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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 conformational activation induced by ligand occupa
4 Mac-1 exhibits a unique inhibitory activity toward IL-13
5 Mac-1(+), CD49b(+), and F4/80(+) cells colocalized with
6 s and macrophages via CD40L-macrophage Ag 1 (Mac-1) interaction is responsible for the sustained resi
12 eptors, FcgammaRs and complement receptor 3 (Mac-1) to cellular cytotoxic responses are poorly unders
14 rated that inflammatory macrophages (F4/80(+)Mac-2(+)) were localized with initiating chondrification
16 hich includes three convenient interfaces: a Mac OS X GUI, a command-line interface and a simple appl
17 indicate that extracellular dsRNA activates Mac-1 to enhance TLR3-dependent signaling and to trigger
19 f beta2 integrins LFA-1 and macrophage-1 Ag (Mac-1) showed that in CD45E613R mutant neutrophils LFA-1
21 tegrins alphaLbeta2 (LFA-1) and alphaMbeta2 (Mac-1) have ratios similar to each other but lower than
23 Mac-1 or LFA-1 revealed that both LFA-1 and Mac-1 contribute to monocyte crawling; however, the LFA-
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
30 Source and binaries for Windows, Linux and Mac OS X are available from http://kumiho.smith.man.ac.u
31 the GNU General Public Licence and Linux and Mac OS X binaries can be downloaded from http://supfam.o
33 h is a Python package that runs on Linux and Mac OS X systems and that enables parameter estimation a
45 LAB, Octave, Python and C) for the Linux and Mac platforms is available at http://sourceforge.net/pro
47 he thrombosis defect in Mac-1(-/-) mice, and Mac-1-dependent regulation of the transcription factor F
48 (+)Ly6C(int)Gr-1(+) cells (neutrophils), and Mac-1(+)Ly6C(low/neg)Gr-1(low/neg) leukocytes (macrophag
49 nhibition of NETosis in an EPCR-, PAR3-, and Mac-1-dependent manner, providing additional mechanistic
50 vivo, both LFA-1-dependent slow rolling and Mac-1-dependent crawling are defective in P-Rex1(-/-) le
52 allers for Windows, Linux, Unix, Solaris and Mac OS X are available at http://apollo.berkeleybop.org,
57 executable downloads for Linux, Windows and Mac OS, with manual and source code, at www.northeastern
59 cell-surface proteoglycans because both anti-Mac-1 function-blocking mAb and heparin were required to
61 lockade of CD40L-Mac-1 interaction with anti-Mac-1 mAb led to spontaneous disease reactivation in hea
63 ith antibodies against Macrophage-1 antigen (Mac-1) or intercellular adhesion molecule 1 and were rep
66 the rationale of using clinically available Mac-1 (CD11b/CD18) antibodies as an adjuvant therapy to
67 ent crawling in unstimulated venules becomes Mac-1 dependent upon inflammation, likely due to increas
68 nstrated that recombinant IL-13Ralpha1 binds Mac-1 in a purified system and supports Mac-1-mediated c
72 gnaling and to trigger TLR3-independent, but Mac-1-dependent, inflammatory oxidative signaling, ident
77 ble 3 binding protein (LGALS3BP, also called Mac-2 binding protein) is a heavily glycosylated secrete
79 present study demonstrated that CD11b/CD18 (Mac-1 [macrophage-1 Ag]), a surface integrin receptor, r
80 rin alpha(v)beta(3), ICAM-1, and CD11b/CD18 (Mac-1) in fibrin(ogen)-mediated melanoma-PMN aggregation
81 cell surface levels of integrins CD11b/CD18 (Mac-1), specifically during transendothelial migration.
