ライフサイエンスコーパス: FABP

1 FABP-deficient mice exhibited a lower incidence of disea

2 FABPs have highly similar tertiary structures consisting

3 Fatty acid binding protein-1 (FABP-1), which is protective against the detergent effec

4 bility to transactivate the C/EBPalpha and a-FABP promoters.

5 The activation by A-FABP was dependent upon its fatty acid binding propertie

6 ed expression of A-FABP, thus establishing A-FABP as a new molecular sensor in triggering macrophage-

7 Inhibition or deficiency of A-FABP in macrophage cell lines decreased sFA-induced Cer

8 Furthermore, we validated the role of A-FABP in promoting sFA-induced macrophage cell death with

9 cell death through elevated expression of A-FABP, thus establishing A-FABP as a new molecular sensor

10 expression of adipose FA binding protein (A-FABP) in macrophages facilitated metabolism of excess sF

11 of new benzophenone-containing fatty acids (FABPs) 1, 5, and 6 and a new route to FABP 3 are describ

12 Our approach adapted FABP-mediated PPARalpha signaling and employed in vitro

13 We investigated the role of adipocyte FABP and epithelial FABP in the development of experimen

14 , yellow fluorescent protein (YFP)-adipocyte FABP, or YFP-liver FABP revealed that under basal condit

15 d that CFP-HSL associated with YFP-adipocyte FABP in both basal and forskolin-treated cells.

16 ed 2-aminfluorene (FAF) and 4-aminobiphenyl (FABP) in order to gain thermodynamic and kinetic insight

17 from fluorinated analogs of 4-aminobiphenyl (FABP), 2-aminofluorene (FAF) or 2-acetylaminofluorene (F

18 uptake and metabolism similar to those of an FABP, but unlike FABP, it does not directly bind 16:0; h

19 ansport proteins, including CD36, Sr-B1, and FABP.

20 tion and PPARalpha activation in a drug- and FABP-dependent manner.

21 -(14)C]ethanolamide ([(14)C]AEA) uptake, and FABP knockdown to demonstrate that transport inhibitors

22 orylation of NFI correlating with GFAP and B-FABP expression.

23 on, we show that NFI occupies the GFAP and B-FABP promoters in NFI-hypophosphorylated GFAP/B-FABP+ve

24 sphatase activity that is enriched in GFAP/B-FABP+ve cells.

25 Calcineurin in GFAP/B-FABP+ve MG cells localizes to the nucleus.

26 P promoters in NFI-hypophosphorylated GFAP/B-FABP+ve MG cells.

27 y expressed in NFI-hypophosphorylated GFAP/B-FABP+ve MG cells.

28 s primarily found in the cytoplasm of GFAP/B-FABP-ve cells, suggesting a dual mechanism for calcineur

29 n of the brain fatty acid-binding protein (B-FABP; FABP7) and glial fibrillary acidic protein (GFAP)

30 Because FABP can influence steady-state lipid mass, brain indivi

31 Because FABPs are expressed in a regionally selective manner, th

32 Drugs also bind FABPs, raising the possibility that FABPs similarly regu

33 nflammatory cytokines and Ag presentation by FABP(-/-) dendritic cells did not promote proinflammator

34 lic-inflammatory pathway cross-regulation by FABPs contributes to adaptive immune responses and subse

35 ection of a vector expressing an antisense C-FABP transcript into the PC-3M prostatic cancer cells yi

36 tively, a 3.8- and a 6.9-fold reduction in C-FABP levels.

37 n of cutaneous fatty acid-binding protein (C-FABP) in prostate tissues was examined by immunohistoche

38 e tumours were associated with the reduced C-FABP.

39 These data show that C-FABP is increased in prostatic carcinoma cells and suppr

40 For the 34 prostatic carcinomas, the C-FABP expression was remarkably increased: 25 (73.5%) sam

41 On the basis of expression, chicken FABP genes seemed to form two major groups: (1) a cluste

42 ffects is different from that of a classical FABP.

43 itions that regulate the levels of competing FABP ligands.

