ライフサイエンスコーパス: MIF

1 MIF also regulated cystic renal epithelial cell apoptosi

2 MIF and FRVs calculated for 83 different 2013 MY vehicle

3 MIF is an inflammatory cytokine but is hepatoprotective

4 MIF is markedly different from other cytokines because i

5 MIF is unique among cytokines in terms of its release pr

6 MIF levels in the cerebrospinal fluid were associated wi

7 MIF motoneurons are located outside the extraocular nucl

8 MIF promoted cystic epithelial cell proliferation by act

9 MIF promoted human CXCR7 internalization up to 40%, peak

10 MIF was upregulated in cyst-lining epithelial cells in p

11 MIF, CD74, and CD44 were upregulated in the glomeruli of

12 MIF-dependent macrophage recruitment was associated with

13 CSF-1, MIF, and MIG levels in both serum and saliva did not dif

14 Levels of calprotectin, CSF-1, MIF, MIG, and MMP-8 were measured using enzyme-linked im

15 than dermal fibroblasts, thereby creating a MIF gradient in skin.

16 Accumulated MIF protein is identified to be low in motor neurons, im

17 e tautomerase/dopachrome isomerase activity (MIF and DDT genes).

18 ly recognized by three mAbs directed against MIF.

19 Depletion of MIF, disruption of the AIF-MIF interaction, or mutation of glutamic acid at positio

20 ISO-1 and MIF knockout (MIFKO) had greater accumulation of Muller

21 positive feedback loop between TNF-alpha and MIF during cyst development.

22 We report here that CD74 and MIF are markedly increased and activated in patients wit

23 Elevated expression of CXCL2 and MIF and an increased number of CD33(+) MDSCs were detect

24 hing is known about the regions of CXCR4 and MIF that are involved in binding to each other.

25 location of the 6-PP adduct to the D-DT and MIF active sites that provide insight into the lack of c

26 rties of the covalent inhibitors of D-DT and MIF that are necessary for the development of therapeuti

27 TNF-alpha induced MIF expression, and MIF subsequently exacerbated TNF-alpha expression in ren

28 ddition, the expression levels of ICBP90 and MIF were correlated in joint synovia from patients with

29 f(-/-)), CD74-deficient (Cd74(-/-)) mice and MIF receptor inhibitor treated mice, we report that MIF

30 Circulating MIF and MIF receptor profiles distinguish PBC from the more infl

31 d in vivo, in particular from podocytes, and MIF stimulation induced proliferation of PECs and mesang

32 young (3-4 mo) or old (24 mo) wild type and MIF knockout (MIF(-/-)) mice.

33 d myocardial ATP availability in aged WT and MIF(-/-) mice.

34 raising the possibility that aggressive anti-MIF treatment of clinically isolated syndrome or RRMS ma

35 ovel findings support the concept of an anti-MIF strategy that targets this enzymatic activity as a p

36 ent with these findings, treatment with anti-MIF immunoglogulin G (IgG) antibodies reduced bacterial

37 elements that govern the interaction between MIF and CXCR4.

38 ed evidence for a direct interaction between MIF and CXCR7.

39 we demonstrate physical interaction between MIF and three receptors: CXCR2, CXCR4, and CD74.

40 ified: (1) bevacizumab bound MIF and blocked MIF-induced M1 polarization of macrophages; and (2) VEGF

41 22 in the catalytic nuclease domain blocked MIF nuclease activity and inhibited chromatinolysis, cel

42 ction were identified: (1) bevacizumab bound MIF and blocked MIF-induced M1 polarization of macrophag

43 To elucidate this role, we bred MIF-deficient mice with SOD1(G85R) mice, which express a

44 in H9C2 myoblasts, the effect was ablated by MIF replenishment.

45 c inflammation, the effect was attenuated by MIF knockout.

46 nM and 30 min, but CXCR7 internalization by MIF was not dependent on CXCR4.

