ライフサイエンスコーパス: MCP

1 MCP substrates were straightforwardly prepared by a pall

2 MCP-1 induces a dose-responsive increase in Nf1(+/-) mac

3 MCP-1 inhibition resulted in reduced CCR2-expressing Ly6

4 MCP-1 inhibition, however, increased glomerular endothel

5 MCP-1 protein stimulates EC proliferation and migration

6 MCP-1 regulates inflammatory cell recruitment and differ

7 MCP-1-induced protein-1 (MCPIP1), a critical regulator o

8 MCPs are fundamentally different from other organelles i

9 MCPs are widely distributed among bacteria and impact pr

10 MCPs manifest as a complex of insertions around a bacter

11 <0.01), IL-7 (P<0.05), IL-8/CXCL8 (P<0.001), MCP-3/CXCCL7 (P<0.05) and MIP-1alpha/CCL-3 (P<0.05) were

12 IL-8/CXCL8 (P<0.001), IP-10/CXCL10 (P<0.05), MCP-1/CCL2 (P<0.05), macrophage inflammatory protein (MI

13 egulation of monocyte chemotactic protein 1 (MCP-1) and inflammatory cytokine TNF-alpha.

14 response to monocyte chemotactic protein 1 (MCP-1) and lipopolysaccharide compared with WT mouse mac

15 6 (IL-6) and monocyte chemotactic protein 1 (MCP-1) expression were assessed using reverse transcript

16 imulated monocyte chemoattractant protein 1 (MCP-1) from macrophages and possible mechanisms.

17 (VEGF), monocyte chemoattractive protein 1 (MCP-1), and granulocyte colony-stimulating factor (G-CSF

18 (IP-10), monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1 beta (MIP-1bet

19 (G-CSF), monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1beta (MIP-1beta

20 such as monocyte chemoattractant protein 1 (MCP-1), TNF-alpha, and IL-6 and hepatic cleaved caspase

21 IL-6 and monocyte chemoattractant protein 1 (MCP-1).

22 (IL-6), and monocyte chemotactic protein 1 (MCP-1).

23 -1beta), and monocyte chemotactic protein 1 (MCP-1).

24 factors, monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) secretion from 3T3-L1 ad

25 cytokine monocyte chemoattractant protein-1 (MCP-1) and MCP-1 induced protein-1 (MCPIP1), a suppresso

26 ation to monocyte chemoattractant protein-1 (MCP-1) as well as IL-17A, which has been linked to cGVHD

27 a), and monocyte chemo attractant protein-1 (MCP-1) in MRSA USA300 skin lesions.

28 imary ligand monocyte chemotactic protein-1 (MCP-1) is critical for monocyte infiltration into the ar

29 report that monocyte chemotactic protein-1 (MCP-1) is secreted by nonpigmented mouse melanocytes by

30 ponectin and monocyte chemotactic protein-1 (MCP-1) levels in culture media were measured by ELISA.

31 S1P and monocyte chemotactic protein-1 (MCP-1) levels were significantly elevated in the broncho

32 4 (TLR4) and monocyte chemotactic protein-1 (MCP-1) that colocalize in neurons from the central nucle

33 produced monocyte chemoattractant protein-1 (MCP-1) upon PIM treatment, and absence of DCAR or FcRgam

34 control, and monocyte chemotactic protein-1 (MCP-1) were identified as the most important distinguish

35 nhibition of monocyte chemotactic protein-1 (MCP-1) with the Spiegelmer emapticap pegol (NOX-E36) sho

36 terleukin-6, monocyte chemotactic protein-1 (MCP-1), and soluble CD40 ligand were also observed in th

37 emokine, monocyte chemoattractant protein-1 (MCP-1), is a mediator of PTH's anabolic effects on bone.

38 hemokine Monocyte Chemoattractant Protein-1 (MCP-1)/CCL2 with different binding affinities.

