ライフサイエンスコーパス: Mac

1 Mac-1 (CD11b/CD18) is a beta2 integrin classically regar

2 Mac-1 alone was responsible for neutrophil crawling in b

3 Mac-1 exhibits a unique inhibitory activity toward IL-13

4 s and macrophages via CD40L-macrophage Ag 1 (Mac-1) interaction is responsible for the sustained resi

5 A-1 required HPK1, but macrophage antigen 1 (Mac-1) affinity regulation was independent of HPK1.

6 epends on the integrin macrophage antigen 1 (Mac-1).

7 ps between adjacent pericytes in an ICAM-1-, Mac-1-, and LFA-1-dependent manner.

8 This newly identified IL-13Ralpha1/Mac-1-dependent pathway may offer novel targets for ther

9 Deletion of macrophage-COX-2 (Mac-COX-2KOs) was attained with LysMCre mice and complet

10 ion of integrin CD11b/CD18 (alpha(M)beta(2), Mac-1, and CR3) shows anti-inflammatory benefits in a va

11 egrin heterodimer complement receptor type 3/Mac-1.

12 rated that inflammatory macrophages (F4/80(+)Mac-2(+)) were localized with initiating chondrification

13 Resident macrophages (F4/80(+)Mac-2(neg)), including osteal macrophages, predominated

14 trengthening and intravascular crawling in a Mac-1-dependent manner.

15 indicate that extracellular dsRNA activates Mac-1 to enhance TLR3-dependent signaling and to trigger

16 In addition, Mac-1 has been described to negatively regulate immune c

17 f beta2 integrins LFA-1 and macrophage-1 Ag (Mac-1) showed that in CD45E613R mutant neutrophils LFA-1

18 BioNetFit can be used on stand-alone Mac, Windows/Cygwin, and Linux platforms and on Linux-ba

19 Although Mac(AIR) comprise the earliest foam cells in plaques, th

20 -Rex1 serves distinct functions in LFA-1 and Mac-1 activation.

21 In sum, both LFA-1 and Mac-1 binding ICAM-1 play a critical role in determining

22 Mac-1 or LFA-1 revealed that both LFA-1 and Mac-1 contribute to monocyte crawling; however, the LFA-

23 D18 expression, the beta2 chain of LFA-1 and Mac-1 integrins.

24 l ICAM-1 and ICAM-2 and neutrophil LFA-1 and Mac-1.

25 been tested on both Windows (Windows 10) and Mac (High Sierra) operating systems.

26 face localization/distribution of alpha4 and Mac-1.

27 eukocyte recruitment to the endothelium, and Mac-1 engagement of platelet GPIbalpha is required for i

28 etermine whether interferon (IFN-)-gamma and Mac-1(+) cells play a role in preventing direct anterior

29 h is a Python package that runs on Linux and Mac OS X systems and that enables parameter estimation a

30 age of stand-alone executables for Linux and Mac OS X under the open-source BSD license.

31 For Linux and Mac OS X, users must install R and then follow instructi

32 code for command line usage under Linux and Mac OS X.

33 d in Python and C and supported on Linux and Mac OS X.

34 ependent, allowing use on Windows, Linux and Mac OS X.

35 ting platforms, including Windows, Linux and Mac OS X.

36 nted in Python and is supported on Linux and Mac OS.

37 rating systems, including Windows, Linux and Mac OS.

38 pliant operating system, including Linux and Mac OS/X.

39 pliant operating system, including Linux and Mac OS/X.

40 ilable as a standalone program for Linux and Mac.

41 n and is compatible with Windows, Linux, and Mac OS systems.

42 open-source software for Windows, Linux, and Mac OS.

43 he thrombosis defect in Mac-1(-/-) mice, and Mac-1-dependent regulation of the transcription factor F

44 (+)Ly6C(int)Gr-1(+) cells (neutrophils), and Mac-1(+)Ly6C(low/neg)Gr-1(low/neg) leukocytes (macrophag

45 nhibition of NETosis in an EPCR-, PAR3-, and Mac-1-dependent manner, providing additional mechanistic

46 vivo, both LFA-1-dependent slow rolling and Mac-1-dependent crawling are defective in P-Rex1(-/-) le

47 eripheral node addressin, E-, L-selectin and Mac-1 but not P-selectin or LFA-1.