47 enes that overlapped with those regulated by MIF shRNA.

48 rimary murine B-cell chemotaxis triggered by MIF, but not by CXCL12.

49 CXCR4 is the dominant receptor used by MIF in the homing tumor context, although some signaling

50 rate the utility of the model by calculating MIFs and FRVs for 37 EVs and 13 ICEVs.

51 Blockade of CD74-MIF interaction reduced AKT phosphorylation and expressi

52 Inhibition of CD74-MIF interaction significantly suppressed tumor growth in

53 es melanoma cell survival by regulating CD74-MIF signaling, suggesting that targeting the CD74-MIF in

54 ignaling, suggesting that targeting the CD74-MIF interaction under IFN-gamma-stimulatory conditions w

55 Circulating MIF and MIF receptor profiles distinguish PBC from the m

56 Circulating MIF levels are increased in the serum of patients with P

57 e mass independent Hg isotopic compositions (MIF; Delta(199)Hg) of the sediments were linearly correl

58 of estimating mass-induced fuel consumption (MIF) and fuel reduction values (FRVs) from fuel economy

59 escription of mass-induced fuel consumption (MIF) and fuel reduction values (FRVs).

60 Depending on the context, MIF signals through 1 or more of its receptors cluster o

61 CXCL2/MIF-stimulated activation of the mitogen-activated prote

62 Overall, our results identify the CXCL2/MIF-CXCR2 axis as an important mediator in MDSC recruitm

63 ll line J82 induced MDSC migration via CXCL2/MIF-CXCR2 signaling in vitro.

64 adder cancer (BC) microenvironment via CXCL2/MIF-CXCR2 signaling.

65 Finally, we demonstrated MIF/CXCR7-mediated functional responses.

66 Loss of keratinocyte-derived MIF leads to a loss of control of epithelial skin tumor

67 Loss of keratinocyte-derived MIF leads to a loss of control of epithelial skin tumor

68 between the two odd Hg isotopes that display MIF (Delta(199)Hg/Delta(201)Hg) was consistent for the l

69 ab-induced VEGF depletion would downregulate MIF.

70 Our findings demonstrate elevated MIF and D-DT levels in males with progressive disease co

71 Elevating MIF in neuronal cells suppresses accumulation of misfold

72 termine the importance of Leishmania-encoded MIF, both LmMIF genes were removed to produce an mif(-/-

73 rast, the complete elimination of endogenous MIF accelerated disease onset and late disease progressi

74 llular membranes, but the role of endogenous MIF in modulating SOD1 misfolding in vivo remains unknow

75 Site-directed biopsies revealed enriched MIF and VEGF at the enhancing edge in bevacizumab-naive

76 ion in the antiapoptotic effect of exogenous MIF.

77 etachment and provide a rationale to explore MIF inhibition as a potential therapeutic option for RD.

78 Xenografts expressing MIF-shRNA grew more rapidly with greater angiogenesis an

79 ng evidence that carriage of high-expression MIF alleles is a genetic marker of morbidity and mortali

80 ages of the CATT7 and -173 C high-expression MIF alleles were associated with unfavorable outcome (P=

81 nd transcription activity of high-expression MIF promoter Luciferase reporter constructs in THP-1 mon

82 ctor (HGF), and migration inhibition factor (MIF) may provide a poor prognosis either by inducing inc

83 fied macrophage migration inhibitory factor (MIF) as a PARP-1-dependent AIF-associated nuclease (PAAN

84 fied macrophage migration inhibitory factor (MIF) as an important regulator of cyst growth in ADPKD.

85 for macrophage migration inhibitory factor (MIF) as the key director of MSC migration and infiltrati

86 Macrophage migration inhibitory factor (MIF) has a cytoprotective effect on lung endothelial cel

87 and macrophage migration inhibitory factor (MIF) have additive effects in neutrophil recruitment.