39 ], IL-8, monocyte chemoattractant protein 1 [MCP-1], and IL-1beta) than do UN individuals.

40 ined by increased renal expression of LLT-1, MCP-1, and VLA-4.

41 ll recruiting (G-CSF, IL-1beta, IL-8, MCP-1, MCP-3, TNF-alpha), polarizing (CXCL13, IL-10, IL-13, IL-

42 1-MCP application maintained higher flesh firmness and red

43 signaling inhibitor, 1-methylcyclopropane (1-MCP), reversed the sHSP gene suppression.

44 atmosphere (CA), CA+1-methylcyclopropene (1-MCP) and dynamic controlled atmosphere monitored by resp

45 Sletr1-1 mutation or 1-methylcyclopropene (1-MCP), resulted in elongated parthenocarpic fruit and inc

46 ated with or without 1-methylcyclopropene (1-MCP).

47 but did not differ from those treated with 1-MCP.

48 (RANTES, monocyte chemoattractant protein 1[MCP-1], and IP-10) were increased.

49 2, IFN-gamma, and chemokines (IP-10/CXCL-10, MCP-1/CCL-2, MIP-1alpha/CCL-3, RANTES/CCL-5, and interle

50 Mean IP-10, MCP-1, MIP-1beta, and IL-18 levels all decline on therap

51 DC), CCL17 (TARC), CCL-2 (MCP-1) and CCL-13 (MCP-4) in both asthma groups after oral corticosteroids.

52 The plasma levels of IL-17A, MCP-1, and monokine induced by IFN-gamma were increased

53 significantly decreased TNF-alpha, IL-1beta, MCP-1, NF-kappaB liver expression and caspase 3 activity

54 0 (IP-10), CCL22 (MDC), CCL17 (TARC), CCL-2 (MCP-1) and CCL-13 (MCP-4) in both asthma groups after or

55 in-2 (IL-2), monocyte chemotactic protein 2 (MCP-2), interferon gamma inducible protein-10 (IP-10), i

56 on of 2-monochlorophenol at 230 degrees C (2-MCP-230) on copper oxide supported by silica, 5% Cu(II)O

57 benzene (1,2-DCBz) and 2-monochlorophenol (2-MCP) over a model surface consisting of 5% CuO/Silica.

58 The higher the 1,2-DCBz to 2-MCP ratio, the lower the PCDD to PCDF ratio.

59 lbumin ratio), and glial activation (YKL-40, MCP-1, and GFAP).

60 the secretion and expression of PAI-1, IL-6, MCP-1 and leptin in mature 3T3-L1 adipocytes under basel

61 educed the expression and secretion of IL-6, MCP-1 and leptin, as well as suppressed the overexpressi

62 many pro-inflammatory cytokines (e.g. IL-6, MCP-1, IL-22, TNF-alpha) and pronounced complement consu

63 IL), cell recruiting (G-CSF, IL-1beta, IL-8, MCP-1, MCP-3, TNF-alpha), polarizing (CXCL13, IL-10, IL-

64 sion of hepatic inflammatory markers (F4/80, MCP-1, TLR4, TLR2 and IL-1beta) and effector caspase (ca

65 t, and absence of DCAR or FcRgamma abrogated MCP-1 production.

66 inflammatory cytokine production (TNF-alpha, MCP-1, and KC).

67 inflammatory cytokines (including TNF-alpha, MCP-1, and keratinocyte-derived protein chemokine [KC])

68 regulated the expression of IL-6, TNF-alpha, MCP-1/CCL2 and IFN-gamma in sera, and ameliorated the or

69 eatment with sodium metal in liquid ammonia, MCPs bearing a C-O bond at allylic position undergo both

70 This is the first evidence of an MCP binding to an aromatic molecule and triggering signa

71 monstrated that intravitreal injection of an MCP-1-neutralizing antibody promoted the recovery of ret

72 +/- 5 versus 9 +/- 2 ng/ml, p < 0.0001) and MCP-1 (867 +/- 150 versus 216 +/- 36 ng/ml, p < 0.0001)

73 ociated with increased levels of PECAM-1 and MCP-1 in lal(-/-) ECs.