48 lpha; and (e) co-culturing of SIRPalpha- and Mac-1-expressing HEK293 cells resulted in the formation

49 ainbowSTORM has been tested with Windows and Mac operating systems and ImageJ/FIJI version 1.52.

50 s are freely available for UNIX, Windows and Mac OS X operating systems at Bioconductor.

51 tested for R 2.14.2 under Linux, Windows and Mac OS X.

52 tested for R 3.2.0 under Linux, Windows and Mac OS X.

53 cell-surface proteoglycans because both anti-Mac-1 function-blocking mAb and heparin were required to

54 lockade of CD40L-Mac-1 interaction with anti-Mac-1 mAb led to spontaneous disease reactivation in hea

55 receptor 3 (PAR3), and macrophage-1 antigen (Mac-1) blocked APC inhibition of NETosis.

56 ith antibodies against Macrophage-1 antigen (Mac-1) or intercellular adhesion molecule 1 and were rep

57 but they also express macrophage-1 antigen (Mac-1), which binds to ICAM-1.

58 CR3 (also known as Mac-1, integrin alphaMbeta2, or CD11b/CD18) is expressed

59 the rationale of using clinically available Mac-1 (CD11b/CD18) antibodies as an adjuvant therapy to

60 orts adhesion of Mac-1-expressing cells; (b) Mac-1-SIRPalpha interaction is mediated through the liga

61 ent crawling in unstimulated venules becomes Mac-1 dependent upon inflammation, likely due to increas

62 nstrated that recombinant IL-13Ralpha1 binds Mac-1 in a purified system and supports Mac-1-mediated c

63 It has been tested on both Mac and Windows.

64 We find that both Mac-1 (CD11b/CD18) and alpha(4)beta(1) (CD49d/CD29) inte

65 The results indicate that both Mac-1 and alphaDbeta2 support macrophage fusion with Mac

66 gnaling and to trigger TLR3-independent, but Mac-1-dependent, inflammatory oxidative signaling, ident

67 yte NADPH oxidase in a TLR3-independent, but Mac-1-dependent, manner.

68 d neutrophil accumulation that is enabled by Mac-1 deficiency.

69 naling events following dsRNA recognition by Mac-1.

70 ble 3 binding protein (LGALS3BP, also called Mac-2 binding protein) is a heavily glycosylated secrete

71 lectrochemical nanoimprinting process-called Mac-Imprint-for directly patterning electronic-grade sil

72 Immunostaining for CD11b (Mac-1)-expressing leukocytes (macrophage, neutrophils) a

73 F4/80(+) and anti-mouse CD11b (Mac-1)(+) histiocytic cells predominated within the tumo

74 present study demonstrated that CD11b/CD18 (Mac-1 [macrophage-1 Ag]), a surface integrin receptor, r

75 rin alpha(v)beta(3), ICAM-1, and CD11b/CD18 (Mac-1) in fibrin(ogen)-mediated melanoma-PMN aggregation

76 cell surface levels of integrins CD11b/CD18 (Mac-1), specifically during transendothelial migration.

77 ue to CD11a/CD18 (LFA-1)- versus CD11b/CD18 (Mac-1)-mediated crawling.

78 The complement receptor CR3 (CD11b/CD18, Mac-1) mediates the phagocytosis of complement protein (

79 ively, our data reveal a novel role of CD40L-Mac-1 interaction in IL-12 production, development, and

80 Blockade of CD40L-Mac-1 interaction with anti-Mac-1 mAb led to spontaneous

81 gives rise to IgM(+)IgD(low)CD45R(low)CD5(+)Mac-1(+)CD19(high)CD43(+)CD23(low) B-1a cells upon adopt

82 king mPGES-1 conditionally in myeloid cells (Mac-mPGES-1-KOs), vascular smooth muscle cells (VSMC-mPG

83 ing) of perfluorcarbon-labeled immune cells, Mac-2/Galectin-3 immunostaining, and FACS (fluorescence-

84 eGFP-L10a upregulation in kidney, confirming Mac(TRAP) responsiveness in vivo.

