ライフサイエンスコーパス: MIF

1 MIF can regulate glucocorticoid-mediated immunosuppressi

2 MIF enzymatic activity has been used for identification

3 MIF is a diffuse and patchy process, appearing as a comb

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

5 MIF levels in the cerebrospinal fluid were associated wi

6 MIF motoneurons are located outside the extraocular nucl

7 MIF overexpression has been reported in several cancer t

8 MIF plays a role in various diseases, including inflamma

9 MIF-2 shares pro-inflammatory and tumorigenic properties

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

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

12 otaxin, IFN-gamma, IL-6, IL-8, IL-16, MCP-1, MIF and MIP-1 beta were significantly higher in all RD g

13 Like MIF-1, MIF-2 has intrinsic keto-enol tautomerase activity and m

14 An in vitro binding assay for MIF-1/MIF-2 to the CD74 ectodomain (sCD74) indicated that 4-CP

15 (DF, ML, MIL, DL), 19-20(DF, ML, MIL), 14-18(MIF), 21(MIF, ML, DL), 22(MF), 23-27(MIL), 24-26(MIL, MF

16 ne macrophage migration inhibitory factor-2 (MIF-2 or D-dopachrome tautomerase) is a recently charact

17 MIL, DL), 19-20(DF, ML, MIL), 14-18(MIF), 21(MIF, ML, DL), 22(MF), 23-27(MIL), 24-26(MIL, MF, DF in 2

18 and loxSOD1(G37R) mice injected with AAV2/9-MIF demonstrated a significant delay in disease onset an

19 were increased in the spinal cords of AAV2/9-MIF-injected mice.

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

21 Accordingly, MIF motoneurons could control mainly gaze in the off-dir

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

23 Apart from its cytokine activity, MIF also harbors enzyme activity for keto-enol tautomeri

24 finity MIF binder as a novel tool to advance MIF-oriented research.

25 Thus, we provide a high-affinity MIF binder as a novel tool to advance MIF-oriented resea

26 Although MIF arises mainly because of alterations in fibrillar co

27 Additionally, we make an MIF toolbox available for the first time.

28 Anatomically, MIF and SIF motoneurons distributed intermingled within

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

30 2, IFN-beta, IL-10, IL-12p40, TNF-alpha, and MIF than young mice, and old mice contained higher level

31 gher levels of CCL2, IL-1beta, IFN-beta, and MIF in their alveolar lining fluid.

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

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

34 defined in different autoimmune diseases and MIF-targeted biologic therapeutics are in early-stage cl

35 and DDX6 interact directly with the MA3 and MIF domains of CNOT1 and compete for binding.

36 oadly distributed florigen promotes MADS and MIF genes, which in turn regulate the rate of vascular m

37 The measured enrichment factors for MDF and MIF (epsilon(202)Hg and E(199)Hg) ranged from 1.10 per m

38 kinase (ERK), protein kinase B and p53, and MIF may also reverse immunosuppression.

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

40 hological studies have revealed that SIF and MIF motoneurons are segregated anatomically and receive

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

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

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

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

45 proof-of-concept that combining antiparasite MIF-blocking antibodies with current standard-of-care an

46 med 3.5 billion years ago do not contain any MIF sulfur.

47 more potent and pharmacologically auspicious MIF-2 inhibitors to investigate the distinct functions o

48 ranslation has been hampered, partly because MIF-2-selective inhibitors have been elusive.

49 CXCR4-binding site to MIF, selectively bind MIF with nanomolar affinity and block MIF/CXCR4 without

50 y bind MIF with nanomolar affinity and block MIF/CXCR4 without affecting CXCL12/CXCR4.

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

52 We identify msR4M-L1, which blocks MIF- but not CXCL12-elicited CXCR4 vascular cell activit

53 nstrate the functional participation of both MIF and SIF motoneurons in fixations and slow and phasic

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

55 enes that overlapped with those regulated by MIF shRNA.

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

57 -L1 does not interfere with cardioprotective MIF/CD74 signaling.

58 [C-C motif chemokine ligand 5], CCL7, CCL4, MIF [macrophage migration inhibitory factor]), cluster 3

59 al functions by engaging the cognate, common MIF family receptor CD74.

60 In comparison, MIF distinctly modulates every step of the transduction

61 imbabwe, and West African cratons do contain MIF sulfur, which suggests craton construction by advect

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

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

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

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

66 We demonstrate that EC-derived MIF decreases PC contractility on 2-dimensional silicone

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

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

69 ab-induced VEGF depletion would downregulate MIF.

