ライフサイエンスコーパス: MFG

1 MFG was administered for 12 days starting 24 hours after

2 MFG were separated into six size groups (1-3 mum) from s

3 MFG-E8 (also termed lactadherin) and developmental endot

4 MFG-E8 also decreased in erbB2(+) human cancers and erbB

5 MFG-E8 and its homologue Del1 may represent relevant tar

6 MFG-E8 augmented melanoma cell resistance to apoptosis,

7 MFG-E8 bound to phosphatidylserine and triggered reorien

8 MFG-E8 can be developed as novel treatment for renal isc

9 MFG-E8 deficiency accelerated the onset of disease in a

10 MFG-E8 deficiency in mice led to the accumulation of une

11 MFG-E8 expression correlated significantly with fractalk

12 MFG-E8 gene expression was significantly decreased in WB

13 MFG-E8 mRNA and protein were increased in angiogenic isl

14 MFG-E8 was shown to attenuate the progression of inflamm

15 MFG-E8(-/-) mice displayed impaired efferocytosis associ

16 MFG-E8-deficient human melanoma cells also showed increa

17 MFG-E8-deficient RPE in primary culture retained normal

18 MFG-E8-mRNA was significantly overexpressed in CP and is

19 MFG-E8-producing myofibroblasts mainly originated from r

20 Intervention Patients participated in 1 of 2 MFGs (MFG-adherence or MFG-standard) or treatment as usu

21 or the expression of milk fat globule EGF 8 (MFG-E8) in antigen-presenting cells, and that MFG-E8-med

22 Here, we show that milk fat globule EGF-8 (MFG-E8), a secreted protein expressed at high levels in

23 regulation of milk fat globule-EGF factor 8 (MFG-E8) as a contributor to breast cancer progression us

24 Milk fat globule EGF factor 8 (MFG-E8) binds to apoptotic cells and facilitates their r

25 Milk fat globule- EGF factor 8 (MFG-E8) is a bridge protein that facilitates efferocytos

26 at globule epidermal growth factor-factor 8 (MFG-E8) is a peripheral glycoprotein that acts as a brid

27 at globule-epidermal growth factor factor 8 (MFG-E8) is expressed in several tissues and mediates div

28 Milk fat globule-EGF factor 8 (MFG-E8) maintains the intestinal homeostasis by enhancin

29 at globule epidermal growth factor-factor 8 (MFG-E8) was originally identified for phagocytosis of ap

30 t globule protein epidermal growth factor 8 (MFG-E8), increases 2.3-fold in abundance in old aorta.

31 geting factor milk fat globule-EGF factor 8 (MFG-E8), stimulated collagen uptake and degradation by a

32 rTK) and Milk fat globule EGF-like factor 8 (MFG-E8), were transiently up-regulated by macrophages/mi

33 milk fat globule-epidermal growth factor 8 (MFG-E8), which promotes apoptotic engulfment, and determ

34 llular ligand milk fat globule-EGF factor 8 (MFG-E8).

35 Milk fat globule-EGF factor 8 (MFG-E8)/lactadherin participates in several cell surface

36 nd its ligand milk fat globule EGF factor-8 (MFG-E8) but not the receptor tyrosine kinase MerTK.

37 Milk-fat globule EGF factor-8 (MFG-E8, SED1, lactadherin) is known to mediate the phago

38 Consistently, exogenously added MFG-E8 inhibited receptor activator of NF-kappaB ligand-

39 Administration of antibody against MFG-E8 significantly attenuated the increase in M2 polar

40 ntration pattern throughout lactation in all MFG size groups.