44 carriers, administration of the competitive FABP ligand oleic acid or the selective non-lipid FABP i

45 Deploying FABP and MPO specific scFvs as receptor molecules onto o

46 On high-fat diet, FABP-deficient mice also exhibit enhanced muscle AMP-act

47 ogether, the data suggest that specific drug-FABP complexes can interact with PPARalpha to effect nuc

48 E-FABP-mediated IFN-beta signaling can further enhance rec

49 drocyte glycoprotein peptide (MOG(35-55)), E-FABP-deficient mice generated reduced levels of Th17 cel

50 that the impaired Th17 differentiation by E-FABP-deficient CD4(+) T cells was associated with lower

51 f IL-21, RORgammat, RORalpha, and IL-17 by E-FABP-deficient T cells to wild-type levels.

52 Collectively, E-FABP represents a molecular sensor triggering HFD-induce

53 rt that host expression of epidermal FABP (E-FABP) protects against mammary tumor growth.

54 kewise, naive CD4(+) T cells isolated from E-FABP-deficient mice showed reduced expression of IL-17 a

55 Furthermore, E-FABP-deficient mice are completely resistant to HFD-indu

56 However, E-FABP-deficient CD4(+) T cells expressed significantly hi

57 These findings identify E-FABP as a new protective factor to strengthen IFN-beta r

58 ther, our data indicate that expression of E-FABP by CD4(+) T cells contributes to the control of IL-

59 The negative influence of E-FABP deficiency on IL-17 expression was attributed to PP

60 Deficiency of E-FABP in obese mice decreased recruitment of CD11c(+) mac

61 , we demonstrate that T cell expression of E-FABP promotes Th17 differentiation, while counterregulat

62 lly, epidermal fatty acid binding protein (E-FABP) was significantly upregulated in skin of obese mic

63 Epidermal fatty acid-binding protein, E-FABP, a lipid chaperone, has been shown to regulate the

64 In the tumor stroma, E-FABP-expressing tumor-associated macrophages (TAM) produ

65 We find that E-FABP is highly expressed in macrophages, particularly in

66 we report that host expression of epidermal FABP (E-FABP) protects against mammary tumor growth.

67 ed the role of adipocyte FABP and epithelial FABP in the development of experimental autoimmune encep

68 ct with HSL such as the heart and epithelial FABPs but not on non-interacting proteins from the liver

69 ence between the two chicken liver-expressed FABPs related to food intake.

70 e chicken genome encodes two liver-expressed FABPs: (1) L-FABP or FABP1; and (2) Lb-FABP.

71 The small and flexible FABP exclusively adopts the less perturbed B conformer w

72 rences in enthalpy-entropy compensations for FABP and FAF.

73 Competition for FABPs may in part or wholly explain the increased circul

74 Dendritic cells deficient for FABPs were found to be poor producers of proinflammatory

75 Here, we provide two new functions for FABPs in NAE signaling.

76 activation, confirming a requisite role for FABPs in this process.

77 Proposed roles for FABPs include assimilation of dietary lipids in the inte

78 Furthermore, FABP Thr54 carriers have higher lipid oxidation rates, w

79 H-FABP gene ablation reduced total heart fatty acid uptake

80 H-FABP gene ablation significantly increased PtdIns mass 1

81 H-FABP predicted the risk of the composite end point both

82 H-FABP was elevated (> 8 ng/mL) in 332 patients (14.5%).

83 l antipsychotics, MBP and lamotrigine, and H-FABP and lithium.

84 tional layers of specially engineered anti-h-FABP and anti-MPO single-chain fragment variables (scFv)

85 In a multimarker approach, H-FABP, troponin I, and B-type natriuretic peptide provide

86 index diagnosis, and troponin I, elevated H-FABP remained a significant predictor of the composite e

87 Patients with an elevated H-FABP were more likely to suffer death (hazard ratio [HR]

88 Rat heart FABP (H-FABP) and rat liver FABP were potent inhibitors of 11,12

89 In brains from H-FABP gene-ablated mice, the incorporation coefficient fo

90 in serum albumin, apolipoprotein B, HSP27, H-FABP, ATP synthase, cytochrome bc-1 subunit 1 and alpha-

91 We measured H-FABP in 2287 patients with acute coronary syndromes from

92 ensor platform for electrical detection of h-FABP and MPO in physiological saline.