85 suggests that integrin alpha(M)beta(2) (CR3, Mac-1, and CD11b/CD18) is the principal leukocyte recept

86 nsistent with the role of Mac-1 in crawling, Mac-1 block (compared with LFA-1) was also significantly

87 rated reactive intermediates and involves DC Mac-1.

88 e we report that mice with Mac-1 deficiency (Mac-1(-/-)) or mutation of the Mac-1-binding site for GP

89 opulations are distinguished by differential Mac-1 and CD11c integrin expression rather than classica

90 ents, we show that PTN contains two distinct Mac-1-binding sites in each of its constitutive domains.

91 Although Dowex Mac 3 had the highest adsorption capacity, material cost

92 Dowex 50 and Dowex Mac 3 showed nearly 100% regeneration efficiencies.

93 clinoptilolite, biochar, Dowex 50, and Dowex Mac 3) were compared in pure salt solutions, synthetic u

94 four-person household were lowest for Dowex Mac 3 (5 L) and highest for biochar (19 L).

95 Blockade of either Mac-1 or LFA-1 revealed that both LFA-1 and Mac-1 contri

96 itation experiments revealed that endogenous Mac-1 forms a complex with IL-13Ralpha1 in solution, and

97 tment, circulating RBC capture, and enhanced Mac-1 activity, whereas FcgammaRIIB was dispensable.

98 We then discuss studies that exemplify Mac-1's pro-inflammatory versus regulatory roles particu

99 , there are astrocytes that normally express Mac-2 (also known as Lgals3 or galectin-3), a gene typic

100 h increased proinflammatory gene expression, Mac-SIRT1 KO mice challenged with a high-fat diet displa

101 at lesional skin from OPN(-/-)mice had fewer Mac-3-positive cells, fewer myofibroblasts, decreased tr

102 ic spinal cord and suggest that a fibrinogen-Mac-1 interaction underpins this response.

103 First, Mac-1 facilitated poly I:C internalization through the a

104 t is available as a packaged application for Mac OS X and Microsoft Windows and can be compiled for L

105 unner binary distributions are available for Mac OS X, Linux and Windows.

106 ions of the program are freely available for Mac OSX and Windows operating systems.

107 adhesion molecule 1, a counter-receptor for Mac-1 and alphaDbeta2, did not alter the fusion rate.

108 identify SIRPalpha as a counter-receptor for Mac-1 and suggest that the Mac-1-SIRPalpha interaction m

109 acted macrophage-specific polysomal RNA from Mac(TRAP) kidneys and conducted RNA sequencing followed

110 Furthermore, Mac 1 is differentially phosphorylated in response to ir

111 ion to a homogenous population of CD11c(high)Mac-1(neg/low) MPhis reflective of lung homeostasis, chr

112 by an additional subpopulation of CD11c(high)Mac-1(pos) MPhis that tracks with lung disease in suscep

113 This study identifies Mac-1 as a novel surface receptor for extracellular dsRN

114 el humanized lupus mouse model, and identify Mac-1 regulation of FcgammaRIIA-mediated neutrophil recr

115 f fluid flow on ICAM-1 surfaces via LFA-1 if Mac-1 is blocked; otherwise, they migrate downstream.

116 acterization found no gross abnormalities in Mac(TRAP) mice and confirmed transgene expression across

117 s revealed markedly reduced atherogenesis in Mac-mPGES-1-KOs, which was concomitant with a reduction

118 te transfer rescues the thrombosis defect in Mac-1(-/-) mice, and Mac-1-dependent regulation of the t

119 e, we demonstrate that P-Rex1 is involved in Mac-1-dependent intravascular crawling.

120 t not adhesion and migration, was reduced in Mac-1-deficient macrophages.

121 ost package is implemented to readily run in Mac or Linux environments.

122 ely twofold higher in wild-type mice than in Mac-1(-/-) mice.

123 emented using Perl and R, and can be used in Mac or Linux environments.

124 we observed that beta2 integrins, including Mac-1, trigger proliferation of AML cells in an AML cell

125 s revealed three major populations including Mac-1(+)Ly6C(high)Gr-1(low/neg) cells (monocytes), Mac-1

126 Because of the increased Mac-1 adhesiveness, neutrophil crawling was impaired in

127 The increased Mac-2 expression by MTZ astrocytes during glaucoma likel

128 ertaken by recruited monocytes, which induce Mac(AIR)-defining genes.