83 The complement receptor CR3 (CD11b/CD18, Mac-1) mediates the phagocytosis of complement protein (
84 ively, our data reveal a novel role of CD40L-Mac-1 interaction in IL-12 production, development, and
86 gives rise to IgM(+)IgD(low)CD45R(low)CD5(+)Mac-1(+)CD19(high)CD43(+)CD23(low) B-1a cells upon adopt
87 king mPGES-1 conditionally in myeloid cells (Mac-mPGES-1-KOs), vascular smooth muscle cells (VSMC-mPG
88 suggests that integrin alpha(M)beta(2) (CR3, Mac-1, and CD11b/CD18) is the principal leukocyte recept
89 nsistent with the role of Mac-1 in crawling, Mac-1 block (compared with LFA-1) was also significantly
91 e we report that mice with Mac-1 deficiency (Mac-1(-/-)) or mutation of the Mac-1-binding site for GP
92 opulations are distinguished by differential Mac-1 and CD11c integrin expression rather than classica
93 ents, we show that PTN contains two distinct Mac-1-binding sites in each of its constitutive domains.
96 clinoptilolite, biochar, Dowex 50, and Dowex Mac 3) were compared in pure salt solutions, synthetic u
99 itation experiments revealed that endogenous Mac-1 forms a complex with IL-13Ralpha1 in solution, and
100 tment, circulating RBC capture, and enhanced Mac-1 activity, whereas FcgammaRIIB was dispensable.
103 , there are astrocytes that normally express Mac-2 (also known as Lgals3 or galectin-3), a gene typic
104 h increased proinflammatory gene expression, Mac-SIRT1 KO mice challenged with a high-fat diet displa
105 at lesional skin from OPN(-/-)mice had fewer Mac-3-positive cells, fewer myofibroblasts, decreased tr
108 t is available as a packaged application for Mac OS X and Microsoft Windows and can be compiled for L
109 IV Therapy Simulator is freely available for Mac OS and Windows at http://sites.google.com/site/hivsi
113 Source code and precompiled binaries for Mac OS X 10.6+ and Linux 2.6.15+ are available from http
115 all fraction of microglia immunoreactive for Mac-1, Iba-1, CD45, and F4/80 but not for NeuN, Dcx, NG2
116 adhesion molecule 1, a counter-receptor for Mac-1 and alphaDbeta2, did not alter the fusion rate.
118 phages with antigen expression similar to GM-Mac (CD68(+)/CD14(-)) were predominant in areas devoid o
120 ion to a homogenous population of CD11c(high)Mac-1(neg/low) MPhis reflective of lung homeostasis, chr
121 by an additional subpopulation of CD11c(high)Mac-1(pos) MPhis that tracks with lung disease in suscep
123 el humanized lupus mouse model, and identify Mac-1 regulation of FcgammaRIIA-mediated neutrophil recr
125 d Dlx3 are transiently expressed in immature Mac-1(lo) NK cells within the BM, with Dlx3 being the pr
126 s revealed markedly reduced atherogenesis in Mac-mPGES-1-KOs, which was concomitant with a reduction
129 te transfer rescues the thrombosis defect in Mac-1(-/-) mice, and Mac-1-dependent regulation of the t
133 of Mac-1 because its activity was reduced in Mac-1-deficient mice and the phenotype in mice deficient
137 we observed that beta2 integrins, including Mac-1, trigger proliferation of AML cells in an AML cell
138 s revealed three major populations including Mac-1(+)Ly6C(high)Gr-1(low/neg) cells (monocytes), Mac-1
141 that preferentially bind activated integrin Mac-1 (alpha(M)beta(2)) and are potent in blocking neutr
142 d whether conformational changes in integrin Mac-1 are sufficient to transmit outside-in signals in h
146 s or lacking the leukocyte-specific integrin Mac-1, neutrophil recruitment, endothelial injury, glome
149 ts identify PTN as a ligand for the integrin Mac-1 on the surface of leukocytes and suggest that this
151 naling partners FcgammaRIIA and the integrin Mac-1, internalizes soluble ICs through a mechanism used