88 Macrophage migration inhibitory factor (MIF) is a key proinflammatory mediator that we have prev

89 Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine that has been implicated

90 Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine that mediates inflammatio

91 Macrophage migration-inhibitory factor (MIF) is a pleiotropic cytokine with chemokine-like funct

92 lian macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine that plays an importa

93 Macrophage migration inhibitory factor (MIF) is an inflammatory cytokine that exhibits chemokine

94 uman macrophage migration inhibitory factor (MIF) is both a keto-enol tautomerase and a cytokine asso

95 kine macrophage migration inhibitory factor (MIF) is encoded in a functionally polymorphic locus that

96 kine macrophage migration inhibitory factor (MIF) plays a role in the maintenance of cardiac homeosta

97 ated macrophage migration inhibitory factor (MIF) to be the most pertinent mediator of increased macr

98 ied a role for macrophage inhibitory factor (MIF) to potentiate the activation of LPS-induced cytokin

99 that macrophage migration inhibitory factor (MIF) was highly expressed by primary AML, and that IL8 w

100 Macrophage migration inhibitory factor (MIF) was identified and evaluated for neurotoxic and pro

101 tly, macrophage migration inhibitory factor (MIF) was shown to directly inhibit the accumulation of m

102 kine macrophage migration inhibitory factor (MIF) were associated with morbidity and mortality of pne

103 e of macrophage migration inhibitory factor (MIF), a pleiotropic proinflammatory cytokine, in this pr

104 Macrophage migration inhibitory factor (MIF), a proinflammatory cytokine and counterregulator of

105 uman macrophage migration inhibitory factor (MIF), a proinflammatory cytokine associated with numerou

106 s of macrophage migration inhibitory factor (MIF), a proinflammatory immunoregulatory cytokine expres

107 that macrophage migration inhibitory factor (MIF), an innate immune mediator, is detrimental for surv

108 ine, macrophage migration inhibitory factor (MIF), and its receptor, CD74, was assessed in autoimmune

109 and, macrophage migration inhibitory factor (MIF), and thereby activates the PI3K/AKT pathway in mela

110 h as macrophage migration inhibitory factor (MIF), its homolog D-dopachrome tautomerase (D-DT), and t

111 )-1, macrophage migration inhibitory factor (MIF), monokine induced by interferon-gamma (MIG), and ma

112 tor, macrophage migration inhibitory factor (MIF), more strongly than dermal fibroblasts, thereby cre

113 kine macrophage migration inhibitory factor (MIF), which results in a M2 shift of microglial cells.

114 onal macrophage migration inhibitory factor (MIF), whose activities include an ATP-independent protei

115 kine macrophage migration inhibitory factor (MIF), whose functions in parasite growth or in the host-

116 kine macrophage migration inhibitory factor (MIF).

117 kine macrophage migration inhibitory factor (MIF).

118 kine macrophage migration inhibitory factor (MIF).

119 multiply innervated nontwitch muscle fibers (MIF).

120 eurons supplying multiply innervated fibers (MIFs) and singly innervated fibers (SIFs) in eye muscles

121 natural antagonist activity of DRalpha1 for MIF that was strongly potentiated by the MOG peptide ext

122 We found that ICBP90 is essential for MIF transcription from monocytes/macrophages, B and T ly

123 MIF, indicating that CXCR7 is essential for MIF-promoted B-cell migration.

124 okine receptor CXCR7 as a novel receptor for MIF.

125 gitis and also suggests a potential role for MIF as a target of immune-modulating adjunctive therapy.

126 We have shown this major role for MIF using in vitro migration and invasion assays, in pre

127 ighly infectious mature intracellular forms (MIFs) of L. pneumophila are considered as infectious par

128 nsignificant mass-independent fractionation (MIF) (-0.12 to +0.15 per thousand for Delta(201)Hg).