74 nocyte chemoattractant protein-1 (MCP-1) and MCP-1 induced protein-1 (MCPIP1), a suppressor of miR-14

75 n of the cytokines IL-1beta, IL-8, IL-10 and MCP-1, whereas exposure to platelets from healthy volunt

76 ted A1-KO mice, but levels of KC, IP-10, and MCP-1 were increased.

77 -8, IL-15, IL-16, IL-17, CXCL10 [IP-10], and MCP-1 [CCL2]) in BAL samples (n=233) from patients with

78 mediated production of TNF, IL-6, IL-13, and MCP-1 in a concentration-dependent manner.

79 secretion of VEGF, IL-6, IL-8, IL-1beta and MCP-1, leading to neovascularization and increased resis

80 IL-10, IL-6, MIP-1alpha, MIP-1beta, and MCP-2 were associated with increased odds of SM.

81 ients (mainly CCL11, CCL24, CCL5, MCP-3, and MCP-4), cell surface expression of adhesion molecules (s

82 e GRO-alpha (CXCL1), RANTES (CCL5), IL-6 and MCP-1 (CCL2).

83 Vaccination decreased expression of IL-6 and MCP-1 and reduced macrophage infiltration in the aorta.

84 e content, elevated plasma interleukin-6 and MCP-1 levels, and decreased skeletal muscle mass.

85 ignificantly attenuates circulating IL-6 and MCP-1 levels, limits the expression of adhesion molecule

86 Blood levels of IL-6 and MCP-1 remained unchanged, and histology analysis showed

87 active oxygen species and increased IL-6 and MCP-1 secretion in lal(-/-) ECs.

88 ukin (IL)-1-dependent expression of IL-6 and MCP-1, enhances beta-cell apoptosis, and impairs mitocho

89 HFD also increased plasma leptin, IL-6, and MCP-1 in WT and increased arcuate expression of Kiss1 an

90 trophils and serum levels of IL-8, IL-6, and MCP-1 which varied with cause of death.

91 reased serum cytokines (IFN-gamma, IL-6, and MCP-1) and acute toxicity similar to cytokine release sy

92 Basal IL-8 and MCP-1 synthesis by monocytes alone did not differ betwee

93 Inhibiting GrmA reduced excessive IL-8 and MCP-1 synthesis in aging to levels similar to younger ad

94 ts, p < 0.05) and governs increased IL-8 and MCP-1 synthesis through TLR4 and caspase-1.

95 tus induced the secretion of IL-6, IL-8, and MCP-1, and the upregulation of CD54 (ICAM-1), consistent

96 eroid treatment, inhibition of TNF-alpha and MCP-1 function or depletion of macrophages suppressed fe

97 lammatory cytokines (including TNF-alpha and MCP-1) in viral-induced exacerbation of asthma and sugge

98 gamma and IL-27, downstream of TNF-alpha and MCP-1, in the mechanism of RSV-induced exacerbation.

99 iated with higher serum IL-6, TNF-alpha, and MCP-1 levels but decreased secretion of IFN-gamma.

100 elevated anti-dsDNA, anti-snRNP, CXCL1, and MCP-1 levels compared to untreated mice; however levels

101 hat NFATc4 siRNA reduced CXCL10, CXCL11, and MCP-1 protein levels.

102 Furthermore, levels of VEGF-D and MCP-1 in patient sera correlated positively with each ot

103 ncludes increase of IL-5, IL-13, eotaxin and MCP-3; infiltration of eosinophils into the airway submu

104 of exosomes was abolished when MSC-Exos and MCP-1 were administrated simultaneously.

105 Mutations in FH and MCP are linked to atypical hemolytic uremic syndrome, a

106 nown as cofactor activity) of C3b via FH and MCP.