152 ability of SLAMF7 to interact with integrin Mac-1 and utilize signals involving immunoreceptor tyros
153 ulates and primes human neutrophil integrin (Mac-1) expression, in response to formylmethionylleucylp
156 Neutrophil adhesion to both cell types is Mac-1-dependent and while ICAM-1 transduction of PCs inc
158 sing a myeloid cell-specific SIRT1 knockout (Mac-SIRT1 KO) mouse model, we show that ablation of SIRT
159 e markers programmed death ligand-1 (PD-L1), Mac-2, and macrophage mannose receptor (CD206) and produ
162 expression, as well as diminished leukocyte Mac-1-integrin activation and cyclic guanosine monophosp
163 ew pathway of thrombosis involving leukocyte Mac-1 and platelet GPIbalpha, and suggest that targeting
164 ntense infiltration with CD45(+) leukocytes, Mac-2(+) macrophages, and alpha-smooth muscle actin (alp
165 source code and precompiled binaries (Linux, Mac OS/X, Windows) are available at github.com/aresio/cu
167 nd tutorials are freely available for Linux, Mac and Windows: http://go.usa.gov/QeH (Note shortened c
171 asyMIFs and SiteHound executables for Linux, Mac OS X, and MS Windows operating systems are freely av
177 s implemented in C++ and supported on Linux, Mac OS X and other platforms supporting standard C++ com
182 with similar antigen expression to that of M-Mac (CD68(+)/CD14(+)) were predominant within atheroscle
183 okine profiles, pathologies, and macrophage (Mac) polarization status in C. neoformans-infected WT, i
184 pump from the fungus Leptosphaeria maculans (Mac) can, when expressed in neurons, enable neural silen
185 uenced 136 microcephaly or macrocephaly (Mic-Mac)-related genes and 158 possible ASD-risk genes in 53
187 addition, we prioritized 39 ASD-related Mic-Mac-risk genes, and showed their interaction and co-expr
190 ed less inflammatory responses in human Mono Mac 6 and murine macrophage RAW264.7 cells in vitro.
192 ifferentiation of the myeloid cell line Mono Mac 6 led to a significant increase in 5-LO protein expr
193 ytokine IL-6 in the monocytic cell line Mono Mac 6, induction of the Toll-interleukin-1 receptor doma
195 In human epithelial DLD-1 and monocytic Mono Mac 6 cells resveratrol decreased the expression of iNOS
197 +)Ly6C(high)Gr-1(low/neg) cells (monocytes), Mac-1(+)Ly6C(int)Gr-1(+) cells (neutrophils), and Mac-1(
198 osine kinase (Btk) was required for multiple Mac-1 activation events involved in neutrophil recruitme
202 tification of the pivotal role of neutrophil Mac-1 and ROS in this process provides a potential targe
203 EM CD4(+) T cell LFA-1 (CD11a/CD18) but not Mac-1 (CD11b/CD18); nectin-2 and poliovirus receptor are
204 However, disease permitted by the absence of Mac-1 is not related to enhanced renal immune complex de
205 tes (at 3 days) and the late accumulation of Mac-2(+) macrophages (at 28 days) in the denudated arter
206 tides leading to the selective activation of Mac-1 and neutrophil recruitment during sterile inflamma
207 ating signals that lead to the activation of Mac-1 at the leading edge of PMNs, thereby allowing RBC
208 d PI3k that promote inside-out activation of Mac-1, thereby enhancing spore internalization by macrop
211 egulated by spatial and temporal cleavage of Mac-1, which is triggered upon interaction with endothel
214 task, consisting of yeast surface display of Mac-1 inserted (I) domain library, directed evolution to
215 Neutrophil elastase is a likely effector of Mac-1 because its activity was reduced in Mac-1-deficien
218 crophages showed that IL-4-induced fusion of Mac-1-deficient cells was strongly reduced compared with
220 eover, we found that genetic inactivation of Mac-1 promotes IL-13-induced JAK/STAT activation in macr