129 evidence of mass independent fractionation (MIF) for mercury (Hg) isotopes have been reported in the

130 on (MDF) and mass-independent fractionation (MIF) may cause characteristic isotope signatures of diff

131 he extent of mass-independent fractionation (MIF) of Hg isotopes preserved in fish is being used to q

132 little to no mass-independent fractionation (MIF, Delta(199)Hg; +/- 0.04 per thousand, 2SD) (0.00 to

133 Two functional MIF promoter polymorphisms, a microsatellite (-794 CATT5

134 Furthermore, MIF inhibition reduced tubular cell proliferation in vit

135 G85R)-MIF(-/-) mice than in their SOD1(G85R)-MIF(+/+) littermates.

136 tly higher in the spinal cords of SOD1(G85R)-MIF(-/-) mice than in their SOD1(G85R)-MIF(+/+) litterma

137 f macrophages; and (2) VEGF increased glioma MIF production in a VEGFR2-dependent manner, suggesting

138 we analyzed the effects of local glomerular MIF/CD74/CD44 signaling in proliferative glomerulonephri

139 Our anatomical findings suggest that C-group MIF motoneurons have different physiological properties

140 with the nocturnal rat the feature of having MIF motoneurons located within the bounds of III.

141 of different types and amounts of DOM on Hg MIF during MMHg photodemethylation were investigated to

142 ns, evidence that Hg isotopes (especially Hg-MIF) can be a useful tracer to identify sources (syngene

143 ere, we reported significant variation in Hg-MIF signature (Delta(199)Hg: -0.24 ~ + 0.18 per thousand

144 However, the magnitude of Hg-MIF in interior pools of the crust is largely unknown.

145 Changing magnitudes of Hg-MIF signals were observed in Zn deposits with different

146 c (Zn) deposits in China, indicating that Hg-MIF can be recorded into the Earth's crust during geolog

147 gs indicate that genetically controlled high MIF expression (and D-DT) promotes MS progression in mal

148 , we investigated the role of E. histolytica MIF (EhMIF) during infection.

149 ding their selectivity of PfMIF versus human MIF.

150 ligation assay, CXCR7 was found to engage in MIF receptor complexes with CXCR4 and CD74, both after e

151 Furthermore, increased MIF and D-DT levels in males with progressive disease we

152 Moreover, increasing MIF expression in neuronal cultures inhibited the accumu

153 Our study indicates MIF is a central and upstream regulator of ADPKD pathoge

154 TNF-alpha induced MIF expression, and MIF subsequently exacerbated TNF-alp

155 Two mechanisms of bevacizumab-induced MIF reduction were identified: (1) bevacizumab bound MIF

156 Pneumolysin-induced MIF production required its pore-forming activity and ph

157 Stress stimuli induced MIF secretion from glomerular cells in vitro and in vivo

158 s, and synovial fibroblasts, and TLR-induced MIF transcription is regulated in an ICBP90- and -794 CA

159 upporting therapies to enhance intracellular MIF chaperone activity.

160 ) or old (24 mo) wild type and MIF knockout (MIF(-/-)) mice.

161 e compounds are likely the most potent known MIF tautomerase inhibitors; the most active ones are mor

162 eport the syntheses of fluorescently labeled MIF inhibitors and their use in the first fluorescence p

163 Conversely, mice lacking MIF or D-DT developed less-severe signs of experimental

164 ovel xenograft models of resistance had less MIF than bevacizumab-naive tumors, and harbored more M2/

165 In polycystin-1-deficient mice, MIF was required for recruitment and retention of renal

166 t that both the extent and signature of MMHg MIF are sensitive to different ligands that bind MMHg in

167 In monkey, MIF motoneurons lie around the periphery of oculomotor n

168 f antigen-presenting cells in the absence of MIF was associated with accelerated and increased format

169 an unexpected tumor-suppressive activity of MIF in murine skin.

170 an unexpected tumor-suppressive activity of MIF in murine skin.-

171 Finally, local administration of MIF was able to restore bacterial clearance and macropha

172 esentative molecules from several classes of MIF inhibitors.