93 We examined the effect of H-FABP gene ablation on brain incorporation of arachidonic

94 Elevation of H-FABP is associated with an increased risk of death and m

95 tive cardiac injury biomarkers (NT-proBNP, H-FABP, hs-cTnT, and cTnI) strongly associated with the pr

96 a biomarkers of cardiac injury (NT-proBNP, H-FABP, hs-cTnT, cTnI, and CK-MB).

97 ue using heart fatty acid-binding protein (H-FABP) gene-ablated mice.

98 for heart-type fatty acid-binding protein (H-FABP) has a role in predicting all-cause mortality after

99 Heart-type fatty acid binding protein (H-FABP) is a cytosolic protein that is released rapidly fr

100 Heart fatty acid binding protein (H-FABP) is expressed in neurons, but its role in brain fat

101 and heart-type fatty acid binding protein (H-FABP) were measured in CSF and analyzed in relation to d

102 her major phospholipid classes, suggesting H-FABP has a role in maintaining steady-state 20:4n-6 mass

103 In summary, H-FABP was important for heart fatty acid uptake and targe

104 esults demonstrate for the first time that H-FABP expression influences brain 20:4n-6 uptake and traf

105 masses were also reduced, suggesting that H-FABP may augment brain plasmalogen synthesis.

106 Multivariable analysis demonstrated that H-FABP quartiles were strongly predictive of outcome: Q1 h

107 The H-FABP was measured 12 to 24 h after onset of symptoms in

108 ortality for unstable angina patients with H-FABP <5.8 microg/l was 2.1% compared with 22.9% for pati

109 omarkers for AD correctly and that CSF heart FABP levels start to increase at very early stages of AD

110 Rat heart FABP (H-FABP) and rat liver FABP were potent inhibitors

111 nt assays, we show that at least three human FABPs bind THC and CBD and demonstrate that THC and CBD

112 CRP, TNF, sIL-6R, I-FABP, sCD14, D-dimer, and HA levels were elevated in acu

113 I-FABP is highly homologous to that of A54 I-FABP, with the same overall three-dimensional fold that

114 for PCTV budding activity; only L-FABP and I-FABP (23% the activity of L-FABP) were active.

115 001); progressors also had higher IL-6 and I-FABP levels over the 5-year study period (P = .02 and .0

116 CRP, IL-6, and I-FABP were not associated with worse cognitive performanc

117 stinal fatty acid-binding proteins (L- and I-FABP) as well as four other proteins.

118 ations between sCD14 and both HIV load and I-FABP, shedding new light on the relationships between pr

119 correlations between HIV load, sCD14, and I-FABP.

120 ntrations (P < .001) and marginally higher I-FABP than other groups (P = .07).

121 erts on the functional properties of human I-FABP.

122 Early ART was associated with increased I-FABP levels but normalization of TNF, sIL-6R, and D-dime

123 nfants had higher sCD14 and IL-6 but lower I-FABP than HIV-exposed and HIV-unexposed infants (P < .00

124 man intestinal fatty acid binding protein (I-FABP) belongs to a family of intracellular lipid binding

125 er (intestinal fatty acid binding protein (I-FABP)) were measured in 253 women (73% HIV-infected).

126 sma intestinal fatty acid binding protein (I-FABP), soluble CD14 (sCD14), interleukin 6 (IL-6), and C

127 dy, intestinal fatty acid-binding protein (I-FABP), soluble CD14 (sCD14), interleukin 6 (IL-6), inter

128 the intestinal fatty acid binding protein (I-FABP), we hypothesize that ligand binding in I-BABP is l

129 and intestinal fatty acid binding protein (I-FABP).

