein coupled rec

226 Bile salt-regulating genes were measured by quantitative

227 major facilitator superfamily, functions in bile salt resistance in E. coli by catalysing secondary

228 d lipopolysaccharide O-antigen synthesis for bile salt resistance.

229 lsB, were previously shown to be involved in bile salts resistance of Enterococcus faecalis and in vi

230 ation of ileal farnesoid X receptor (FXR) by bile salts results in transcriptional induction of FGF19

231 Bile salt secretion is mediated primarily by the bile sa

232 sP3R2 plays an important role in maintaining bile salt secretion through posttranslational regulation

233 normal serum liver tests, bile flow, biliary bile salt secretion, fecal bile salt loss, and expressio

234 atment of patients with cholestasis with the bile salt sequestrant, colesevelam, but not placebo, eff

235 in patients with pruritus not responding to bile salt sequestrants.

236 ed as a biofilm has coopted the host-derived bile salt signal to detach from the biofilm and go on to

237 Bile salt synthesis and intestinal bile salt signaling were not affected, as evidenced by n

238 Myrcludex B blocked NTCP transport of bile salts; small hairpin RNA-mediated knockdown of NTCP

239 The bile salt sodium deoxycholate (SDC) enabled efficient ex

240 ant showed an increase in sensitivity to the bile salts sodium taurocholate and sodium deoxycholate a

241 lica-based beads as the stationary phase and bile salt solution as the mobile phase.

242 In the presence of bile salts, some released peptide monomers were bound to

243 On the other hand, bile salts stimulate hepatic synthesis of nitric oxide.

244 ary cholesterol mass secretion under maximal bile salt-stimulated conditions is fully dependent on AB

245 lk composition and structure by inactivating bile salt-stimulated lipase (BSSL) and partially denatur

246 d revealed the involvement of WxL operons in bile salt stress and endocarditis pathogenesis.

247 hat an ompU deletion mutant was sensitive to bile salt stress but resistant to polymyxin B stress, in

248 c antimicrobial peptide polymyxin as well as bile salts, suggesting a role in outer membrane integrit

249 is accomplished by exchanging strong binding bile salt surfactant coating with DNA in methanol/water

250 om the maltoside and thiomaltoside families, bile salt surfactant, and the steryl derivative choleste

251 Furthermore, bile salt survival assays and animal models using a muta

252 Hrn mice have strongly impaired bile salt synthesis and (re)hydroxylation capacity and a

253 Bile salt synthesis and intestinal bile salt signaling w

254 echanisms may shed light on the evolution of bile salt synthesis and possible therapy for infant bili

255 o known mechanisms, such as the reduction of bile salt synthesis in liver.

256 Bile salt synthesis is a specialized liver function in v

257 n an evolutionarily transitional state where bile salt synthesis occurs in both liver and intestine.

258 nd cytochrome P450 7a1, the key regulator of bile salt synthesis, indicating that elevated serum bile

259 cascade that provides feedback inhibition of bile salt synthesis.

260 se (CYP7A1), a key enzyme for the control of bile salt synthesis.

261 role in the negative feedback regulation of bile salt synthesis.

262 GF19 signaling results in down-regulation of bile salt synthesis.

263 mature biofilms to physiologic levels of the bile salt taurocholate, a host signal for the virulence

264 owever, when insulin was co-infused with the bile salt taurocholate, this was followed by a marked hy

265 One of these was revealed to be the bile salt taurocholate.

266 X bound to 7alpha-hydroxycholesterol and the bile salt tauroursodeoxycholate (TUDCA), showing how the

267 upon infusion with increasing amounts of the bile salt tauroursodeoxycholic acid, Abcg5 became fully

268 a higher critical micelle concentration for bile salts than for SDS.

269 uctal fibrosis, and sensitivity toward human bile salt toxicity.

270 NA-sequencing analysis verified an important bile salt transcriptional profile in S. flexneri 2457T,

271 he established cell line displayed vectorial bile salt transport and specific phosphatidylcholine sec

272 TCDC regulates bile salt transport at the sinusoidal membrane by protei

273 asolateral membrane localization of multiple bile salt transport proteins in central hepatocytes and

274 dent retrieval of sinusoidal and canalicular bile salt transport systems from the corresponding membr

275 tance protein 3, and apical sodium-dependent bile salt transporter.

276 loss, and expression of major hepatocellular bile salt transporters and cytochrome P450 7a1, the key

277 tion of orthologs of known organic anion and bile salt transporters in the kidney, with lesser effect

278 estine of anaesthetised rats by means of the bile salt transporters of the ileum.

279 holyl-insulin had been taken up by the ileal bile salt transporters.

280 disulfide stress conditions are sensitive to bile salt treatment.

281 Bile salts trigger recruitment of the first hydrophobic

282 tal bile salt load this mechanism may adjust bile salt uptake along the acinus and protect periportal

283 cotransporting polypeptide (Ntcp), the major bile salt uptake system at the sinusoidal membrane of he

284 transporting polypeptide (Ntcp) is the major bile salt uptake transporter at the sinusoidal membrane

285 sis demonstrated near absence of basolateral bile salt uptake transporters OATP1B2, OATP1A1, OATP1A4,

286 Net bile salt uptake was investigated in perfused rat liver

287 onditions, such as in the presence of serum, bile salts, urine, and collagen and at 46 degrees C.

288 ndant and very closely related physiological bile salts, vary substantially in their destabilizing ef

289 < 0.0001), and the ratio of phospholipids to bile salt was greater (6.8 +/- 1.3 vs. 3.2 +/- 1.6, P =

290 ndicated that hepatic uptake of unconjugated bile salts was strongly impaired whereas uptake of conju

291 rongly impaired whereas uptake of conjugated bile salts was unaffected.

292 Plasma total bile salts were 10-fold increased and were mostly presen

293 Bile salts were rarely detected.

294 Bile salts were undetectable, using spectrophotometry an

295 tromyzonol sulfate (PZS) was the predominant bile salt, whereas the major bile salts in adult liver w

296 The results demonstrate that the presence of bile salts, which are found in the intestine and thought

297 Here we show that mnhF confers resistance to bile salts, which can be abrogated by efflux pump inhibi

298 s multiple mechanisms to survive exposure to bile salts, which may have important implications for mu

299 nter in the gut is the high concentration of bile salts, which not only aid in food absorption but al

300 C NMR titration and negative controls with a bile salt with no secondary binding site (glycocholate)