107 al chemoattractants like chemerin, fMLF, and MCP-1; and doubled the phagocytic activity of these macr

108 on of immune mediators GM-CSF, IFN-gamma and MCP-1, while suppressing an excessive and potentially ha

109 increased production of TNF, IFN-gamma, and MCP-1/CCL2.

110 ulation of macrophages with a CD86(high) and MCP-1(high) M1-like phenotype that suppressed tumor grow

111 VCAM-1 (vascular cell adhesion molecule) and MCP-1 (monocyte chemotactic protein) were reduced in mic

112 , normal T cell expressed and secreted), and MCP-1.

113 Increased levels of TNFalpha and MCP-1 correlated with IgE-mediated tumor cytotoxicity by

114 ntinuously infused female wild-type (WT) and MCP-1(-/-) mice with hPTH or vehicle.

115 otential connections between CheD, CheX, and MCPs and discuss how these interactions play critical ro

116 Intravenous PDNF also augments MCP-1 and FKN in TLR signaling-deficient MyD88-knockout

117 onsiderable interest in exploiting bacterial MCPs for metabolic engineering applications, but little

118 ttle is known about the interactions between MCP signal sequences and the protein shells of different

119 n into the cryoEM map reveals that SCP binds MCP largely via hydrophobic interactions and the kinked

120 ression and secretion of the chemokine CCL2 (MCP-1).

121 ession of AIMP1 (OMIM 603605) (EMAP2), CCL2 (MCP-1) (OMIM +158105), and IL1b (OMIM *147720).

122 d, and massive astroglial induction of CCL2 (MCP-1), a chemokine for CCR2(+) monocytes.

123 L-18, monocyte chemotactic protein-1 (CCL2) (MCP-1), tissue plasminogen activator inhibitor (PAI-1),

124 Moreover, expression of chemokine CCL2, MCP-1 and its receptor CCR2, which play an important rol

125 ion of COX-2 abrogated the induction of CCL2/MCP-1 expression by beta-adrenergic activation and preve

126 mokine gradients (mainly CCL11, CCL24, CCL5, MCP-3, and MCP-4), cell surface expression of adhesion m

127 inflammatory state with elevated Ly6C, CCR5, MCP-1 and reduced SR-B1.

128 superfamily, unlike previously characterized MCP hydrolases, which are serine-dependent enzymes of th

129 TNFalpha and the macrophage chemoattractant MCP-1 in lung bronchoalveolar lavage fluid.

130 expression of the proinflammatory chemokine MCP-1.

131 nd in vivo studies identified the chemokines MCP-1, RANTES, and CXCL10 as MAP3K14 targets in tubular

132 ll-described chemotaxis elements CheY, CheW, MCP, and CheA.

133 how 2.3-fold decreased levels of circulating MCP-1.

134 At 30 days after treatment completion, MCP-1 levels remained lower in the experimental group th

135 The most complex MCP elucidated so far is the propanediol utilizing (Pdu)

136 increase in proinflammatory cytokine (CXCL1, MCP-1, TNF-alpha, and IL-6) expression and infiltration

137 tic factor Bim and proinflammatory cytokines MCP-1, IL-6, and E-selectin.

138 protein 10]), and proinflammatory cytokines (MCP-1 [monocyte chemoattractant protein 1], MIP-1alpha/b

139 iverges from what occurs in serine-dependent MCP hydrolases.

140 equences and the protein shells of different MCP systems.

141 DN/MCP and DN-to-pons ratios were significantly different b

142 DN/MCP, DN-to-pons, GP-to thalamus, and GP-to-cerebrospinal

143 Results DN/MCP (rho = 0.51, P < .0001) and DN-to-pons (rho = 0.41,

144 A significant increase in GP:TH and DN:MCP is associated with multiple gadodiamide-enhanced stu

145 t trend toward an increase in Rchange for DN:MCP (P = .013).