129 m increased affinity of the beta(2)-integrin Mac-1 after prolonged chemokine stimulation of neutrophi

130 specific for the activated beta(2)-integrin Mac-1.

131 that preferentially bind activated integrin Mac-1 (alpha(M)beta(2)) and are potent in blocking neutr

132 The leukocyte integrin Mac-1 (also known as integrin alphaMbeta2, or CD11b/CD18

133 Among beta2 family members, integrin Mac-1 (alphaMbeta2, CD11b/CD18) is abundantly expressed

134 ptor (IL-13R), as a novel ligand of integrin Mac-1, using a co-evolution-based algorithm.

135 quired neutrophil expression of the integrin Mac-1 (alphaMbeta2).

136 Here, we identified the integrin Mac-1 (alphaMbeta2, CD11b/CD18) as the receptor mediatin

137 extracellular matrix (ECM) via the integrin Mac-1 and NE, respectively, causing the hallmarks of chr

138 ts identify PTN as a ligand for the integrin Mac-1 on the surface of leukocytes and suggest that this

139 naling partners FcgammaRIIA and the integrin Mac-1, internalizes soluble ICs through a mechanism used

140 ability of SLAMF7 to interact with integrin Mac-1 and utilize signals involving immunoreceptor tyros

141 ulates and primes human neutrophil integrin (Mac-1) expression, in response to formylmethionylleucylp

142 he mice additionally lack the CD18 integrin, Mac-1.

143 Therefore, integrins Mac-1 and alpha(4)beta(1) have a pivotal role in prevent

144 Neutrophil adhesion to both cell types is Mac-1-dependent and while ICAM-1 transduction of PCs inc

145 s the interaction between fibrinogen and its Mac-1 integrin receptor.

146 sing a myeloid cell-specific SIRT1 knockout (Mac-SIRT1 KO) mouse model, we show that ablation of SIRT

147 e markers programmed death ligand-1 (PD-L1), Mac-2, and macrophage mannose receptor (CD206) and produ

148 expression, as well as diminished leukocyte Mac-1-integrin activation and cyclic guanosine monophosp

149 ew pathway of thrombosis involving leukocyte Mac-1 and platelet GPIbalpha, and suggest that targeting

150 source code and precompiled binaries (Linux, Mac OS/X, Windows) are available at github.com/aresio/cu

151 hensive R Archive Network (CRAN), for Linux, Mac OS and Windows platforms.

152 Source code and binaries for Linux, Mac OS X and Microsoft Windows are available.

153 GeNN is available for Linux, Mac OS X and Windows platforms.

154 any Unix-based operating system (e.g. Linux, Mac OSX).

155 The package can be run on Linux, Mac and Windows systems and also provides a graphical us

156 It can run on Linux, Mac and Windows.

157 tware implemented using C# and run on Linux, Mac OS X & Windows operating systems.

158 implemented in Perl and supported on Linux, Mac OS X and MS Windows.

159 s implemented in C++ and supported on Linux, Mac OS X and other platforms supporting standard C++ com

160 OSA has been tested extensively on Linux, Mac OS X and Windows platforms.

161 s written in C++, and is supported on Linux, Mac OSX and MS Windows.

162 okine profiles, pathologies, and macrophage (Mac) polarization status in C. neoformans-infected WT, i

163 cialized aortic intima resident macrophages (Mac(AIR)) that depend upon colony-stimulating factor 1 a

164 pump from the fungus Leptosphaeria maculans (Mac) can, when expressed in neurons, enable neural silen

165 direct laryngoscopy 98.5% (254/258), McGrath Mac Video Laryngoscope 98.1% (251/256) (difference, 0.4%

166 The McGrath Mac Video Laryngoscope (Medtronic, Minneapolis, MN) has

167 This trial compared the McGrath Mac Video Laryngoscope and direct laryngoscopy for the p

168 ical problems was increased with the McGrath Mac Video Laryngoscope.

