ライフサイエンスコーパス: MCP

1 MCP-1 and IL-7 concentrations increased after lymphodepl

2 MCP-1 antibody significantly decreased tumor burden and

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

4 MCP-1 inhibition, however, increased glomerular endothel

5 MCP-1 regulates inflammatory cell recruitment and differ

6 MCP-1-induced monocyte chemotaxis is a crucial event in

7 MCP-4 and the tryptase MCP-6 emerge to be protective in

8 MCPs manifest as a complex of insertions around a bacter

9 of the four N-linked glycans from the PBCV-1 MCP consist of nonasaccharides, and similar glycans are

10 mble four of the nine residues of the PBCV-1 MCP N-glycans.

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

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

13 ncluding monocyte chemoattractant protein 1 (MCP-1), interleukin (IL) 6, and IL-8.

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

15 ight and monocyte chemoattractant protein 1 (MCP-1).

16 ction of monocyte chemoattractant protein 1 (MCP-1).

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

18 -1beta), and monocyte chemotactic protein 1 (MCP-1).

19 p<0.05), monocyte chemoattractant protein-1 (MCP-1) (0.798, p<0.005), transforming growth factor-beta

20 nd decreased monocyte chemotactic protein-1 (MCP-1) (513.3 pg/mL vs 809.5 pg/mL; P = .0.042) concentr

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

22 um day 0 monocyte chemoattractant protein-1 (MCP-1) and peak interleukin-7 (IL-7) concentrations abov

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

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

25 /MDC, and monocyte chemoattactant protein-1 (MCP-1) levels were higher in subjects with SAR, whereas

26 ligand, monocyte chemoattractant protein-1 (MCP-1) promotes cancer progression by directly stimulati

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

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

29 (IP-10), monocyte chemoattractant protein-1 (MCP-1), IFN-gamma, interleukin (IL)-6, IL-8 and IL-1ra (

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

31 N-gamma, monocyte chemoattractant protein 1 [MCP-1; chemokine (C-C motif) ligand 2 (CCL2)], and tumor

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

33 9, monocyte chemoattractant protein (MCP)-1, MCP-2, MCP-3, CXCL9, CXCL10, CXCL5, ENRAGE, and poly (AD

34 23p40, IL-12p70, IL-13, IL-16, IP-10, MCP-1, MCP-4, MDC, MIP-1a, TARC, TNFB) was associated with dimi

35 1-MCP application maintained higher flesh firmness and red

36 formation regarding how blockage caused by 1-MCP may be circumvented at the metabolic level, thus ope

37 suppressed by the ET perception inhibitor 1-MCP.

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

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

40 1-methylcyclopropene (1-MCP) in an ethylene receptor antagonist that blocks ethy

41 ene (NC), as well as 1-methylcyclopropene (1-MCP) on ethylene production and fruit quality of Cripps

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

43 ever, in European pear, the application of 1-MCP irreversibly obstructs the onset of system 2 ethylen

44 ort that activation of AOX via exposure of 1-MCP treated 'D'Anjou' pear fruit to glyoxylic acid trigg

45 whilst the Granny Smith fruit treated with 1-MCP exhibited lowest ethylene production followed by NC

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

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

48 flammatory proteins, including; IL-6, IL-10, MCP-1, sVCAM-1, MIP-1alpha, IP-10, GM-CSF, M-CSF, TNF-al

49 -12/IL-23p40, IL-12p70, IL-13, IL-16, IP-10, MCP-1, MCP-4, MDC, MIP-1a, TARC, TNFB) was associated wi

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

51 ls of eotaxin, IFN-gamma, IL-6, IL-8, IL-16, MCP-1, MIF and MIP-1 beta were significantly higher in a

52 flammatory cytokines (IL-1beta, IL-6, IL-17, MCP-1, MIP-1alpha, MIP-2, RANTES, and TNF-alpha), inflam

53 a, IL-5, IL-6, TNF-alpha, RANTES, MIP-1beta, MCP-1, KC and IL-10).

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 cyte chemoattractant protein (MCP)-1, MCP-2, MCP-3, CXCL9, CXCL10, CXCL5, ENRAGE, and poly (ADP-ribos

57 roinflammatory genes (CXCL1/KC, CXCL2/MIP-2, MCP-1/CCL2, CXCR2, IL-6, ICAM-1, P-selectin, and C5aR) w

58 gher plasma levels of KIM-1, TNFR-1, TNFR-2, MCP-1, suPAR, and YKL-40 were associated with increased

59 her concentrations of KIM-1, TNFR-1, TNFR-2, MCP-1, suPAR, and YKL-40 were each associated with a gre

60 mation, and fibrosis (KIM-1, TNFR-1, TNFR-2, MCP-1, suPAR, and YKL-40).