146 Rchange (P = .001 for GP:TH, P < .001 for DN:MCP).

147 odiamide showed a significant increase in DN:MCP and GP:TH (P < .001 for both) and in Rchange (P = .0

148 p 2, there was no significant increase in DN:MCP or GP:TH over time or in Rchange for GP:TH, but ther

149 sters (clusters 1 and 3) with genes encoding MCPs lacking cyanobacteriochrome sensory domains, are up

150 s article, we show that the endoribonuclease MCP-1-induced protein 1 (MCPIP1; also known as regnase-1

151 stable transgenic zebrafish lines expressing MCP, validated the MBS-MCP interaction and applied the s

152 uction, and proinflammatory gene expression (MCP-1).

153 ken together, this study implicates the FMOD/MCP-1 pathway in the regulation of angiogenesis by local

154 200-fold difference in binding affinity for MCP-1.

155 of the two distinct conformations known for MCP-1 dimers.

156 BMMs from MCP-1(-/-) mice showed decreased multinucleated osteocla

157 n vitro, bone marrow macrophages (BMMs) from MCP-1(-/-) and WT mice were cultured with M-CSF, RANKL a

158 Monokine induced by IFN-gamma, MCP-1, and IFN-gamma production induced in T. cruzi-infe

159 udy, we investigated the factors that govern MCP assembly by performing scanning mutagenesis on the s

160 cluding the glycyl-radical propanediol (Grp) MCP.

161 Human MCP-1-induced protein 1 (MCPIP1, also known as ZC3H12A a

162 sticity, thoracic scoliosis, hyperextendable MCP joints, rocker-bottom feet, hyperextended elbows and

163 These studies identify MCP-1 as a potent chemokine for Nf1(+/-) monocytes/macro

164 esses the TLR9 (toll-like receptor 9), IFNG, MCP-1 (monocyte chemoattractant protein-1) and GM-CSF ge

165 mice results in a dose-dependent increase in MCP-1 and FKN in the heart and liver with pulse-like kin

166 om homozygous carriers showed an increase in MCP-1 release in carriers of the minor allele, with the

167 tly elevated inflammatory markers including: MCP-1 SDF-1a, IL-Ra, MIP-1b, IL-8, and VEGF in compariso

168 hough single PDNF injections do not increase MCP-1 and FKN receptors, multiple PDNF injections at sho

169 imicrobial peptide expression, and increased MCP-1/CCL2 secretion.

170 r GRP78 or linoleic acid treatment increased MCP-1 serum levels, decreased CD47 expression, and incre

171 ionine-beta-synthase pathway, with increased MCP-1 protein and mRNA expression in both THP-1 cells an

172 f C. albicans repressed F. nucleatum-induced MCP-1 and TNFalpha production in macrophages.

173 upregulating TNFalpha, which in turn induced MCP-1 production by monocytes and tumor cells to promote

174 s also associated with reduced inflammation (MCP-1, MIP-2, TNF-alpha, IL-6 and CD68), decreased accum

175 xpressed the proinflammatory mediators iNOS, MCP-1 and IL-1beta.

176 tokines (IL-1beta, IL-6) and chemokines (KC, MCP-1) known to drive tissue damage.

177 Plasma leukocyte chemokines (KC, MCP-1, and RANTES) and myeloperoxidase activity were als

178 the ILFs and IFOFs (p<0.001) and in the left MCP and right SLF (p<0.05), compared to the normal subje

179 n the two cell types showed that the ligand (MCP-1) is more highly expressed in KCs than in RHMs, whe

180 d the expression of THP-1-derived macrophage MCP-1 by enhancing NF-kappaB p65 phosphorylation, nuclea

181 sulted in a reduced THP-1-derived macrophage MCP-1 generation.

182 d the expression of THP-1-derived macrophage MCP-1.