41 Mfge8 knock-out mice or by coinjection of an MFG-E8 receptor (VR) inhibitor into the rat striatum.

42 ed that p63 regulates MFG-E8 expression, and MFG-E8 knockdowns sensitized triple-negative breast canc

43 to-parietal attentional network, the IPS and MFG/IFG appear to be most heavily involved in attentive

44 functional connectivity between the PCC and MFG/vACC during a working memory task and at rest by exa

45 Our results indicate that the SC and MFG transcriptome are representative of MGT and LCMEC an

46 ing MFG-E8 in mice by administration of anti-MFG-E8 antibody or targeted deletion of the MFG-E8 gene

47 Accordingly, local microinjection of anti-MFG-E8 mAb exacerbated periodontal bone loss in wild-typ

48 ranslation analysis demonstrated that aortic MFG-E8 mRNA and protein levels increase with aging in se

49 The data indicate that arterial MFG-E8 significantly increases with aging and is a pivot

50 SED1, also known as MFG-E8, is a secreted protein composed of two EGF repeat

51 tors such as c-mer and glycoproteins such as MFG-E8 were found to participate in the clearance of apo

52 Using a wound-healing assay, MFG-E8 was shown to promote the migration of intestinal

53 uman CD34 cells used the retroviral backbone MFG.

54 as a hemispheric asymmetry in the MDMR-based MFG findings, with literacy associated with the left MFG

55 um that was affected by Cx43 was found to be MFG-E8 (milk fat globule epidermal growth factor 8), whi

56 ce suggests an immunomodulatory link between MFG-E8 and the pro-inflammatory chemokine fractalkine, w

57 Our data show that blocking MFG-E8-dependent phagocytosis preserves live neurons, im

58 sufficient to fully restore phagocytosis by MFG-E8-deficient RPE.

59 hat osteoclasts express and are regulated by MFG-E8.

60 nversely dependent manner when stimulated by MFG-E8 and efferocytosis.

61 In human melanoma cells, MFG-E8 knockdown attenuated Akt and Twist signaling and

62 In conclusion, MFG-E8 is a novel homeostatic regulator of osteoclasts t

63 cting these cells with retroviral construct (MFG) expressing TGF-beta RII.

64 ressed the activity of a reporter containing MFG-E8 3'UTR.

65 In contrast, MFG-E8 expression was present at high levels in triple-n

66 In contrast, MFG-E8(-/-) mice that received wild-type bone marrow sho

67 gyrus and ventral anterior cingulate cortex (MFG/vACC).

68 Finally, reduced local efficiency of dACC/MFG during the task was significantly associated with an

69 in flexibility of local efficiency of R dACC/MFG significantly predicted inhibition performance, cons

70 ingulate cortex/medial frontal gyrus (R dACC/MFG).

71 Depleting MFG-E8 in mice by administration of anti-MFG-E8 antibody

72 Wound macrophage-derived MFG-E8 was recognized as a critical driver of wound angi

73 After detecting MFG-E8 mRNA in murine tumor cell lines, we sought to det

74 ncer cells increased efferocytosis, elevated MFG-E8 protein expression levels, and induced macrophage

75 nged cells with SNA-NC(anti-miR99b) enhanced MFG-E8 expression in the cells.

76 fronto-parietal regions, including IPS, FEF, MFG and IFG, in addition to regions in visual cortex.

77 Following MFG-E8-mediated engulfment of apoptotic cells, myofibrob

78 e isolated from CP tissues and evaluated for MFG-E8 mRNA expression after fractalkine stimulation.

79 that serum response factor is important for MFG-E8 production in myofibroblasts.

80 (n = 9) and 95% and 100%, respectively, for MFG (n = 19).

81 ese findings delineate pleiotropic roles for MFG-E8 in the tumor microenvironment and raise the possi

82 Less fractionated MFG regimens of every 48 and 72 hours are safe and as ef

83 ne marrow-derived osteoclast precursors from MFG-E8-deficient (Mfge8(-/-)) mice underwent increased r

84 tudied mice lacking expression of functional MFG-E8 to test the contribution of this integrin ligand

85 Furthermore, MFG-E8 supplementation strongly increased POS binding by

86 potential/current, a microfluidic generator (MFG) is demonstrated using patterned micropillar arrays

87 mes to DCs is mediated via milk fat globule (MFG)-E8/lactadherin, CD11a, CD54, phosphatidylserine, an

88 sm underlying the shift in milk-fat-globule (MFG) mean diameter upon changing the concentrate-to-fora

89 epithelial cells (LCMEC), milk fat globules (MFG) and antibody-captured milk mammary epithelial cells

90 pid composition of bovine milk fat globules (MFG) and their membranes (MFGM) was investigated.