130 of intestinal fatty acid-binding protein (I-FABP/FABP2), a marker of gut damage, and of soluble CD14

131 er (intestinal fatty acid binding protein [I-FABP]), lipopolysaccharide-induced monocyte activation (

132 ssociations between progression and sCD14, I-FABP, and IL-6 levels were unchanged in models controlli

133 nonprogressors, the association of sCD14, I-FABP, and IL-6 levels with liver disease progression sug

134 tly stronger binding of fatty acids to T54 I-FABP does not originate from residues in direct contact

135 irect comparison between human A54 and T54 I-FABP has now been performed to help elucidate the struct

136 The solution structure of T54 I-FABP is highly homologous to that of A54 I-FABP, with th

137 These two I-FABP forms display differential binding and transport of

138 oligodendrocyte glycoprotein 35-55-immunized FABP(-/-) mice showed reduced proliferation and impaired

139 tty acid-binding proteins (FABP), intestinal FABP (IFABP; FABP2) and liver FABP (LFABP; FABP1).

140 L-FABP also increased the targeting of fluorescent LCFAs (

141 L-FABP bound fluorescent VLC-PUFA with affinity and specif

142 L-FABP deletion attenuates both diet-induced hepatic steat

143 L-FABP gene ablation resulted not only in loss of L-FABP b

144 L-FABP overexpression selectively increased the targeting

145 ome encodes two liver-expressed FABPs: (1) L-FABP or FABP1; and (2) Lb-FABP.

146 kers of kidney injury (IL-18, NGAL, KIM-1, L-FABP, and albumin) and five plasma biomarkers of cardiac

147 Urine NGAL, IL-18, L-FABP, and KIM-1 are sequential predictive biomarkers for

148 hepatocytes isolated from L-FABP (+/+) and L-FABP (-/-) mice demonstrated for the first time a physio

149 demonstrated that higher urinary NGAL and L-FABP concentrations associated with slightly lower 6-mon

150 At 6 h, NGAL, IL-18, and L-FABP each improved the AUC from 0.72 to 0.91, 0.84, and

151 IL-18 and L-FABP increased at 6 h, and KIM-1 increased at 12 h.

152 differentiation/maturation markers such as L-FABP, kruppel-like factor 4 (KLF4), and keratin 20.

153 Our findings show that reducing both L-FABP and MTP is an effective means to reduce VLDL secret

154 ast, in L35 cells the DR1 elements of both L-FABP and MTP promoters are occupied by chicken ovalbumin

155 In FAO cells, the DR1 elements of both L-FABP and MTP promoters are occupied by peroxisome prolif

156 the fraction that normally comprises both L-FABP and sterol carrier protein-2 (SCP-2).

157 The vesicles generated by L-FABP were sealed, contained apolipoproteins B48 and AIV,

158 PUFA, correlating with its high binding by L-FABP.

159 We have therefore created L-FABP null mice and report here their initial analysis, f

160 in but did not fuse with cis-Golgi nor did L-FABP generate COPII-dependent vesicles.

161 Gene-disrupted L-FABP mouse cytosol had 60% the activity of wild type mou

162 FAO rat hepatoma cells express L-FABP and MTP and demonstrate the ability to assemble and

163 cell clone from FAO cells, do not express L-FABP or MTP nor do they assemble and secrete VLDL.

164 ntracellular lipid binding protein family, L-FABP is of particular interest as it can i), bind two fa

165 on promotes HSC activation in vivo, we fed L-FABP(-/-) and WT mice a high-fat diet supplemented with

166 In addition, TFF-fed L-FABP(-/-) mice exhibited decreased hepatic fibrosis, wit

167 TFF-fed L-FABP(-/-) mice exhibited reduced hepatic steatosis along

168 tudies provided three new insights: First, L-FABP gene ablation reduced maximal, but not initial, upt

169 cultured primary hepatocytes isolated from L-FABP (+/+) and L-FABP (-/-) mice demonstrated for the fi

170 Gel-filtered cytosol from L-FABP null liver lacked the main fatty acid binding peak

171 Primary HSCs isolated from L-FABP(-/-) mice contain fewer LDs than wild-type (WT) HSC

172 Freshly isolated HSCs from L-FABP(-/-) mice correspondingly exhibited decreased palmi

173 Comparison of the human apo and holo L-FABP structures revealed no evidence for an "open-cap" c

174 The overall conformation of human L-FABP shows the typical beta-clam motif.

175 vestigated structure and dynamics of human L-FABP with and without bound ligands by means of heteronu

176 ng according to the structure of the human L-FABP/OA complex.