173 Depletion of MIF, disruption of the AIF-MIF interaction, or mutation

174 atic and biological activities, discovery of MIF inhibitors has focused on monitoring the tautomerase

175 , demonstrated significant downregulation of MIF, Hsp70, Hsp90beta, and CDK4, and upregulation of Hsp

176 The detrimental effect of MIF knockout was associated with accentuated loss in car

177 s (MLECs) abrogated the protective effect of MIF, including decreased hyperoxia-mediated AKT phosphor

178 The proliferative effects of MIF may involve CD74 together with the coreceptor and PE

179 vides a rationale for further exploration of MIF as a therapeutic target for ADPKD.

180 sts that older adults with low expression of MIF may be predisposed to hyporesponsiveness to lipopoly

181 Inhibition of MIF activity or MIF expression reduced microbial product

182 etic deletion or pharmacologic inhibition of MIF aggravated fibrosis and inflammation, whereas treatm

183 report that MIF deficiency or inhibition of MIF receptor binding results in increased sensitivity to

184 The inhibition of MIF signaling or its receptor CD74 promotes IFN-gamma re

185 Inhibition of MIF's nuclease activity is a potential therapeutic targe

186 f animals with a small-molecule inhibitor of MIF improves survival by reducing inflammation and impro

187 treatment with a small molecule inhibitor of MIF reduced systemic inflammatory response, bacterial pr

188 , noncompetitive, and covalent inhibitors of MIF in a manner that can be scaled for high-throughput s

189 IF represents the disease-related isoform of MIF; oxMIF is therefore a new diagnostic marker for infl

190 We show that one of the two isoforms of MIF, that is, oxidized MIF (oxMIF), is specifically reco

191 Newborn monocytes expressed high levels of MIF and released MIF upon stimulation with Escherichia c

192 once infection is established high levels of MIF are detrimental to the host, treatment with a small

193 We have extended our physics-based model of MIF and FRVs for internal combustion engine vehicles (IC

194 AIF was required for recruitment of MIF to the nucleus, where MIF cleaves genomic DNA into l

195 rotective effect and that down-regulation of MIF by NFkappaB-mediated signaling under hypoxia acceler

196 ndings identify ICBP90 as a key regulator of MIF transcription and provide functional insight into th

197 s study was designed to evaluate the role of MIF in aging-induced cardiac anomalies and the underlyin

198 ruitment, mediating the exacerbating role of MIF in atherosclerosis and contributing to the wealth of

199 We investigated the role of MIF in high-fat or methionine- and choline-deficient die

200 phosphorylation abrogated in the setting of MIF deficiency.

201 ur (S(red)-DOM), the extent and signature of MIF is likely dependent on whether MMHg is dominantly bo

202 Additionally, selective targeting of MIF:CD74 signaling might provide an effective, trackable

203 ell crosstalk by which local upregulation of MIF and its receptor complex CD74/CD44 mediate glomerula

204 Inhibition of MIF activity or MIF expression reduced microbial product-induced phospho

205 ve association was observed between CXCL2 or MIF expression and the number of tumor-infiltrating CD33

206 y, we show that knockdown of either CXCR4 or MIF abrogates MSC homing to tumors in an in vivo pulmona

207 ssive kidney disease, global Mif deletion or MIF inhibition also worsened fibrosis and inflammation a

208 three in vivo models, global Mif deletion or MIF inhibition caused similar effects and attenuated the

209 ines macrophage colony-stimulating factor or MIF.

210 osis and contributing to the wealth of other MIF biological activities.

211 f the two isoforms of MIF, that is, oxidized MIF (oxMIF), is specifically recognized by three mAbs di

212 sight into the regulation of the polymorphic MIF locus.

213 s for 22 compounds show that the most potent MIF inhibitors bind with Kd values of ca. 50 nM; two are

214 nalysis of melanoma cell lines, all produced MIF constitutively.