169 uenced 136 microcephaly or macrocephaly (Mic-Mac)-related genes and 158 possible ASD-risk genes in 53

170 Our results indicate some of Mic-Mac-risk genes are involved in ASD.

171 addition, we prioritized 39 ASD-related Mic-Mac-risk genes, and showed their interaction and co-expr

172 to generate c-fms-eGFP-L10a transgenic mice (Mac(TRAP)).

173 This cytokine interplay modulates Mac differentiation, including generation of an intermed

174 o JAM-C via the neutrophil adhesion molecule Mac-1.

175 Mon/Mac cells were also differentiated by levels of Ki67 and

176 dosing of a CSF-1R inhibitor to deplete Mon/Mac cells significantly reduced several inflammatory med

177 tissue suggesting a pathogenic role for Mon/Mac.

178 er characterize the monocyte/macrophage (Mon/Mac) population when the IL-23 pathway is activated, a m

179 ta point to an important contribution of Mon/Mac cells in IL-23 related skin inflammation and suggest

180 Flow cytometry revealed that Mon/Mac cells were the dominant immune population, particula

181 The Mon/Mac cells were also shown to have high expression for TN

182 ed less inflammatory responses in human Mono Mac 6 and murine macrophage RAW264.7 cells in vitro.

183 oteins in the human monocytic cell line Mono Mac 6 (MM6).

184 ifferentiation of the myeloid cell line Mono Mac 6 led to a significant increase in 5-LO protein expr

185 ytokine IL-6 in the monocytic cell line Mono Mac 6, induction of the Toll-interleukin-1 receptor doma

186 man primary and immortalized monocytes (Mono Mac 6) were measured.

187 In human epithelial DLD-1 and monocytic Mono Mac 6 cells resveratrol decreased the expression of iNOS

188 In undifferentiated Mono Mac 6 (MM6) cells, full-length Dicer was undetectable; o

189 +)Ly6C(high)Gr-1(low/neg) cells (monocytes), Mac-1(+)Ly6C(int)Gr-1(+) cells (neutrophils), and Mac-1(

190 osine kinase (Btk) was required for multiple Mac-1 activation events involved in neutrophil recruitme

191 Using multiple Mac activation markers, we further demonstrate that IL-4

192 s to cancer cells was mediated by neutrophil Mac-1/ICAM-1.

193 TEM, which increases neutrophil Mac-1 surface expression, concomitantly increases the ab

194 tification of the pivotal role of neutrophil Mac-1 and ROS in this process provides a potential targe

195 EM CD4(+) T cell LFA-1 (CD11a/CD18) but not Mac-1 (CD11b/CD18); nectin-2 and poliovirus receptor are

196 However, disease permitted by the absence of Mac-1 is not related to enhanced renal immune complex de

197 tides leading to the selective activation of Mac-1 and neutrophil recruitment during sterile inflamma

198 ating signals that lead to the activation of Mac-1 at the leading edge of PMNs, thereby allowing RBC

199 ough NOD2 and a second through activation of Mac-1 by T cell-derived GPIbalpha.

200 associated with clustering and activation of Mac-1-positive microglia around disrupted vessels.

201 mCLCA1-mediated adhesion of Mac-1- or LFA-1-expressing leukocytes to lymphatic vesse

202 ectodomain of SIRPalpha supports adhesion of Mac-1-expressing cells; (b) Mac-1-SIRPalpha interaction

203 Immunohistological analyses of Mac(TRAP) kidneys identified eGFP-L10a expressing cells

204 s to general principles governing binding of Mac-1 to many of its ligands; (d) SIRPalpha reportedly b

205 egulated by spatial and temporal cleavage of Mac-1, which is triggered upon interaction with endothel

206 nzymes that control constitutive cleavage of Mac-1.

207 Deletion of Mac-COX-2 appeared to remove a restraint on COX-2 expres

208 task, consisting of yeast surface display of Mac-1 inserted (I) domain library, directed evolution to

209 rough the ligand-binding alpha(M)I-domain of Mac-1; (c) recognition of SIRPalpha by the alpha(M)I-dom

210 We also found that expression of Mac-1 on the surface of human embryonic kidney (HEK) 293

211 ation, likely due to increased expression of Mac-1.