177 ostulate that the lipid binding process in L-FABP is associated with backbone dynamics.

178 A synthase mRNA was selectively reduced in L-FABP null liver.

179 fatty acid content of the culture medium, L-FABP expression also increased the cellular LCFA-CoA poo

180 oA binding was absent from Fraction III of L-FABP (-/-) mice.

181 CFA-CoA pool size, LCFA-CoA acyl chains of L-FABP (-/-) mouse livers were enriched 2.1-fold in C16:1

182 omoter element present in the promoters of L-FABP and MTP affects transcription, expression, and VLDL

183 gene ablation resulted not only in loss of L-FABP but also in concomitant upregulation of two other i

184 To address this issue, the effect of L-FABP gene ablation on liver cytosolic LCFA-CoA binding,

185 rimary hepatocytes isolated from livers of L-FABP gene-ablated (-/-) and wild type (+/+) mice.

186 nothing is known regarding the function of L-FABP in peroxisomal oxidation and metabolism of branched

187 for the first time a physiological role of L-FABP in the uptake and metabolism of branched-chain fatt

188 Additional studies show that ablation of L-FABP prevents hepatic steatosis caused by treating mice

189 nly L-FABP and I-FABP (23% the activity of L-FABP) were active.

190 scuous binding and transport properties of L-FABP, we investigated structure and dynamics of human L-

191 ere tested for PCTV budding activity; only L-FABP and I-FABP (23% the activity of L-FABP) were active

192 ssion of liver fatty-acid binding protein (L-FABP) and adipocyte fatty acid-binding protein (aP2), tw

193 roteins, liver fatty acid-binding protein (L-FABP) and MTP, which cooperatively shunt fatty acids int

194 ing liver-type fatty acid-binding protein (L-FABP) by real time multiphoton laser scanning microscopy

195 and liver-type fatty acid binding protein (L-FABP) from 1304 deceased donors at organ procurement, am

196 Liver fatty acid binding protein (L-FABP) has been proposed to limit the availability of lon

197 role of liver fatty acid-binding protein (L-FABP) in the uptake, transport, mitochondrial oxidation,

198 Although liver fatty acid binding protein (L-FABP) is known to bind not only long chain fatty acid (L

199 and liver-type fatty acid binding protein (L-FABP) were measured in spot urine samples and standardiz

200 Liver fatty acid binding protein (L-FABP), a cytosolic protein most abundant in liver, is as

201 1), liver-type fatty acid binding protein (L-FABP), and albumin differed between etiologies and were

202 1), liver-type fatty acid binding protein (L-FABP), and interleukin (IL)-18, is reviewed.

203 wed that liver fatty acid-binding protein (L-FABP; binds LCFA-CoA as well as LCFA) significantly colo

204 [IL]-18, liver fatty acid-binding protein [L-FABP], and kidney injury molecule [KIM]-1) for cardiac s

205 lbumin, liver fatty acid binding proteins (L-FABP), and organic anion transporters--determine the dis

206 Regarding n-3 and n-6 VLC-PUFA, L-FABP expression enhanced uptake into the cell and cytopl

207 n upon ligand binding, as proposed for rat L-FABP.