215 The most prominent MIF motoneuron group is the C group, which innervates th

216 Purified MIF is shown to directly inhibit mutant SOD1 misfolding.

217 Recombinant MIF exerted opposing effects on tubular cells in vitro a

218 Recombinant MIF increased IL8 expression in BM-MSCs via its receptor

219 Recombinant MIF used at newborn, but not adult, concentrations count

220 nas aeruginosa can utilize human recombinant MIF (rMIF) to significantly (P < 0.01) enhance its endog

221 t xenograft-derived cells, while recombinant MIF drove M1 polarization.

222 ammation, whereas treatment with recombinant MIF was beneficial, even in established fibrosis.

223 bevacizumab resistance is driven by reduced MIF at the tumor edge causing proliferative expansion of

224 Protein kinase C beta (PKCbeta) regulated MIF-induced IL8 in BM-MSCs.

225 reptococcus pneumoniae strongly up-regulated MIF production in whole blood and transcription activity

226 potential therapeutic role of up-regulating MIF within the nervous system to modulate the selective

227 es expressed high levels of MIF and released MIF upon stimulation with Escherichia coli and group B S

228 Renal MIF expression was reduced in tubular cells in fibrotic

229 itself remained anoxic with its attendant S-MIF signature.

230 Consequently, S-MIF is considered some of the strongest evidence for the

231 Earth's formation, a common mechanism for S-MIF production was established in the atmosphere.

232 ffected by mass-independent fractionation (S-MIF down to Delta(33)S = -0.8), something which is thoug

233 ur isotope mass-independent fractionation (S-MIF), an Archean signature of atmospheric anoxia that be

234 ependent fractionation of sulfur isotopes (S-MIF) results from photochemical reactions involving shor

235 The presence of negative S-MIF in the deep mantle may also help resolve the problem

236 investigated to track the early origins of S-MIF.

237 previously thought despite the presence of S-MIF.

238 Although temporal variations in the S-MIF record are thought to depend on changes in the abund

239 chanisms complicates interpretation of the S-MIF record in terms of atmospheric composition.

240 nd that, in addition to exhibiting selective MIF inhibition in vitro and in vivo, iguratimod also has

241 Using an in vitro model of senescence, MIF knockdown exacerbated doxorubicin-induced premature

242 Distal injections labeled smaller MIF motoneurons located ventrolaterally and rostrally wi

243 BEVs have much smaller MIF and FRVs, both in the range 0.04-0.07 Le/(100 km 100

244 targeting the microenvironment, specifically MIF and IL8.

245 sing this knowledge to yield two more strong MIF inhibitors/binders.

246 Blockade of CXCR7 suppressed MIF-mediated ERK- and zeta-chain-associated protein kina

247 a small-molecular-weight inhibitor targeting MIF's tautomerase activity (SCD-19) significantly reduce

248 Thus, the concept of targeting MIF for therapeutic intervention is challenging because

249 Our results demonstrate that MIF is essential for maintaining innate immunity in skin

250 In summary, we demonstrate that MIF mediates hepatoprotection through the CD74/AMPK path

251 Our study demonstrates that MIF exerts a neuronal protective effect and that down-re

252 Our work demonstrates that MIF modulates beneficial versus detrimental inflammatory

253 We determined that MIF inhibitors exhibit distinct profiles of anti-inflamm

254 ide biochemical and functional evidence that MIF is an alternative ligand of CXCR7 and suggest a func

255 4-Cre(+/tg); Mif(fl/fl)) mice, we found that MIF both recruits and maintains antigen-presenting cells

256 This led us to hypothesize that MIF may have the capacity to interact with external subs

257 These findings indicate that MIF plays a significant role in the folding and misfoldi

258 Our data indicated that MIF knockout exacerbates aging-induced cardiac remodelin

259 eptor inhibitor treated mice, we report that MIF deficiency or inhibition of MIF receptor binding res