212 crophages showed that IL-4-induced fusion of Mac-1-deficient cells was strongly reduced compared with

213 eover, we found that genetic inactivation of Mac-1 promotes IL-13-induced JAK/STAT activation in macr

214 ypothesized this was due to the influence of Mac-1.

215 r impairment was seen with the inhibition of Mac-1, a receptor for ICAM-1.

216 olecule 1 (ICAM-1), an established ligand of Mac-1, did not impair macrophage fusion, suggesting the

217 the conclusion that SIRPalpha is a ligand of Mac-1: (a) recombinant ectodomain of SIRPalpha supports

218 I domain, the major ligand-binding region of Mac-1, and PTN.

219 Consistent with the role of Mac-1 in crawling, Mac-1 block (compared with LFA-1) was

220 However, the role of Mac-1 in macrophage fusion leading to the formation of m

221 However, the role of Mac-1 in thrombosis is undefined.

222 may shed light on how the opposing roles of Mac-1 may be elicited.

223 dance was reduced in the liver and spleen of Mac-1 KO mice after administration of MDP compared with

224 Moreover, stimulation of Mac-1 or FcgammaRI intensifies the constitutive Syk-medi

225 Antibody and small-molecule targeting of Mac-1:GPIbalpha inhibits thrombosis.

226 recognition specificity overlapping that of Mac-1, is unknown.

227 infection concurrently display both types of Mac polarization markers.

228 While binding to PTN, Mac-1 on Mac-1-expressing HEK293 cells appears to cooperate with

229 irculation into lungs, neutrophils depend on Mac-1 and alpha(4)beta(1), whereas the T cells are entir

230 The toolkit can be executed on Mac OS X 10.5 and above or any Linux distribution.

231 sis framework is written in Perl and runs on Mac OS and Linux/Unix systems.

232 using an open-source R package that runs on Mac OS X, Linux and Windows systems.

233 has been implemented in Java for support on Mac OS X, Linux and MS Windows.

234 It is implemented in C++14 and supported on Mac OS X, Linux and MS Windows.

235 PyIOmica has been tested on Mac OS X, Unix/Linux and Microsoft Windows.

236 s available under a BSD license and works on Mac OS X and Linux systems.

237 ptor 3 (CR3, alpha(M)beta(2), CD11b/CD18, or Mac-1) of myeloid phagocytes, penetrates their plasma me

238 The leukocyte integrin alphaMbeta2 (CR3 or Mac-1) has both proinflammatory and immune regulatory fu

239 etermine whether the absence of IFN-gamma or Mac-1(+) macrophages affected the sites or timing of vir

240 ~3 h on a desktop computer running Linux or Mac OS with R support.

241 n be deployed on any server running Linux or Mac OS.

242 ted nearly instantaneously on a modern PC or Mac computer.

243 s can be <1 h using a standard desktop PC or Mac.

244 reported cognate ligands vWF, P-selectin or Mac-1, offering a potential target against NASH.

245 or as a binary without MATLAB (on Windows or Mac).

246 Peter Mac and Deauville showed better fit than EORTC and PERCI

247 bserver agreements for EORTC, PERCIST, Peter Mac, and Deauville had kappa values of 0.76, 0.76, 0.87,

248 nt of Cancer (EORTC), PERCIST 1.0, the Peter Mac metabolic visual criteria, and the Deauville criteri

249 Unlike most NIL processes, Mac-Imprint does not rely on plastic deformation, and th

250 Accordingly, PTN promoted Mac-1-dependent cell spreading and initiated intracellul

251 While binding to PTN, Mac-1 on Mac-1-expressing HEK293 cells appears to cooper

252 l proteins, especially the integrin receptor Mac-1, the Fc-gamma receptor I (FcgammaRI), and the tran

253 ed blockade of GPIbalpha or of its receptor, Mac-1 integrin, inhibited the secretion of PGE(2), IL-1b

254 on of high shear stress through TAVI reduces Mac-1 activation, cellular adhesion, phagocytosis, oxidi

255 lacking gamma-synuclein fail to up-regulate Mac-2 at the MTZ after elevation of intraocular pressure

256 a models, MTZ astrocytes further up-regulate Mac-2 expression.