222 uent thrombosis relied on the interaction of Mac-1 on recruited neutrophils with glycoprotein Ibalpha
224 early as 12 hours pi, and the percentage of Mac-1(+) cells increased in the injected eye beginning a
235 irculation into lungs, neutrophils depend on Mac-1 and alpha(4)beta(1), whereas the T cells are entir
243 The leukocyte integrin alphaMbeta2 (CR3 or Mac-1) has both proinflammatory and immune regulatory fu
244 etermine whether the absence of IFN-gamma or Mac-1(+) macrophages affected the sites or timing of vir
250 PrtS/ScpC and the integrin-like/IgG protease Mac/IdeS, findings that suggest a coordinated GAS virule
252 l proteins, especially the integrin receptor Mac-1, the Fc-gamma receptor I (FcgammaRI), and the tran
253 te attenuation of acute rejection, recipient Mac-1-deficiency did not prevent late graft arterial dis
254 lacking gamma-synuclein fail to up-regulate Mac-2 at the MTZ after elevation of intraocular pressure
257 IIB-mediated neutrophil recruitment requires Mac-1 and is associated with the removal of intravascula
258 iplexed analysis of RAS-dependent signaling, Mac-1(Low) cells, which harbor leukemia stem cells, were
259 re, we demonstrate that the R77H-substituted Mac-1 can be expressed on the cell surface in transfecte
262 The predicted sequence of the cloned OA/TA(Mac) receptor consists of 1,579 base pairs (bp), with an
264 ken together, these results demonstrate that Mac-1(+) cells are important IFNgamma-producing cells in
268 ertheless, recent reports have revealed that Mac-1 also plays significant immunoregulatory roles, and
269 in the cremasteric vasculature reveals that Mac-1 mitigates FcgammaRIIA-dependent neutrophil recruit
270 and confocal immunofluorescence showed that Mac-1, especially the CD11b subunit, interacted and colo
271 c-1 playing a dominant role and suggest that Mac-1 may mediate cell-cell interactions with a previous
273 , which is coexpressed with CD18 to form the Mac-1/CR3 complement receptor and adhesion molecule.
274 phism conferring an amino acid change in the Mac-1 integrin extracellular domain, R77H, was shown to
275 g promoted switchblade-like extension of the Mac-1 extracellular domain and separation of the alpha(M
276 1 deficiency (Mac-1(-/-)) or mutation of the Mac-1-binding site for GPIbalpha have delayed thrombosis
278 e revealed that neutrophils make use of this Mac-1 ligand, not for lung entry or for migration within
279 mation, and injury, whereas thrombocytopenic Mac-1-deficient mice remained resistant to disease, indi
280 firm adhesion of monocytes to ICAM-1 through Mac-1, which may explain the prominence of monocytes dur
283 g neutrophil shear resistant arrest, whereas Mac-1 was dominant over LFA-1 in mediating neutrophil po
285 he first time a molecular mechanism by which Mac-1 regulates the signaling activity of IL-13 in macro
287 k is freely available for Microsoft Windows, Mac OS X, Linux and Solaris, and can be downloaded from
288 B and runs either within MATLAB (on Windows, Mac or Linux) or as a binary without MATLAB (on Windows
289 versions of R 3.1.1 (and higher) on Windows, Mac OS X and Linux using Bioconductor 3.0 and is availab
292 The program has been tested on Windows, Mac, and Linux operating systems, and is implemented bot
293 re has been developed and tested on Windows, Mac, and Linux platforms and is available publicly under
296 The source code is available (along with Mac OS and Windows binaries) under the GPL from http://a
297 ) had enough contact time to form bonds with Mac-1 via Fn, which could not otherwise occur at a shear
299 d alphaDbeta2 support macrophage fusion with Mac-1 playing a dominant role and suggest that Mac-1 may
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