61 formerly monocyte chemoattractant protein-3 (MCP-3)) using chimeras between CCL7 and the non-cognate

62 e investigated whether plasma KIM-1, YKL-40, MCP-1, suPAR, TNFR-1, and TNFR-2 are associated with GFR

63 improves from R(2) = 35.8% (MTAG) to 42.5% (MCP + CTPR) or 42.8% (Lasso + CTPR) with UK Biobank data

64 PD reduced IL-6, MCP-1, GM-CSF, and IFN-gamma in brains of WT mice and re

65 n of proinflammatory molecules such as IL-6, MCP-1, ICAM-1 and VCAM-1.

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

67 Levels of IP-10, HGF, IL-6, MCP-1, MIP-1alpha, IL-12p70, IL-18, VEGF-A, PDGF-BB and

68 Genotypes IC-2489-88, M-633, MCP-632, HUJM 1080, GR-325 and DJ-65 recorded high NUE a

69 nflammatory stress response in plasma (IL-8, MCP-1 and CRP collected two hours after temporary separa

70 Production of IL-6, IL-8, MCP-1, and OPG was significantly increased by Poly I:C o

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

72 robes useful to selectively report on type-A MCPs activity in complex media.

73 tory response, such as CXCL1, CXCL6, PDGF-A, MCP-1 and IL-6.

74 romoted bacterial killing but did not affect MCP-1 production.

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

76 +/- 5 versus 9 +/- 2 ng/ml, p < 0.0001) and MCP-1 (867 +/- 150 versus 216 +/- 36 ng/ml, p < 0.0001)

77 R2 (0.265, p<0.05), IL-6 (0.129, p<0.05) and MCP-1 (0.779, p<0.05) and lower levels of IL-8 (-1.293,

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

79 lpha, intracellular adhesion molecule 1, and MCP-1; P < 0.05), and reduced oxidative stress, while ma

80 (interleukin-4 [IL-4], IL-6, and IL-10) and MCP-1/CCL2 were detected early after P. yoelii yoelii 17

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

82 by their contrasting effects on IL-1beta and MCP-1 production.

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

84 etion of inflammatory mediators IL-1beta and MCP-1.

85 D11c expression or secretion of IL-1beta and MCP-1.

86 , IL-22, IL-33, IL-17alpha, IL-2, MIP-2, and MCP-1), and neutrophil infiltration (myeloperoxidase sta

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

88 ration reduced TRAF6 (~20%), CRF (~30%), and MCP-1 (~20%) levels, as well as TLR4 binding to GABA(A)

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

90 produced significantly less G-CSF, IL-6, and MCP-1 in the serum, spleen, and liver on day 1 postinfec

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

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

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

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

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

96 ion synergistically triggers IL-6, IL-8, and MCP-1 production, which was not observed for OPG.

97 ion of the CSF biomarkers T-tau, Abeta40 and MCP-1 separates iNPH from cognitive and movement disorde

98 T-tau, Abeta40 and MCP-1 together yielded an area under the curve of 0.86,

99 n algorithm consisting of T-tau, Abeta40 and MCP-1 was designed as a diagnostic tool using CSF biomar

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

101 cirrhosis was associated with higher ATX and MCP-1, female sex with higher ATX and IL-6, older age wi

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

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

106 terol concentrations are similar for MCC and MCP, but sphingolipids are enriched in MCP.

107 The starch and MCP mobilities appeared similar at a micron scale.

108 ing close interaction between the starch and MCP.

109 cell, with decrease levels of IL-10, TNF and MCP-1.

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

111 Baseline concentrations of VEGF and MCP-1 are associated with anatomic response to anti-VEGF

112 pokines/cytokines including IGF-1, VEGF, and MCP-1, along with decreased AR, Ki67, and microvessel de

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

114 vaccine in soluble factors release, such as MCP-1 or IL-15.