70 acute lung injury, selective deletion of EC MIF decreases neutrophil infiltration to the bronchoalve

71 gate the effects of selective deletion of EC MIF.

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

73 ket of MIF have been valuable in elucidating MIF mechanisms and developing translational strategies.

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

75 addition, complete elimination of endogenous MIF accelerated disease onset and late disease progressi

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

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

78 Its potency compares well with established MIF inhibitors, whereas msR4M-L1 does not interfere with

79 F), 28(MF, ML, DL), 29-31(all 6 sites except MIF 30,31).

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

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

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

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

84 tory macrophage migration inhibitory factor (MIF) cytokine homolog, a virulence factor linked to seve

85 kine macrophage migration inhibitory factor (MIF) has been characterized as a key immunomodulator and

86 Macrophage migration inhibitory factor (MIF) has been recognized as a major player in the pathog

87 e of macrophage migration inhibitory factor (MIF) in autoimmunity is underscored by data showing that

88 ived macrophage migration inhibitory factor (MIF) in inhibiting PC contractility and facilitating neu

89 kine macrophage migration inhibitory factor (MIF) in regulating a metabolic rhythm in the model light

90 Macrophage migration inhibitory factor (MIF) is a cytokine found to be associated with chronic o

91 Macrophage migration inhibitory factor (MIF) is a cytokine with key roles in inflammation and ca

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

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

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

95 pes, macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine with critical and support

96 Macrophage migration-inhibitory factor (MIF) is an atypical chemokine that promotes atherosclero

97 uman macrophage migration-inhibitory factor (MIF) is an evolutionarily-conserved protein that has bot

98 Macrophage migration inhibitory factor (MIF) is an upstream mediator of host defense that up-reg

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

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

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

102 n of macrophage migration inhibitory factor (MIF) was identified in human GBM specimens that were MGM

103 tly, macrophage migration inhibitory factor (MIF) was shown to directly inhibit mutant SOD1 misfoldin

104 n of macrophage migration inhibitory factor (MIF), a cytokine involved in host-microbe interactions a

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

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

107 h as macrophage migration inhibitory factor (MIF), also promote tumorigenesis.

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

109 )-1, macrophage migration inhibitory factor (MIF), monokine induced by interferon-gamma (MIG), and ma

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

111 and macrophage migration inhibitory factor (MIF), using Forster resonance energy transfer-based appr

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

113 kine macrophage migration inhibitory factor (MIF).

114 kine macrophage migration inhibitory factor (MIF).

115 ]-9, macrophage migration inhibitory factor [MIF], MIP-1alpha, and MIP-2alpha) was measured using rea

116 gene expression of members of the MIF family MIF, D-Dopachrome Tautomerase (DDT) and DDT-like (DDTL)

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

118 bers, and multiply innervated muscle fibers (MIFs).

119 Myocardial interstitial fibrosis (MIF) is a histological hallmark of several cardiac disea

120 ed followed by molecular interaction fields (MIFs), a global descriptor class that typically has the

121 ations, we propose a multitaper approach for MIF and compare its performance with coherence in simula

122 An in vitro binding assay for MIF-1/MIF-2 to the CD74 ectodomain (sCD74) indicated tha

123 Since none of our significant eSNPs for MIF or DDTL have been described in GWAS for COPD or lung

124 0.3 per mille for MDF, +/-0.05 per mille for MIF, 2SD).

125 ize a small-molecule inhibitor selective for MIF-2 that interferes with receptor binding and cell sig

126 IC(50) of 27 mum and 17-fold selectivity for MIF-2 versus MIF-1.

127 usions with mass-independently fractionated (MIF) sulfur isotopes that trace Archean surficial signat

128 all negative mass-independent fractionation (MIF) owing to nuclear volume effects.

129 Whereas no mass independent fractionation (MIF) was observed during sampling, the mass dependent fr

130 te potential mass-independent fractionation (MIF).

131 introduced mutual information in frequency (MIF) technique makes no model assumptions and measures n

132 described in GWAS for COPD or lung function, MIF expression in COPD patients is more likely a consequ

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

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

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

142 We found higher MIF and DDT expression in COPD patients compared to non-

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

144 azole when combined with anti-E. histolytica MIF antibodies, compared to metronidazole alone.

