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

6 highlights emerging roles of adipose FABP (A-FABP) and epidermal FABP (E-FABP) in the fields of obesi

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 ase and highlights emerging roles of adipose FABP (A-FABP) and epidermal FABP (E-FABP) in the fields

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

38 ffects is different from that of a classical FABP.

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

40 e pattern recognition receptor for conserved FABPs found in common mite allergens that initiate type

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

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

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

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

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

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

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

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

49 adipose FABP (A-FABP) and epidermal FABP (E-FABP) in the fields of obesity, chronic inflammation, an

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

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

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

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

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

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

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

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

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

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

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

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

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

63 roles of adipose FABP (A-FABP) and epidermal FABP (E-FABP) in the fields of obesity, chronic inflamma

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 H-FABP gene ablation significantly increased PtdIns mass 1

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

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

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

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

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

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

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

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

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

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

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

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

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

92 Postoperatively a combination of H-FABP, midkine and sTNFR2 had the highest predictive abil

93 Post operatively a combination of H-FABP, sTNFR1 and MK had the highest predictive ability t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 74 PFASs assessed, 20 were identified as hL-FABP ligands in which eight of them have high binding af

110 then developed an SECC method to identify hL-FABP ligands, and all eight high-affinity ligands were s

111 rming foam (AFFF) product in which 31 new hL-FABP ligands were identified.

112 o human liver fatty acid binding protein (hL-FABP).

113 the existence of many previously unknown hL-FABP ligands.

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

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

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

117 temic inflammatory response, with IL-6 and I-FABP as independent markers of disease severity and fata

118 eastfeeding, sCD14, BDG, LBP, zonulin, and I-FABP correlated with several markers of systemic inflamm

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

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

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

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

123 IL-6 and I-FABP, the latter a marker for intestinal damage, were by

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

125 Higher baseline I-FABP levels were associated with increases in VAT, TAT,

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

127 An overall 1.7-fold increase in I-FABP was observed throughout 96 weeks, with no differenc

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

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

130 Intestinal fatty acid binding protein (I-FABP) and lipopolysaccharide binding protein (LBP) did n

131 Intestinal fatty acid binding protein (I-FABP) arteriovenous (V-A) concentrations differences wer

132 ker Intestinal fatty acid binding protein (I-FABP) than IR.

133 and intestinal fatty acid-binding protein (I-FABP) than survivors.

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

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

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

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

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

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

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

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

142 acid and ileal bile acid binding proteins (I-FABP and I-BABP) were assessed over 96 weeks.

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

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

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

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

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

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

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

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

151 L-FABP overexpression selectively increased the targeting

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

223 AA1 interacted directly with allergenic mite FABPs (Der p 13 and Blo t 13).

224 The interaction between mite FABPs and SAA1 activated the SAA1-binding receptor, form

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

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

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

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

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

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

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

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

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

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

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

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

237 Snapshot describes the overall functions of FABPs in health and disease and highlights emerging role

238 Identification of FABPs as targets of transport inhibitors undermines the

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

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

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

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

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

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

245 of CCL5, CXCL10, fatty acid binding protein (FABP) 2, fas ligand (FASLG), matrix metalloproteinase (M

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

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

248 allergens of the fatty acid-binding protein (FABP) family are sensed by an evolutionarily conserved a

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

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

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

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

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

254 ort proteins (FATP) and FA binding proteins (FABP) are up-regulated and fetal plasma FA concentration

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

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

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

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

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

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

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

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

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

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

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

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

267 Fatty acid binding proteins (FABPs) serve as intracellular chaperones for fatty acids

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

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

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

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

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

273 annabinoid transmembrane transporter, target FABPs.

274 ar uptake and catabolism of AEA by targeting FABPs.

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

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

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

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

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

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

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

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

283 d new functions of individual members of the FABP family.

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