208 pha and PGC-1beta coordinately up-regulate L-FABP and MTP expression, by competing with chicken ovalb

209 Second, L-FABP gene ablation inhibited phytanic acid peroxisomal o

210 inaric acid displacement assay showed that L-FABP bound BODIPY-C12 and BODIPY-C16 with K(i)s of 10.1

211 We conclude that L-FABP can select cargo for and bud PCTV from intestinal E

212 Third, lipid analysis of the L-FABP gene-ablated hepatocytes revealed an altered fatty

213 Thus, L-FABP may function as a carrier for selectively enhancing

214 ein fraction (Fraction III) from wild-type L-FABP (+/+) mice, isolated by gel permeation chromatograp

215 Urine L-FABP did not associate with any study outcomes.

216 Here, we used L-FABP null mice to test this hypothesis.

217 luorescence photobleaching recovery, where L-FABP gene ablation reduced the cytoplasmic, but not memb

218 iving cells and suggested a model, whereby L-FABP facilitated VLC-PUFA targeting to nuclei by enhanci

219 To investigate whether L-FABP deletion promotes HSC activation in vivo, we fed L-

220 While L-FABP gene ablation did not alter liver LCFA-CoA pool siz

221 essed FABPs: (1) L-FABP or FABP1; and (2) Lb-FABP.

222 ligand oleic acid or the selective non-lipid FABP inhibitor BMS309403 attenuated AEA uptake and hydro

223 P), intestinal FABP (IFABP; FABP2) and liver FABP (LFABP; FABP1).

224 hain fatty acid, with the exception of liver FABP, which binds two fatty acids or other hydrophobic m

225 Rat heart FABP (H-FABP) and rat liver FABP were potent inhibitors of 11,12-EET and 14,15-EET c

226 t protein (YFP)-adipocyte FABP, or YFP-liver FABP revealed that under basal conditions each protein w

227 ld be detected between CFP-HSL and YFP-liver FABP.

228 In animals lacking the adipocyte/macrophage FABP isoforms aP2 and mal1, there is strong protection a

229 Nine separate mammalian FABPs have been identified, and their tertiary structure

230 pression of different and sometimes multiple FABPs in these tissues and may be driven by protein-prot

231 ng profiles similar to oleic acid, a natural FABP substrate.

232 PPARalpha to effect nuclear accumulation of FABP and NHR activation.

233 Nuclear accumulation of FABP on drug binding is driven largely by reduced nuclea

234 Antagonism of FABP function through chemical inhibition, dominant-nega

235 macrophages negated the protective effect of FABP loss and increased ER stress in response to palmita

236 Consistent with a reported effect of FABP on plasmalogen mass, ethanolamine plasmalogen mass

237 tion and that insulin-sensitizing effects of FABP deficiency are, at least in part, independent of it

238 on and purification of a recombinant form of FABP (Fh15).

239 Consistent with the roles of FABP as AEA carriers, administration of the competitive

240 ent studies have demonstrated the ability of FABPs to simultaneously regulate metabolic and inflammat

241 Deletion of FABPs in adipocytes resulted in reduced expression of in

242 Identification of FABPs as targets of transport inhibitors undermines the

243 dually could account for the total impact of FABPs on systemic metabolism and suggest that interactio

244 pports our hypothesis that the inhibition of FABPs and subsequent elevation of anandamide is a promis

245 rs exert their effects through inhibition of FABPs, thereby providing a molecular rationale for the u

246 termine the biologic basis of lumican and/or FABP-1 dysregulation in NAFLD.

247 compensatory changes in the levels of other FABP mRNA in the gene-ablated mice.

248 The charge quartet is conserved on other FABPs that interact with HSL such as the heart and epith

249 f CSF heart-type fatty acid binding protein (FABP) and 12 other correlated analytes increase as AD pr

250 The adipocyte fatty acid-binding protein (FABP) aP2 is expressed by adipocytes and macrophages and

251 a member of the fatty acid-binding protein (FABP) family.