145 mechanistic understanding of the MIF homolog MIF-2/d-dopachrome tautomerase (d-DT) and its clinical t

146 However, there is no consensus on how MIF levels differ in COPD compared to control conditions

147 However, MIF motoneurons presented an overall reduced firing rate

148 However, MIF tautomerase activity assays are troubled by irregula

149 nd leukocyte recruitment capacities of human MIF by its plant orthologs.

150 Surprisingly, AtMDLs bind to the human MIF receptors CD74 and CXCR4.

151 condary structure characteristics with human MIF, yet only have minimal residual tautomerase activity

152 g cats, of electrophysiologically identified MIF and SIF motoneurons in the abducens nucleus.

153 wing that common functional polymorphisms in MIF are associated with disease susceptibility or clinic

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

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

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

157 pathogenesis of COPD, as SNPs that influence MIF expression are also associated with symptoms of COPD

158 ent manner (0.01-10 mum) without influencing MIF-1-CD74 binding.

159 Notably, 4-CPPC inhibited MIF-2-mediated activation of CD74 and reduced CD74-depen

160 Inhibiting MIF activity in cell culture and in preclinical animal m

161 omain (sCD74) indicated that 4-CPPC inhibits MIF-2-CD74 binding in a dose-dependent manner (0.01-10 m

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

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

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

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

166 Like MIF-1, MIF-2 has intrinsic keto-enol tautomerase activit

167 Furthermore, the platform used to measure MIF (microarray or RNAseq) was found to influence the sp

168 nic properties with the clinical target MIF (MIF-1), but the precise contribution of MIF-2 to immune

169 , we used Entamoeba histolytica as the model MIF-secreting protozoan, and a mouse model that mirrors

170 A small molecule MIF inhibitor and an allosteric CXCR4 inhibitor countera

171 directing the development of small-molecule MIF antagonists.

172 te in the whole repertoire of eye movements, MIF motoneurons would contribute only to slow eye moveme

173 Additionally, multitaper MIF and coherence are computed between macaque visual co

174 Our multitaper MIF estimator produces low variance and performs better

175 Simulations further suggest that multitaper MIF captures more information than coherence.

176 the macaque data set, coherence and our new MIF estimator largely agree.

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

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

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

180 MIF (MIF-1), but the precise contribution of MIF-2 to immune physiology or pathology is unclear.

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

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

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

184 significantly influencing gene expression of MIF and DDTL.

185 Further specific functions of MIF are now being defined in different autoimmune diseas

186 y controls carrying 3 different genotypes of MIF gene rs755622.

187 activity has been used for identification of MIF binding molecules that also interfere with its biolo

188 also contribute to the detrimental impact of MIF.

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

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

191 n of a selective small-molecule inhibitor of MIF-2.

192 l hits for potential catalytic inhibitors of MIF-2 and identified 4-(3-carboxyphenyl)-2,5-pyridinedic

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

194 pe carriers had the highest plasma levels of MIF than other genotype carriers.

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

196 s based on the conserved enzymatic pocket of MIF have been valuable in elucidating MIF mechanisms and

197 The polymorphism of MIF gene (rs755622, rs1007888 and rs2096525) was analyze

198 ned the association between polymorphisms of MIF gene and acute coronary syndrome (ACS).

199 The levels (both mRNA and protein) of MIF were increased at 2 weeks post-surgery and those of

200 erapeutic potential role of up-regulation of MIF in modulating the specific accumulation of misfolded

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

202 Moreover, the relevance of MIF's partially functionally redundant family member, D-

203 ffect on glial overactivation as a result of MIF up-regulation.

204 een made in our understanding of the role of MIF (and its family member D-dopachrome tautomerase (DDT

205 Studies of the role of MIF (which largely functions via the type II transmembra

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

207 nt discoveries demonstrating direct roles of MIF in supporting NLR Family Pyrin Domain-Containing 3 (

208 Evidence that the catalytic site of MIF family cytokines has a structural role in receptor b

209 The unique structure of MIF is also directing the development of small-molecule

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

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

212 equently the direction of the SNP effects on MIF expression.

213 ntrol conditions and there are no reports on MIF expression in lung tissue.

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

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

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

217 y intervening in pathogenesis and overcoming MIF-related genetic susceptibility to many rheumatic dis

218 ssociated viral (AAV) vectors to overexpress MIF in the spinal cord of mutant SOD1(G93A) and loxSOD1(

219 Plasma MIF level was also measured in part of ACS patients (139

220 sight into the regulation of the polymorphic MIF locus.