183 We report that in murine macrophages MCP-1-induced protein (MCPIP), induced by KLF4, inhibits

184 fish lines expressing MCP, validated the MBS-MCP interaction and applied the system to investigate zy

185 ased expression of proinflammatory mediators MCP-1 and nuclear factor-kappaB.

186 a human cadaver distal metacarpophalangeal (MCP) joint with the ammonium nanoparticles showed good v

187 a in synovial tissue in metacarpophalangeal (MCP) joints of 16 patients were imaged, and compared to

188 gas-phase conversion of methylcyclopentane (MCP) to acyclic isomer, olefins, cyclohexane, and benzen

189 ive isomerization of methylenecyclopropanes (MCPs) to vinylcyclopropanes (VCPs).

190 nal diversity of bacterial microcompartment (MCP) systems, which serve as protein-based metabolic org

191 Bacterial microcompartments (MCPs) are protein-bound organelles that carry out divers

192 nelles known as bacterial microcompartments (MCPs), enabling the metabolism of carbon sources to enha

193 nelles known as bacterial microcompartments (MCPs).

194 The MS2-MCP system enables researchers to image multiple steps o

195 ses a kinked helix to cross-link neighboring MCP subunits.

196 kinked helix of SCP bridges over neighboring MCPs to form noncovalent cross-links.

197 luding the expression of TGF-beta, NFkappaB, MCP-1, IL-1, IL-6, ICAM-1, VCAM-1 and CD68 macrophages.

198 Notably, MCP-1(-/-) mice were protected against PTH-induced corti

199 The expression of ICAM-1, VCAM-1 and of MCP-1 was elevated and apoptosis was increased.

200 Downregulation of MCP-1/CCL2 release was also observed during OASL knock d

201 ssociated with increased renal expression of MCP-1 (monocyte chemoattractant protein-1) and VLA-4 (ve

202 ystathionine could inhibit the expression of MCP-1 in THP-1-derived macrophages induced by ox-LDL via

203 High or low expression of MCP-1, eotaxin, and IL-8 discriminates between eosinophi

204 The presence of high or low expression of MCP-1, eotaxin, and IL-8 identified two separate blood e

205 ha receptor signaling abrogated induction of MCP-1, implicating it in the antitumor effects of IgE.

206 n podocytes in vitro led to an inhibition of MCP-1 and IL-6 expression in response to TNF-alpha and I

207 aucasians have 2-fold higher serum levels of MCP-1 than African Americans.

208 Loss of MCP-1 or CCR2 expression effectively inhibited Nf1(+/-)

209 Conversely, augmented production of MCP-1 and IL-6 was observed in the glomeruli of C/EBP-al

210 Acute-phase production of MCP-1 correlated with viremia at 3 months postinfection

211 injury partially through down-regulation of MCP-1.

212 ease of adiponectin and inhibited release of MCP-1 from the fat.

213 thy volunteers only induced the secretion of MCP-1.

214 lavages as well as impaired upregulation of MCP-1/CCL2.

215 c studies determine that FMOD is upstream of MCP-1 and promotes its secretion from both melanocytes a

216 New types of MCPs have been identified, including the glycyl-radical

217 induce TNF-alpha, IL-1beta, IL-6, IL-12, or MCP-1 production in STING(-/-) mice.

218 emonstrated a defect in binding to FH and/or MCP, whereas 2 demonstrated reduced binding to CR1.

219 of pulmonary macrophage by TNF-alpha and/or MCP-1 in the mechanisms of RSV-induced exacerbation.

220 pulmonary macrophages with TNF-alpha and/or MCP-1 induced expression of both IFN-gamma and IL-27.

221 mice were cultured with M-CSF, RANKL and/or MCP-1.

222 mice did not show elevated levels of S1P or MCP-1.

223 for scrambled siRNA did not inhibit TLR4 or MCP-1 expression nor reduce binge drinking, identifying

224 Infusion of amplicons for TLR4 or MCP-1 siRNA into the CeA or VTA from the P rats inhibite

225 some cytokines (TNF-a, IL-3) but not others (MCP-1, IL-4).