91 rmation about the role of milk fat globules (MFGs) in high-fat dairy systems, such as cheese, and con

92 The glycoprotein MFG-E8 mediates phagocytic clearance of apoptotic cells

93 ttributed to increased secretion of F1-group MFG, while fat content and composition in the other MFG

94 cessus group (MCAG), the M. fortuitum group (MFG), and M. mucogenicum.

95 x, primarily within the middle frontal gyri (MFG).

96 e middle frontal and inferior temporal gyri (MFG and ITG) and resistant (cerebellum) to classical AD

97 eased rsFC in the left middle frontal gyrus (MFG) and bilateral inferior parietal lobe (IPL) of the D

98 cycle within the left middle frontal gyrus (MFG) and the right prefrontal cortex.

99 iFC), highlighting the middle frontal gyrus (MFG) for both competencies.

100 rence and in the right middle frontal gyrus (MFG) for the double interference condition.

101 ontal eye field (FEF), middle frontal gyrus (MFG), and inferior frontal gyrus (IFG).

102 rontal junction (IFJ), middle frontal gyrus (MFG), inferior frontal gyrus, and intraparietal sulcus c

103 r frontal gyrus (SFG), middle frontal gyrus (MFG), LIP, anterior intraparietal sulcus (IPSa)] that ma

104 recentral gyrus (PcG), middle frontal gyrus (MFG), orbital frontal cortex, and two regions of inferio

105 of damage to the left middle frontal gyrus (MFG).

106 The right middle/inferior frontal gyrus (MFG/IFG), which is included in the FPCN, showed greater

107 The higher MFG mean diameter in whole raw LCHF milk might therefore

108 a retroviral vector expressing human apoA-I (MFG-HAI) had 95% lower atherosclerotic lesion area than

109 We first identified MFG-E8 downregulation in invasive lesions in transgenic

110 These results identify MFG-E8 as the first extracellular ligand in the retina t

111 tumor cell lines, we sought to determine if MFG-E8 influenced tumorigenesis in Rip1-Tag2 transgenic

112 nt stimuli in the frontal regions (ACG, IFG, MFG) than the control group.

113 A 60-hr survival study was conducted in MFG-E8 and recombinant murine MFG-E8-treated wild-type m

114 c islets and tumor burdens were decreased in MFG-E8-deficient Rip1-Tag2 mice compared with those in c

115 Mice deficient in MFG-E8 develop lupus-like autoimmunity associated with a

116 nic islets and tumors, were also detected in MFG-E8-deficient mice.

117 fractalkine led to a significant increase in MFG-E8 expression.

118 less likely to be hospitalized than those in MFG-standard (chi(2) = 8.2; P = .04) and treatment as us

119 carcinomas were modestly underrepresented in MFG-E8-deficient mice, but tumor frequencies and surviva

120 o advanced glycated end products inactivated MFG-E8, recognizing a key mechanism that complicates dia

121 on of extracellular growth factors including MFG-E8.

122 tidylserine-recognizing molecules, including MFG-E8, TIM-1, -3, and -4, CD300a, BAI1, and stabilin-1

123 n of MFG-E8 in CP, with noticeably increased MFG-E8 immunoreactivity in tubular complexes.

124 g aorta to angiotensin II markedly increases MFG-E8 and enhances invasive capacity to levels observed

125 east cancer progression and small inhibitory MFG-E8 RNAs accelerated ER(+) breast cancer cell prolife

126 After renal ischemia-reperfusion injury, MFG-E8 mRNA and protein expressions were significantly d

127 esults suggest that a decrease in intestinal MFG-E8 impairs intestinal mucosal repair in sepsis.

128 Moreover, in septic mice, intestinal MFG-E8 expression was downregulated, which correlated wi

129 ssociated with down-regulation of intestinal MFG-E8 and impairment of enterocyte migration.