221 Plants possess MIF orthologs but lack the associated receptors, suggest

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

223 We develop a powerful MIF estimator optimized for correlating frequency coupli

224 effectiveness of targeting parasite-produced MIF as combination therapy with standard antibiotics to

225 ions, and assist the development of putative MIF-targeting therapeutics for a variety of pathologies.

226 l competition-based assay format to quantify MIF binding.

227 macrophages via the chemoattractants RANTES, MIF, CCL2, and CXCL12 and activation of their tumor cell

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

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

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

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

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

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

234 Among the SNPs found to regulate MIF expression, the major LD block identified was linked

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

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

237 Renal MIF expression was reduced in tubular cells in fibrotic

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

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

240 gether with identification of an E. scolopes MIF (EsMIF) in the light-organ transcriptome, led us to

241 nd flow cytometry, we found that ECs secrete MIF, and PCs upregulate CD74 in response to TNF-alpha.

242 Secreted MIF binds to cell-surface immune receptors such as CD74

243 Endothelial cell-secreted MIF reduces pericyte contractility and enhances neutroph

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

245 ct photolysis caused a small but significant MIF (Delta(33)S = 0.55 +/- 0.04 mUr, n = 3), demonstrati

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

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

248 We repurposed ibudilast, a specific MIF inhibitor, and treated patient derived cell lines.

249 For the first time, an EC-specific MIF knockout mouse was used to investigate the effects o

250 targeting the microenvironment, specifically MIF and IL8.

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

252 origenic properties with the clinical target MIF (MIF-1), but the precise contribution of MIF-2 to im

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

254 we characterized three MIF orthologs (termed MIF/d-dopachrome tautomerase-like proteins or MDLs) of t

255 the human EC-PC barrier, we demonstrate that MIF decreases the PC barrier to human neutrophil transmi

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

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

258 4-Cre(+/tg); Mif(fl/fl)) mice, we found that MIF both recruits and maintains antigen-presenting cells

259 echanisms and strengthen the hypothesis that MIF acts as a chaperone for misfolded SOD1 in vivo and m

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

261 These data indicate that MIF deficiency is associated with a compensatory amplifi

262 Our findings indicate that MIF gene rs755622 variant C allele is associated with in

263 Our findings indicate that MIF plays a significant role in SOD1 folding and misfold

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

265 Our data show that MIF mRNA and protein levels were increased in the spinal

266 Our study shows that MIF levels are affected not only by disease but also by

267 This suggests that MIF may be contributing to the pathogenesis of COPD, as

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

269 The MIF level in ACS patients with CC genotype was significa

270 The MIF promoter contains a 4-nucleotide microsatellite poly

271 marin fluorophore with high affinity for the MIF tautomerase active site (K(i) = 18 +/- 1 nM) that bi

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

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

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

275 recently characterized second member of the MIF cytokine superfamily in mammalian genomes.

276 we studied gene expression of members of the MIF family MIF, D-Dopachrome Tautomerase (DDT) and DDT-l

277 ntrast, our mechanistic understanding of the MIF homolog MIF-2/d-dopachrome tautomerase (d-DT) and it

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

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

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

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

282 creen of 1.6 million compounds targeting the MIF-2 tautomerase site yielded several hits for potentia

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

284 roxycoumarin fluorophore interfered with the MIF-CD74 interaction and inhibited proliferation of A549

285 This MIF enrichment was lost in bevacizumab-resistant gliobla

286 o investigate the distinct functions of this MIF family member in vivo.

287 Identification of this MIF gene polymorphism may help for predicting the risk o

288 Here, we characterized three MIF orthologs (termed MIF/d-dopachrome tautomerase-like

289 Finally, msR4M-L1 binds to MIF in plaques from human carotid-endarterectomy specime

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

291 vidence on the complex mechanisms leading to MIF, as well as its contribution to systolic and diastol

292 designed to mimic the CXCR4-binding site to MIF, selectively bind MIF with nanomolar affinity and bl

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

294 indings may offer new clues to understanding MIF's multiple functions, and assist the development of

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

296 mum and 17-fold selectivity for MIF-2 versus MIF-1.

297 conclude that paracrine signals from EC via MIF decrease PC contraction and enhance PC-regulated neu

298 , AIF translocates to the nucleus along with MIF causing chromatinolysis.

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

300 termingled within the abducens nucleus, with MIF motoneurons being smaller and having a lesser somati