260 In this article, we report that MIF occurs in two redox-dependent conformational isoform

261 Our data revealed that MIF knockout exacerbated aging-induced unfavorable struc

262 We show that MIF-CD74 signaling inhibits interferon (IFN)-gamma secre

263 In this study, we showed that MIF expression is down-regulated by 0.75 +/- 0.10-fold o

264 ditions of severe infection, suggesting that MIF could represent a potential attractive target for im

265 The MIF and FRVs for HEVs and PHEVs mostly lie between those

266 The MIF promoter contains a 4-nucleotide microsatellite poly

267 acies of curative treatments with either the MIF antagonist ISO-1 or anti-CD74 neutralizing antibodie

268 ession promoter polymorphisms located in the MIF gene, a -794CATT5-8 microsatellite repeat and a -173

269 the wild-type mice to 9.07 +/- 0.66% in the MIF-knockout mice.

270 Moreover, the MIF inhibitor ISO-1 inhibited AML-induced IL8 expression

271 s with monkeys, cats show segregation of the MIF and SIF medial rectus motoneuron pools, albeit in a

272 Systemic administration of the MIF inhibitor ISO-1 significantly blocked photoreceptor

273 suggest that therapeutic manipulation of the MIF-CD74 axis in lung endothelial cells may be a novel a

274 Activation of the MIF-CXCR2 and -CXCR4 axes promotes leukocyte recruitment

275 Although the structural basis of the MIF-CXCR2 interaction has been well studied and was foun

276 f CXCR7 and suggest a functional role of the MIF-CXCR7 axis in B-lymphocyte migration.

277 Our data show the feasibility of the MIF-inhibitor ISO-1 to block pathological damage respons

278 dulation of the functional activities of the MIF/CD74 complex.

279 The combination of GM-CSF plus the MIF inhibitor 4-iodo-6-phenyl-pyrimidine achieved the be

280 We postulate that the MIF receptor CD74 mediates this protective effect.

281 We hypothesized that the MIF/CD74 signaling pathway is overexpressed in idiopathi

282 , we found that curative treatments with the MIF antagonist ISO-1 or anti-CD74 neutralizing antibodie

283 1) is the major protein interacting with the MIF microsatellite.

284 Our data reveal that interference with the MIF signaling pathway represents a viable therapeutic op

285 This MIF enrichment was lost in bevacizumab-resistant gliobla

286 )Hg: -0.2 per thousand to -0.5 per thousand; MIF Delta(199)Hg: -0.05 per thousand to -0.10 per thousa

287 or two of the most potent compounds bound to MIF are also reported here.

288 ay crystal structures for 3a and 3b bound to MIF are reported and provided a basis for the modeling e

289 luable new candidate for drug repurposing to MIF-relevant diseases, including multiple sclerosis.

290 ibited an ablated transmigration response to MIF, indicating that CXCR7 is essential for MIF-promoted

291 and in vivo Our data identify renal tubular MIF as an endogenous renoprotective factor in progressiv

292 esistant xenografts transduced to upregulate MIF exhibited the opposite changes.

293 hase fuel consumption can be estimated using MIF and FRVs in life cycle assessments (LCAs) of vehicle

294 g a drastic decrease in both processes using MIF inhibitor.

295 ion were investigated to assess how variable MIF enrichment factors may be with respect to changing D

296 for recruitment of MIF to the nucleus, where MIF cleaves genomic DNA into large fragments.

297 ssibility of pharmacologic intervention with MIF pathway agonists, which are in advanced preclinical

298 Treatment with MIF decreased hyperoxia-mediated H2AX phosphorylation in

299 Similarly, treatment with MIF receptor antagonist resulted in a 59% and 91% increa

300 Using adult wild-type (WT), MIF-deficient (Mif(-/-)), CD74-deficient (Cd74(-/-)) mic