226 Overall, MCPs consist of metabolic enzymes encased within a prote

227 t Eut proteins might be localized to the Pdu MCP in vivo.

228 eting sequences for encapsulation in the Pdu MCP.

229 I) network governing the assembly of the Pdu MCP.

230 esh insight into the organization of the Pdu MCP.

231 eterologous proteins encapsulated within Pdu MCPs.

232 ins to the 1,2-propanediol utilization (Pdu) MCP, and that this localization is mediated by a conserv

233 o-pons and DN-to-middle cerebellar peduncle (MCP) ratios by subtracting the SI ratio at the first MR

234 o-pons and DN-to-middle cerebellar peduncle (MCP) ratios in a region-of-interest-based analysis, and

235 ity ratio, DN-to-middle cerebellar peduncle (MCP) signal intensity ratio and relative percentage chan

236 relation to the middle cerebellar peduncle (MCP), pons, and thalamus after repeated administration o

237 including: the middle cerebellar peduncles (MCP), the inferior longitudinal fasciculi (ILF), inferio

238 complexed with alpha-maltose-C-phosphonate (MCP), a non-hydrolyzable substrate analogue, was solved

239 resulted in a significant decrease in plasma MCP-1 on day 3 and reduced exhaled breath condensate aci

240 se from the ELIT using a microchannel plate (MCP) enables the acquisition of multireflection time-of-

241 the hydrolysis of the meta-cleavage product (MCP) 4,11-dicarboxy-8-hydroxy-9-methoxy-2-hydroxy-6-oxo-

242 t stabilize the shell of the 1,2-propanediol MCP.

243 pression of monocyte chemoattractant protein MCP-1, which in peripheral blood mononuclear cells (PBMC

244 ression of the complement inhibitory protein MCP on quiescent EC, but does not induce complement depo

245 (Eut) and glycyl radical-generating protein MCPs are able to target reporter proteins to the 1,2-pro

246 eighth the size of the major capsid protein (MCP), the smallest capsid protein (SCP) of human tumor h

247 th AHR and monocyte chemoattractant protein (MCP)-1 with asthma severity and fast LF decline.

248 ectin, and monocyte chemoattractant protein (MCP)-1.

249 -regulation of monocyte chemotactic protein (MCP)-1 in the retina was found after MSC-Exos injection.

250 of the methyl-accepting chemotaxis protein (MCP)-null mutant CNB-1Delta20.

251 fluorescent MS2 bacteriophage coat protein (MCP) and an RNA of interest tagged with multiple copies

252 , the tight binding of the MS2 coat protein (MCP) to the MS2 binding sites (MBS) protects the RNA fro

253 FH) in plasma and membrane cofactor protein (MCP) on the cell surface.

254 ns factor H (FH), membrane cofactor protein (MCP; CD46), and complement receptor 1 (CR1; CD35).

255 of the herpesvirus-conserved capsid proteins MCP, Tri1, Tri2, and SCP and the HCMV-specific tegument

256 rescently tagged viral RNA-binding proteins (MCP and PCP) to specific genomic sites.

257 tative methyl-accepting chemotaxis proteins (MCPs), revealed that pcaY encodes the MCP required for m

258 computational all-atom Monte Carlo pulling (MCP) approach that enables us to model results at pullin

259 or LPS - secretory responses (VEGF, RANTES, MCP-1, IL-17A, IFN-gamma, GM-CSF, eotaxin, MIP1-alpha, M

260 We present crystal structures of human RCA (MCP, DAF, and CR1) and a smallpox virus homolog (SPICE)

261 thyl-accepting chemotaxis protein receptors (MCPs) and by increasing the receptor kinase activity or

262 had a greater effect on calponin reduction, MCP-1 inhibition, and p38 MAP kinase inhibition than any