257 Summarizing, ArhGAP15 specifically regulates Mac-1, but not LFA-1, and affects leukocyte recruitment

258 IIB-mediated neutrophil recruitment requires Mac-1 and is associated with the removal of intravascula

259 iplexed analysis of RAS-dependent signaling, Mac-1(Low) cells, which harbor leukemia stem cells, were

260 by murine macrophages independent of SLAMF7-Mac-1 interaction.

261 re, we demonstrate that the R77H-substituted Mac-1 can be expressed on the cell surface in transfecte

262 inds Mac-1 in a purified system and supports Mac-1-mediated cell adhesion.

263 s1143679, a single nucleotide non-synonymous Mac-1 polymorphism associated with SLE.

264 The predicted sequence of the cloned OA/TA(Mac) receptor consists of 1,579 base pairs (bp), with an

265 We also mapped the OA/TA(Mac) receptor distribution by in-situ hybridization to t

266 Indeed, we found that Mac-1(-/-)LDLR(-/-) mice develop significantly more foam

267 The prevailing view is that Mac-1 on macrophages is responsible for immune complex c

268 Importantly, we observed that Mac-1(-/-) macrophages exhibit increased expression of f

269 ertheless, recent reports have revealed that Mac-1 also plays significant immunoregulatory roles, and

270 in the cremasteric vasculature reveals that Mac-1 mitigates FcgammaRIIA-dependent neutrophil recruit

271 and confocal immunofluorescence showed that Mac-1, especially the CD11b subunit, interacted and colo

272 c-1 playing a dominant role and suggest that Mac-1 may mediate cell-cell interactions with a previous

273 The Mac-1 integrin is expressed mainly on myeloid cells and

274 phism conferring an amino acid change in the Mac-1 integrin extracellular domain, R77H, was shown to

275 1 deficiency (Mac-1(-/-)) or mutation of the Mac-1-binding site for GPIbalpha have delayed thrombosis

276 nter-receptor for Mac-1 and suggest that the Mac-1-SIRPalpha interaction may be involved in macrophag

277 e revealed that neutrophils make use of this Mac-1 ligand, not for lung entry or for migration within

278 firm adhesion of monocytes to ICAM-1 through Mac-1, which may explain the prominence of monocytes dur

279 in this pathway required for fMLF-triggered Mac-1 activation and neutrophil recruitment.

280 StochKit2 runs on Linux/Unix, Mac OS X and Windows.

281 g neutrophil shear resistant arrest, whereas Mac-1 was dominant over LFA-1 in mediating neutrophil po

282 impaired, and avidity was enhanced, whereas Mac-1 adhesiveness was increased.

283 he first time a molecular mechanism by which Mac-1 regulates the signaling activity of IL-13 in macro

284 system with R installed, including Windows, Mac OS and most Linux distributions.

285 0 license and can be run locally on Windows, Mac and Linux systems capable of running R and/or Docker

286 B and runs either within MATLAB (on Windows, Mac or Linux) or as a binary without MATLAB (on Windows

287 versions of R 3.1.1 (and higher) on Windows, Mac OS X and Linux using Bioconductor 3.0 and is availab

288 compatible with R 3.2 and above on Windows, Mac OS X and Linux.

289 ns of PathVisio 2.0.11 and later on Windows, Mac OS X and Linux.

290 mplemented in Java and supported on Windows, Mac OS X and Linux.

291 The program has been tested on Windows, Mac, and Linux operating systems, and is implemented bot

292 re has been developed and tested on Windows, Mac, and Linux platforms and is available publicly under

293 for execution on popular platforms (Windows, Mac and Linux).

294 .3 open source license and supports Windows, Mac and Linux platforms.

295 PathVisio is compatible with Windows, Mac OS X and Linux.

296 ) had enough contact time to form bonds with Mac-1 via Fn, which could not otherwise occur at a shear

297 d alphaDbeta2 support macrophage fusion with Mac-1 playing a dominant role and suggest that Mac-1 may

298 en implicated in cell fusion, interacts with Mac-1.

299 t (68)Ga-FOL radioactivity co-localized with Mac-3-positive macrophage-rich atherosclerotic plaques.

300 Here we report that mice with Mac-1 deficiency (Mac-1(-/-)) or mutation of the Mac-1-b