252 asciola hepatica fatty acid binding protein (FABP) termed Fh12 is a powerful anti-inflammatory protei

253 ctin, perilipin, fatty acid-binding protein (FABP), leptin, C/EBPalpha, and PPARgamma but not uncoupl

254 Fatty-acid binding proteins (FABP) and myeloperoxidases (MPO) are associated with man

255 Fatty acid-binding proteins (FABP) are known central regulators of both metabolic and

256 for cytoplasmic fatty acid-binding proteins (FABP) in lipid metabolism, although a similar function i

257 e expresses two fatty acid-binding proteins (FABP), intestinal FABP (IFABP; FABP2) and liver FABP (LF

258 Fatty acid-binding proteins (FABPs) act as intracellular receptors for a variety of h

259 serum albumin, fatty acid binding proteins (FABPs) and organic anion transporters (OATs) have been i

260 cyte/macrophage fatty acid-binding proteins (FABPs) aP2 (FABP4) and mal1 (FABP5) to examine the contr

261 Fatty acid-binding proteins (FABPs) are a widely expressed group of calycins that pla

262 Fatty acid-binding proteins (FABPs) are abundant intracellular proteins that bind lon

263 e intracellular fatty acid-binding proteins (FABPs) are abundantly expressed in almost all tissues.

264 Fatty acid-binding proteins (FABPs) are cytosolic fatty acid chaperones that play a c

265 Fatty acid-binding proteins (FABPs) are intracellular proteins that mediate AEA trans

266 , we identified fatty acid-binding proteins (FABPs) as intracellular NAE carriers.

267 Three fatty acid binding proteins (FABPs) known to be expressed in brain were examined as p

268 ther vertebrate fatty acid binding proteins (FABPs) supported the hypothesis that several gene duplic

269 nd by cytosolic fatty acid-binding proteins (FABPs) with K(d) values of approximately 0.4 microM.

270 , including the fatty acid-binding proteins (FABPs), can chaperone ligands to the nucleus and promote

271 Fatty acid binding proteins (FABPs), in particular FABP5 and FABP7, have recently bee

272 Recent studies, however, have recast FABPs as active participants in vital lipid-signaling pa

273 at intestinal fatty acid binding protein (rI-FABP) with acrylodan.

274 annabinoid transmembrane transporter, target FABPs.

275 ar uptake and catabolism of AEA by targeting FABPs.

276 ed three to four times more efficiently than FABP and FAF.

277 classification is incomplete suggesting that FABP contributes independent information as a predictor

278 We demonstrate that FABPs mediate the nuclear translocation of the NAE oleoy

279 lso bind FABPs, raising the possibility that FABPs similarly regulate drug activity at the NHRs.

280 erging in the last decade has suggested that FABPs have tissue-specific functions that reflect tissue

281 The FABP and FAF lesions exist in a simple mixture of 'stack

282 The FABP-Abeta42 ratio demonstrates a similar hazard ratio f

283 Several members of the FABP family have been shown to function directly in the

284 ysical complex that presumably positions the FABP to accept a product fatty acid generated during cat

285 reduced UCP2 expression, suggesting that the FABP-FFA equilibrium controls UCP2 expression.

286 armacologic inhibition of FABP4/aP2 with the FABP inhibitor HTS01037 also upregulated UCP2 and reduce

287 The FABPs appear to be involved in the extranuclear compartm

288 The FABPs have unique tissue-specific distributions that hav

289 understanding the specific functions of the FABPs and, in some cases, their mechanisms of action at

290 ese emerging functions and mechanisms of the FABPs, highlighting the unique functional properties of

291 Combined with the known 2 and 4, these FABPs comprise a set of photoactivatable fatty acid anal

292 lomyelitis to test the hypothesis that these FABPs impact adaptive immune responses and contribute to

293 acids (FABPs) 1, 5, and 6 and a new route to FABP 3 are described.

294 Taken together, FABPs represent the first proteins known to transport AE

295 ltrafast, label-free screening of heart type-FABP and MPO.

296 lism similar to those of an FABP, but unlike FABP, it does not directly bind 16:0; hence, the mechani

297 t the earliest duplication in the vertebrate FABP family led to the divergence of a gut-specialized g

298 r of fibrosis in nonhepatic tissues, whereas FABP-1 is paradoxically underexpressed in NASH, suggesti

299 y and extracellular spaces, association with FABP in the liver, and renal elimination and reabsorptio

300 rrow transplantation, we generated mice with FABP deficiency in bone marrow and stroma-derived elemen