263 In vitro, MSC-Exos also down-regulated MCP-1 mRNA expression in primarily cultured retinal cell

264 Taurocholate induced LPCs to release MCP-1, MIP1alpha, and RANTES into conditioned medium cau

265 ta1, and TNF-alpha cytokines while restoring MCP-2 levels, suggesting that H4K12ac may be playing a m

266 over, CheD specifically binds two of the six MCPs, indicating that CheD may also modulate the recepto

267 ntreated mice; however levels of anti-snRNP, MCP-1, and CXCL1 were reduced in pristane-treated Psgl-1

268 duction and exacerbated TNF-alpha-stimulated MCP-1 and IL-8 secretion.

269 is review, we discuss the three best-studied MCPs highlighting atomic-level models for shell assembly

270 r expression of ETS-1 and two ETS-1 targets, MCP-1 and MMP2, did not increase as substantially in ES

271 Taken together, our work demonstrates that MCP-1 has a role in PTH's catabolic effects on bone incl

272 n diabetic nephropathy, we hypothesized that MCP-1 inhibition restores glomerular barrier function th

273 We show that MCP-1 inhibition restores glomerular endothelial glycoca

274 teins (MCPs), revealed that pcaY encodes the MCP required for metabolism-independent chemotaxis to va

275 this SCP model and a homology model for the MCP upper domain into the cryoEM map reveals that SCP bi

276 system (MBSV6) with reduced affinity for the MCP, which allows mRNA degradation while preserving sing

277 showed that the expression of MCP2901 in the MCP-null mutant restored chemotaxis toward nine tested a

278 sidues of PduA, a major shell protein of the MCP used for 1,2-propanediol degradation.

279 n, nuclear translocation, and binding of the MCP-1 promoter sequence after entry into the nucleus.

280 A comparison of the MCP-1/C-C chemokine receptor type 2 (CCR2) chemokine sys

281 perfamily, is likely to localize outside the MCP, interacting with the protruding beta-barrel of the

282 DNA binding activity, and recruitment to the MCP-1 promoter in ox-LDL-treated macrophages.

283 DNA binding activity, and recruitment to the MCP-1 promoter.

284 and DNA binding level of NF-kappaB with the MCP-1 promoter, which resulted in a reduced THP-1-derive

285 clear translocation and DNA binding with the MCP-1 promoter.

286 ge accumulation and expression of p65, TLR4, MCP-1, and osteopontin.

287 To examine the potential role of a TLR4/MCP-1 signal, we used Herpes Simplex Virus (HSV) vectors

288 binge drinking, identifying a neuronal TLR4/MCP-1 signal that regulates the initiation of voluntary

289 ncluding significant reductions in TNFalpha, MCP-1 (CXCL2), RANTES (CCL5) and KC (CCL5).

290 nocompetent animal, and we identify TNFalpha/MCP-1 signaling as an IgE-mediated mechanism of monocyte

291 ncentrations between 1 and 3% in relation to MCP and phenol adsorption.

292 strate an enhanced proliferative response to MCP-1 when compared with WT SMCs.

293 r DN-to-pons ratio = 0.09 and that for DN-to-MCP ratio = 0.12).

294 e (0.10 for DN-to-pons ratio; 0.27 for DN-to-MCP ratio).

295 s ratio: -0.0032 +/- 0.0154, P = .248; DN-to-MCP ratio: -0.0011 +/- 0.0093, P = .521), and one-sided

296 s ratio: -0.0012 +/- 0.0101, P = .436; DN-to-MCP ratio: 0.0007 +/- 0.0088, P = .604), and one-sided B

297 We then used MCP to analyze AFM spectroscopy experiments that probed

298 rminal sequence from the ethanol utilization MCP system that previously did not act as a Pdu signal s

299 ions of C3b involved in the interaction with MCP and CR1 and interrogated relative to known FH bindin

300 f signaling arrays through interactions with MCP-proteins and CheA.