130 on of SNA-NC(anti-miR99b) rescued intestinal MFG-E8 expression in LPS-induced septic mice and attenua

131 an cancers and erbB2 transgenic mice lacking MFG-E8 showed accelerated tumor formation.

132 mine concentration was constant in the large MFG, but dropped twofold in the small MFG.

133 ing left intraparietal sulcus (IPS) and left MFG/IFG.

134 task-set) to the right IFG/POp and the left MFG respectively.

135 In addition, the rsFC of the left MFG was inversely correlated with the Trail Making Test-

136 ings, with literacy associated with the left MFG, whereas numeracy associated with the right MFG (R.M

137 sMerTK release, whereas the integrin ligand MFG-E8 markedly increases both phagocytosis and sMerTK l

138 alphavbeta5 integrin receptor and its ligand MFG-E8, thus generating a phagocytic peak.

139 In a murine model of melanoma, MFG-E8 enhanced tumorigenicity and metastatic capacity t

140 ention Patients participated in 1 of 2 MFGs (MFG-adherence or MFG-standard) or treatment as usual.

141 of alternate dosing regimens of micafungin (MFG) for the treatment of experimental subacute dissemin

142 In wild-type mice, MFG-E8 attenuates the vaccination activity of GM-CSF-sec

143 In septic WT mice, MFG-E8 mRNA and protein levels were suppressed by 49 and

144 Moreover, MFG-E8 administration into infarcted hearts restored car

145 Moreover, MFG-E8 knockdown tumor cells cultured with wild-type or

146 Using ectopically expressed mouse MFG-E8, a secreted phosphatidylserine-binding protein, w

147 a microRNA that is predicted to target mouse MFG-E8 3'UTR.

148 A recombinant murine MFG-E8 (0.4 mug/20 g) was given intraperitoneally at the

149 Treatment with recombinant murine MFG-E8 recovered renal dysfunction, significantly suppre

150 Administration of recombinant murine MFG-E8 reduces neutrophil migration through upregulation

151 oration and, in contrast, recombinant murine MFG-E8-treated wild-type mice showed a significant impro

152 s conducted in MFG-E8 and recombinant murine MFG-E8-treated wild-type mice.

153 ng PS blocking antibodies, annexin V, mutant MFG-E8 unable to bind VR, or VR antagonist).

154 Mutated MFG-E8, which binds viral envelope phosphatidylserine wi

155 Treg induction, whereas a dominant-negative MFG-E8 mutant potentiates GM-CSF-stimulated tumor destru

156 tion was affected by lactation stage but not MFG size.

157 Absence of MFG-E8 also led to decreases in tumor vascular permeabil

158 chemistry analysis confirmed accumulation of MFG-E8 in CP, with noticeably increased MFG-E8 immunorea

159 y was to determine whether administration of MFG-E8 attenuates renal ischemia-reperfusion injury.

160 previously shown that the administration of MFG-E8-rich exosomes from immature dendritic cells promo

161 In situ analyses of MFG-E8 expression in estrogen receptor (ER) positive cas

162 Study groups consisted of MFG at 1 mg/kg every 24 hours (MFG1), 2 mg/kg every 48 h

163 r strengthened differential contributions of MFG connections to each competency.

164 ed enterocyte migration, whereas deletion of MFG-E8 impeded mucosal healing in mice with sepsis.

165 Mean diameter of MFG, determined in raw whole milk, was 0.4 mum larger in

166 ile retaining the single promoter feature of MFG responsible for high virus titer and enhanced protei

167 e studies clearly indicate the importance of MFG-E8 in ameliorating neutrophil infiltration and sugge

168 uggests the role of miR-99b in inhibition of MFG-E8 gene expression.

169 Lack of MFG-E8 only minimally reduced retinal adhesion.

170 In contrast, lack of MFG-E8, like lack of alphavbeta5 receptor, eliminated al

171 e cancer patients presented higher levels of MFG-E8 compared with controls, a novel finding in human

172 The expression and localization of MFG-E8 was investigated in CP (n=62), and normal pancrea

173 Conversely, microinjection of MFG-E8 inhibited bone loss in experimental mouse periodo

174 PK of MFG were determined on day 7 by high-performance liquid

175 PK of MFG were linear and the parameter means +/- SD were Vc =

176 ation of closure, upholding the potential of MFG-E8-directed therapeutics in diabetic wound care.