115 r (such as YKL-40), or inflammation (such as MCP-1, suPAR, TNF receptor-1 [TNFR-1], and TNFR-2) may i

116 d a significant association between baseline MCP-1 levels and higher risk of ischemic stroke (HR, 1.1

117 overlap were highly variable, likely because MCP and SEA inherently include or exclude unused areas i

118 SAP reduced serum levels of IL-23, IFN-beta, MCP-1, and tumor necrosis factor-alpha, whereas 1866 red

119 ific Src kinase isoform that is activated by MCP-1 and acts upstream of Pyk2 in primary monocytes.

120 ithelial growth factor), GM-CSF, IL-10, CCL2/MCP-1, CCL3/MIP-1a, CXCL10/IP-10, CCL5/RANTES, and CCL20

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

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

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

124 expression of the proinflammatory chemokine MCP-1.

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

126 ed associations between baseline circulating MCP-1 levels and risk of any stroke, ischemic stroke, an

127 to compensate for release of SPs that clasp MCP capsomeres together.

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

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

130 Furthermore, by composing a four-CCP DAF-MCP chimera with robust CFA (for C3b and C4b) and DAA (f

131 rleuckin-6 (r = 0.47; P = .02) and decreased MCP-1 (r = -0.45; P = .03).

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

133 In order to simultaneously disrupt MCP-1/CCR2 signaling and target CCR2-expressing cancer c

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

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

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

137 The DN/MCP SI ratio increased linearly with the amount of gadob

138 erived proteins in combination with elevated MCP-1 compared with HI and the non-iNPH disorders.

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

140 increasingly clear that aberrantly expressed MCPs can support multiple hallmarks of carcinogenesis by

141 L7 and the non-cognate ligand CCL2 (formerly MCP-1).

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

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

144 Results of niche size from MCP, SEA and KUD were highly correlated but divergent am

145 However, chemokine release (e.g. MCP-1, RANTES and TARC) was significantly reduced in inh

146 ranulocyte colony-stimulating factor (GCSF), MCP-1, tumor necrosis factor alpha (TNF-alpha), and IgG

147 of archaeal viruses possess hetero-hexameric MCPs which mimic the PRD1-adeno lineage trimer.

148 ses-uses its N-terminal half to bridge hexon MCP subunits and possesses a C-terminal flexible half em

149 sex, race, and vascular risk factors, higher MCP-1 levels were associated with increased risk of any

150 ch of combining cardiac phenotyping in human MCPs and in the in vivo Drosophila heart at high through

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

152 L-4, 5, 10, 13, 17 A, Eotaxin, GM-CSF, IFNy, MCP-1, TARC, TNFalpha, Total IgE, and Endotoxin) were qu

153 ammation (increased IL1beta, IL8, IL4, IL10, MCP, MIP1alpha).

154 e of multiple cytokines including IL6, IL17, MCP-1, and GM-CSF in the tumor-bearing host, and persist

155 ced cord inflammation (reduced IL1beta, IL8, MCP, MIP1alpha, MIP1beta).

156 C and MCP, but sphingolipids are enriched in MCP.

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

158 Notably, knockdown (KD) in MCPs of RPL13, a ribosomal gene and SON, an RNA splicing

159 HMGB1, and inflammatory mediators, including MCP-1 and TNFalpha.

160 various pro-inflammatory molecules including MCP-1 and IP-10.

161 hat an inflammatory response with increasing MCP-1 and KIM-1 levels precedes loss of renal function.

162 GM-CSF-induced MCP-1/CCR2 signaling plays an important role in the cros

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

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

165 metastasis at least partially by inhibiting MCP-1 secretion from adipocytes independent of direct ef

166 ressing cancer cells for drug delivery, KLAK-MCP-1 micelles consisting of a CCR2-targeting peptide se

167 In vitro, KLAK-MCP-1 micelles were observed to bind and induce cytotoxi

168 In vivo, KLAK-MCP-1 micelles inhibited tumor growth (34 +/- 11%) in a

169 governing selectivity for type-A of the M14A MCP family.

170 und to be associated with a decrease in mean MCP width only in those individuals who developed FXTAS

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

172 Metallocarboxypeptidases (MCPs) of the M14 family are Zn(2+)-dependent exoprotease

173 e corroborated using a computational method (MCP-counter(18)) to estimate the immune and stromal comp

174 alculated for the superficial (SCP), middle (MCP), and deep capillary plexuses (DCP): parafoveal vess

175 Moreover, MCPs also reorganize the biomechanical properties of the

176 Both an MS2-MCP system and an engineered CRISPR-Cas13 system were us

177 dCas13 proteins or combining dCas13 and MS2-MCP allows dual-color imaging of RNAs in single cells.