177 sis, we hypothesized that down-regulation of MFG-E8 is mediated via the LPS-CD14 pathway, eventually

178 dependent manner and the down-regulation of MFG-E8 mRNA expression in CLP-induced sepsis was attenua

179 esent in the gut, the physiological roles of MFG-E8 in the intestinal mucosa have not been explored.

180 Thus, targeting of MFG-E8 within this signaling axis pathway is a potential

181 Transplantation of MFG-E8(-/-) bone marrow to MFG-E8(+/+) mice resulted in

182 of 293GPG cells using a modified version of MFG.SnlsLacZ, in which the cytomegalovirus IE promoter w

183 ant change in the size and zeta-potential of MFGs.

184 articipated in 1 of 2 MFGs (MFG-adherence or MFG-standard) or treatment as usual.

185 oglia were genetically deficient in MerTK or MFG-E8, both of which mediate phosphatidylserine-recogni

186 e isolation of total RNA directly from SC or MFG released into milk during lactation.

187 kdown tumor cells cultured with wild-type or MFG-E8-deficient macrophages resulted in increased SOCS3

188 ile fat content and composition in the other MFG size groups remains unchanged.

189 hPSCs overexpress MFG-E8 upon fractalkine stimulation in vitro, which unde

190 Using the proposed MFG to power a single nanowire-based pH sensor, a self-p

191 soluble phosphatidylserine-binding protein, MFG-E8, enhances transduction.

192 athways, and is inhibited by blocking the PS/MFG-E8/VR pathway (by adding PS blocking antibodies, ann

193 n iFC profiles to both competencies (e.g., R.MFG with cerebellum).

194 as numeracy associated with the right MFG (R.MFG).

195 as that numeracy was negatively related to R.MFG connections with the default network, which has been

196 cultures, but restored by adding recombinant MFG-E8, without affecting inflammation.

197 Soluble or POS-bound recombinant MFG-E8 was sufficient to fully restore phagocytosis by M

198 mucosal healing and suggest that recombinant MFG-E8 may be beneficial for the treatment of bowel inju

199 Topical recombinant MFG-E8 induced resolution of wound inflammation, improve

200 Treatment with recombinant MFG-E8 restored enterocyte migration, whereas deletion o

201 Endotoxemia reduced MFG-E8 mRNA expression in a dose dependent manner and th

202 Silencing MFG-E8 RNA substantially reduces MFG-E8 expression and VSMCs invasion capacity.

203 eporter assays all showed that p63 regulates MFG-E8 expression, and MFG-E8 knockdowns sensitized trip

204 ively, our study suggests that LPS represses MFG-E8 expression and disrupts enterocyte migration via

205 nd F-actin recruitment via Rac1 both require MFG-E8-ligated alphavbeta5 integrin.

206 l nanoparticle-conjugate capable of rescuing MFG-E8 gene expression and maintaining intestinal epithe

207 present study, we have used the retrovirus, MFG-IRAP, to transfer the human IL-1 receptor antagonist

208 We therefore aimed to reveal MFG-E8 roles in regulating lung neutrophil infiltration

209 y using offline TMS over right IPS and right MFG.

210 f the DAN, as well as the left IPL and right MFG/IFG of the VAN.

211 , whereas numeracy associated with the right MFG (R.MFG).

212 In contrast, perturbation of the right MFG had no effect on any of the conflict types.

213 right hemisphere frontal regions (FEF, SFG, MFG).

214 Silencing MFG-E8 RNA substantially reduces MFG-E8 expression and V

215 compositional regulation for large and small MFG at different lactation stages.

216 large MFG, but dropped twofold in the small MFG.

217 between treatments were found in a specific MFG subgroup with the diameter of 3.3 mum (F1), with hig

218 Splenic MFG-E8 expression, phagocytic activity, and apoptosis we

219 In the survival study, MFG-E8 mice showed a significant deterioration and, in c

220 iorating neutrophil infiltration and suggest MFG-E8 as a novel therapeutic potential for ALI.

221 ment and raise the possibility that systemic MFG-E8 blockade might prove therapeutic for melanoma pat

222 ciated with higher medication adherence than MFG-standard or treatment as usual only (F = 6.41; P = .

223 FG-E8) in antigen-presenting cells, and that MFG-E8-mediated uptake of apoptotic cells is a key deter

224 However, we show here that MFG-E8 can mediate phagocytosis of viable neurons during

225 In this work, we test the hypothesis that MFG-E8 helps resolve inflammation, supports angiogenesis

226 This study investigated the hypothesis that MFG-E8-mediated efferocytosis promotes M2 polarization.

227 These experiments indicate that MFG activation is reliably evoked by exemplars from arbi

228 Together, our data indicate that MFG-E8 plays an important role in the maintenance of int

229 Taken together, our results show that MFG-E8 is expressed in triple-negative breast cancers as

230 Here we show that MFG-E8 was expressed in intestinal lamina propria macrop

231 Here, we have shown that MFG-E8 controls phagocytic ingestion of cell fragments a

232 We have recently shown that MFG-E8 treatment attenuates organ injury, inflammatory r

233 Dual immunolabeling shows that MFG-E8 colocalizes with both angiotensin II and monocyte

234 together, these novel findings suggest that MFG-E8 blockade may be a promising tool for future immun

235 These observations suggest that MFG-E8 deficiency promotes immune responses to self anti

236 udy, we demonstrated for the first time that MFG-E8 is significantly up-regulated in CP patients and

237 The MFG-adherence participants had a longer time to first ho

238 ted with AD when comparing the groups in the MFG and ITG, respectively: linoleic acid (p < 0.0001, p

239 e former novels now evoked activation in the MFG, but the former target circles did not.

240 caudal/medial SFG and a small region of the MFG in a majority of the subjects analyzed.

241 -MFG-E8 antibody or targeted deletion of the MFG-E8 gene resulted in a slowing of enterocyte migratio

242 n of the 293GPG packaging cell line with the MFG.SnlsLacZ retroviral vector construct, it was possibl

243 This MFG activation did not differ as a function of the requi

244 The continuous electrical output makes this MFG particularly suitable as a power source in self-powe

245 Thus, MFG-E8 production is down-regulated in sepsis by LPS-CD1

246 Thus, MFG-E8 stimulates rhythmic POS phagocytosis by ligating

247 ransplantation of MFG-E8(-/-) bone marrow to MFG-E8(+/+) mice resulted in impaired wound closure and

248 At the end of the 1-year treatment, MFG-adherence was associated with higher medication adhe

249 Using MFG-based retrovirus vectors containing oxidase genes, w

250 The replication-defective retroviral vector MFG was used for GM-CSF gene transfer.

251 The retroviral vector MFG was used to transfer the G156A MGMT (deltaMGMT) cDNA

252 C were transduced with the retroviral vector MFG-enhanced green fluorescence protein as a marker gene

253 urine leukemia virus-based retroviral vector MFG-S encoding the human form of p47phox, we performed e

254 el, we have used a murine retroviral vector, MFG, that expresses the green fluorescent protein (GFP)

255 s uncover a unique role of efferocytosis via MFG-E8 as a mechanism for macrophage polarization into t

256 e epidermal growth factor (EGF)-factor VIII (MFG-E8) mediates the clearance of apoptotic cells.

257 globule-epidermal growth factor-factor VIII (MFG-E8), a membrane-associated secretory glycoprotein, i

258 rrow cells infected with the parental virus (MFG).

259 , and green tea extract were added to washed MFGs to examine possible interactions.

260 However, whether MFG-E8 can regulate neutrophil function to alleviate inf

261 elated WM performance, FFA connectivity with MFG predicted LTM improvements.

262 Treatment of VSMCs with MFG-E8 increases MCP-1 expression and VSMCs invasion tha