178 Compared to the aptamer-based MS2-MCP strategy, an optimized dCas13 system is user friendl

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

180 Using the MS2-MCP system to visualize nascent transcripts in single ce

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

182 nary biomarkers including ATP, ACh, nitrite, MCP-1 and IL-5 and participants' confounders, age and ge

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

184 bsequent DNA packaging instigates bending of MCP A domain loops outwards, closing the hexons central

185 nse elicited by IL-4, sequential delivery of MCP-1/IL-4 and coating components was distinct in young

186 ved in aged mice, the sequential delivery of MCP-1/IL-4 was capable of restoring both recruitment and

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

188 feration correlated with decreased levels of MCP (monocyte chemoattractant protein)-1 and IL (interle

189 Conclusions: Higher circulating levels of MCP-1 are associated with increased long-term risk of st

190 : To determine whether circulating levels of MCP-1 are associated with risk of incident stroke in the

191 cided with altered mRNA transcript levels of MCP-1, Cx43 and TGFbeta.

192 Structure-guided phylogeny of MCP suggests that Yaravirus groups together with the MCP

193 cular freedom of movement in the presence of MCP.

194 e largest mobility change in the presence of MCP.

195 intracellular calcium, and the production of MCP 1 (CCL-2) in murine bone marrow-derived MCs.

196 among individuals in the upper quartiles of MCP-1 levels as compared with the first quartile (HRs, s

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

198 nd Mendelian randomization suggest a role of MCP-1 (monocyte chemoattractant protein-1) in atheroscle

199 ion, Th2 skewing, and increased secretion of MCP-1.

200 The morphology and sizes of MCP microspheres can be easily controlled by a dual-surf

201 Together this suggests a novel target of MCP-1/CCR-2 axis that could benefit ovarian cancer patie

202 pendent mechanism that results in release of MCPs (monocyte chemoattractant proteins) and monocyte mo

203 ibitory potential against a large variety of MCPs, combined with high-resolution crystal structures o

204 s realization is stimulating new research on MCPs as reliable and accessible biomarkers in cancer, as

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

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

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

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

209 propanediol-utilising microcompartment (Pdu MCP), a specialised proteinaceous organelle that is esse

210 eins and internal enzymes of the natural Pdu MCP by QconCAT-driven quantitative mass spectrometry.

211 The structural insights into the Pdu MCP are critical for both delineating the general princi

212 Pdu MCPs are a family of bacterial microcompartments that ar

213 remodelling of metabolically functional Pdu MCPs.

214 iometric composition and organisation of Pdu MCPs.

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

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

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

218 y, including the middle cerebellar peduncle (MCP), superior cerebellar peduncle (SCP), pons, and midb

219 te nucleus (DN)-to-middle cerebral peduncle (MCP) SI ratio showed a mean increase of 6.7% +/- 3.9 in

220 Using minimax concave penalty (MCP) and smoothly clipped absolute deviation (SCAD) anal

221 the Elastic Net and Minimax Concave Penalty (MCP) regression.

222 h the Lasso and the minimax concave penalty (MCP) to incorporate the shared genetic effects across mu

223 Plasma MCP-1, suPAR, and YKL-40 were not independently associat

224 rophage content within these lesions, plasma MCP-1 levels decreased upon WTD feeding.

225 Here, we use a microchannel plate (MCP) based Timepix soft X-ray detector to conduct a time

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

227 rated it into an imaging microchannel plate (MCP).

228 he Micro-Compartment-of-Can1 (MCC) and Pma1 (MCP), which have different lipid compositions.

229 ial metrics, such as minimum convex polygon (MCP) and standard ellipse area (SEA), and add novel metr

230 ividual cells using metal-chelating polymer (MCP) based reagents.

231 -diaminopyridine-based multichamber polymer (MCP) with a high nitrogen content up to 20 wt%.

232 Metal-chelating polymers (MCPs) are widely used to profile and quantify cellular b

233 starch and Mesona chinensis polysaccharide (MCP) was found to change the molecular mobility of the w

234 using the Microenvironment Cell Populations (MCP)-counter package and compared with immunohistochemis

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

236 PSC)-derived multipotent cardiac progenitor (MCPs) cells and, in parallel, in the Drosophila in vivo

237 deling by alpha-chymase (mast cell protease [MCP] 5) is crucial for successful embryo implantation.

238 a fusion to the MS2 aptamer binding protein MCP, allowing the construction of a doxycycline-regulata

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

240 the double jelly-roll major capsid protein (MCP) p72, arranged in trimers displaying a pseudo-hexame

241 bly by chaperoning the major capsid protein (MCP) to build an icosahedral lattice.

242 presenting a divergent major capsid protein (MCP) with a predicted double jelly-roll domain.

243 sid, consisting of 955 major capsid protein (MCP), 900 small capsid protein (SCP), 640 triplex dimer

244 red to glycosylate its major capsid protein (MCP).

245 ree copies of a single major capsid protein (MCP).

246 )-6, IL-8, monocyte chemoattractant protein (MCP)-1, and osteoprotegerin (OPG) were measured with qPC

247 MIP-1beta, monocyte chemoattractant protein (MCP)-1, interferon gamma-induced protein (IP)-10, monoki

248 10, IL-19, monocyte chemoattractant protein (MCP)-1, MCP-2, MCP-3, CXCL9, CXCL10, CXCL5, ENRAGE, and

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

250 leukin 18, monocyte chemoattractant protein (MCP-1), autotaxin (ATX), and Mac2-binding protein (Mac2B

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

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

253 exhibits DAA and membrane cofactor protein (MCP) that exhibits CFA.

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

255 g tissue remodeling, matricellular proteins (MCP) are secreted into the ECM.

256 everal methyl-accepting chemotaxis proteins (MCPs), rather than a specific MCP.

257 d concept of the soil microbial carbon pump (MCP) emphasizes the active role of soil microbes in SOC

258 us cytokines such as I-TAC, Eotaxin, RANTES, MCP-1, IFNgamma and MIG demonstrated a biphasic peak tha

259 cascade in primary monocytes that regulates MCP-1-induced monocyte adhesion and migration.

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

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

262 nt, sCD14 levels did not change, and sCD163, MCP-1, and IL-6 levels changed at a single time point.

263 nflammatory factors (eg, ICAM-1, E-selectin, MCP-1) in endothelial cells or vascular smooth muscle ce

264 isting of a CCR2-targeting peptide sequence (MCP-1 peptide) and the apoptotic KLAKLAK peptide were sy

265 er delineate and suggest two parameters-soil MCP capacity and efficacy-reflecting the conversion of p

266 We interrogate the soil MCP concept by investigating the asynchronous responses

267 This suggests that the soil MCP was stimulated in diversified perennial agroecosyste

268 axis proteins (MCPs), rather than a specific MCP.

269 water and carbohydrate populations in starch-MCP gels, when measured using proton and carbon nuclear

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 Here, we show that MCP-1 produced by omental adipocytes binding to its cogn

275 We showed that MCP-1 induces Src phosphorylation in a similar time fram

276 netic and experimental evidence suggest that MCP-1 signaling might represent a therapeutic target to

277 Additionally, the MCP-1/CCR2 signaling axis drives the migration of circul

278 ing PRP, except for decreased density at the MCP at the latest timepoint in the adjusted multivariabl

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

280 In this study, we investigated the MCP-1-mediated activation of Pyk2 (particularly by the p

281 anded state associated with unfolding of the MCP N-terminus and straightening of E-loops.

282 r U-IRI reveals high-level expression of the MCP-1 receptor Ccr2.

283 ylation in a similar time frame and that the MCP-1-induced Pyk2 tyrosine phosphorylation is controlle

284 ests that Yaravirus groups together with the MCPs of Pleurochrysis endemic viruses.

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

286 b attenuated the release of IL-6, IL-8, TNF, MCP-1, MIP-1alpha, IFN-gamma, LTB-4, MMP-8 and -9, and I

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

288 he intermediate state, SPs are bound only to MCP pentons and to adjacent subunits from hexons.

289 ting implants showed a preserved response to MCP-1 in both young and aged animals, restoring delayed

290 k2 activation/phosphorylation in response to MCP-1 stimulation.

291 nsable for monocyte migration in response to MCP-1 stimulation.

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

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

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

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

296 oke (HR per 1-SD increment in ln-transformed MCP-1, 1.07; 95% CI, 1.01-1.14).

297 MCP-4 and the tryptase MCP-6 emerge to be protective in central nervous system

298 response towards an M2-like phenotype, using MCP-1 (macrophage chemotactic protein-1) and IL-4 (inter

299 a, and IL-6 predominated in WT mice, whereas MCP-1 and IL-6 predominated in IRF3-KO mice.

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