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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
7 A-1 required HPK1, but macrophage antigen 1 (Mac-1) affinity regulation was independent of HPK1.
8 m the microvillus tips in the case of LFA-1, Mac-1, and PSGL-1.
9 ps between adjacent pericytes in an ICAM-1-, Mac-1-, and LFA-1-dependent manner.
10           This newly identified IL-13Ralpha1/Mac-1-dependent pathway may offer novel targets for ther
11                Deletion of macrophage-COX-2 (Mac-COX-2KOs) was attained with LysMCre mice and complet
12 eptors, FcgammaRs and complement receptor 3 (Mac-1) to cellular cytotoxic responses are poorly unders
13 egrin heterodimer complement receptor type 3/Mac-1.
14 rated that inflammatory macrophages (F4/80(+)Mac-2(+)) were localized with initiating chondrification
15                Resident macrophages (F4/80(+)Mac-2(neg)), including osteal macrophages, predominated
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
18                                 In addition, Mac-1 has been described to negatively regulate immune c
19 f beta2 integrins LFA-1 and macrophage-1 Ag (Mac-1) showed that in CD45E613R mutant neutrophils LFA-1
20         BioNetFit can be used on stand-alone Mac, Windows/Cygwin, and Linux platforms and on Linux-ba
21 tegrins alphaLbeta2 (LFA-1) and alphaMbeta2 (Mac-1) have ratios similar to each other but lower than
22 -Rex1 serves distinct functions in LFA-1 and Mac-1 activation.
23  Mac-1 or LFA-1 revealed that both LFA-1 and Mac-1 contribute to monocyte crawling; however, the LFA-
24 D18 expression, the beta2 chain of LFA-1 and Mac-1 integrins.
25 l ICAM-1 and ICAM-2 and neutrophil LFA-1 and Mac-1.
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                           Windows, Linux and Mac binaries are available from our website.
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
32                                    Linux and Mac OS X binaries free for academic use are available at
33 h is a Python package that runs on Linux and Mac OS X systems and that enables parameter estimation a
34 age of stand-alone executables for Linux and Mac OS X under the open-source BSD license.
35                                For Linux and Mac OS X, users must install R and then follow instructi
36 ependent, allowing use on Windows, Linux and Mac OS X.
37  implemented in C and supported on Linux and Mac OS X.
38 ting platforms, including Windows, Linux and Mac OS X.
39  code for command line usage under Linux and Mac OS X.
40 d in Python and C and supported on Linux and Mac OS X.
41 nted in Python and is supported on Linux and Mac OS.
42 pliant operating system, including Linux and Mac OS/X.
43 pliant operating system, including Linux and Mac OS/X.
44 pliant operating system, including Linux and Mac OS/X.
45 LAB, Octave, Python and C) for the Linux and Mac platforms is available at http://sourceforge.net/pro
46 open-source software for Windows, Linux, and Mac OS.
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
51 eripheral node addressin, E-, L-selectin and Mac-1 but not P-selectin or LFA-1.
52 allers for Windows, Linux, Unix, Solaris and Mac OS X are available at http://apollo.berkeleybop.org,
53 re available for Windows, Linux, Solaris and Mac OS X at http://bioinf.scri.ac.uk/strudel/.
54 s are freely available for UNIX, Windows and Mac OS X operating systems at Bioconductor.
55 tested for R 2.14.2 under Linux, Windows and Mac OS X.
56  tested for R 3.2.0 under Linux, Windows and Mac OS X.
57  executable downloads for Linux, Windows and Mac OS, with manual and source code, at www.northeastern
58 ad.html, and operates on Linux, Windows, and Mac OS.
59 cell-surface proteoglycans because both anti-Mac-1 function-blocking mAb and heparin were required to
60 effects were abrogated by anti-CD40L or anti-Mac-1 monoclonal antibody.
61 lockade of CD40L-Mac-1 interaction with anti-Mac-1 mAb led to spontaneous disease reactivation in hea
62 receptor 3 (PAR3), and macrophage-1 antigen (Mac-1) blocked APC inhibition of NETosis.
63 ith antibodies against Macrophage-1 antigen (Mac-1) or intercellular adhesion molecule 1 and were rep
64 reely available for Microsoft Windows, Apple Mac OS X, Linux and Solaris.
65                           CR3 (also known as Mac-1, integrin alphaMbeta2, or CD11b/CD18) is expressed
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
69                   It has been tested on both Mac and Windows.
70                            We find that both Mac-1 (CD11b/CD18) and alpha(4)beta(1) (CD49d/CD29) inte
71               The results indicate that both Mac-1 and alphaDbeta2 support macrophage fusion with Mac
72 gnaling and to trigger TLR3-independent, but Mac-1-dependent, inflammatory oxidative signaling, ident
73 yte NADPH oxidase in a TLR3-independent, but Mac-1-dependent, manner.
74 nd acts as a coreceptor for spore binding by Mac-1.
75 d neutrophil accumulation that is enabled by Mac-1 deficiency.
76 naling events following dsRNA recognition by Mac-1.
77 ble 3 binding protein (LGALS3BP, also called Mac-2 binding protein) is a heavily glycosylated secrete
78                    Immunostaining for CD11b (Mac-1)-expressing leukocytes (macrophage, neutrophils) a
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.
82 ue to CD11a/CD18 (LFA-1)- versus CD11b/CD18 (Mac-1)-mediated crawling.
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
85                            Blockade of CD40L-Mac-1 interaction with anti-Mac-1 mAb led to spontaneous
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
90 rated reactive intermediates and involves DC Mac-1.
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.
94                               Although Dowex Mac 3 had the highest adsorption capacity, material cost
95                           Dowex 50 and Dowex Mac 3 showed nearly 100% regeneration efficiencies.
96 clinoptilolite, biochar, Dowex 50, and Dowex Mac 3) were compared in pure salt solutions, synthetic u
97  four-person household were lowest for Dowex Mac 3 (5 L) and highest for biochar (19 L).
98                           Blockade of either Mac-1 or LFA-1 revealed that both LFA-1 and Mac-1 contri
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.
101                 These observations establish Mac-1 on neutrophils as a critical molecular link betwee
102       We then discuss studies that exemplify Mac-1's pro-inflammatory versus regulatory roles particu
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
106                                       First, Mac-1 facilitated poly I:C internalization through the a
107        Executable versions of AlphaMPSim for Mac and Linux and a user manual are available at http://
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
110 unner binary distributions are available for Mac OS X, Linux and Windows.
111 ions of the program are freely available for Mac OSX and Windows operating systems.
112           RULEBENDER is freely available for Mac, Windows and Linux at http://rulebender.org.
113     Source code and precompiled binaries for Mac OS X 10.6+ and Linux 2.6.15+ are available from http
114 obal conformational changes are critical for Mac-1-dependent outside-in signal transduction.
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.
117                                 Furthermore, Mac 1 is differentially phosphorylated in response to ir
118 phages with antigen expression similar to GM-Mac (CD68(+)/CD14(-)) were predominant in areas devoid o
119 ammatory marker CD14 in M-Mac relative to GM-Mac.
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
122                        This study identifies Mac-1 as a novel surface receptor for extracellular dsRN
123 el humanized lupus mouse model, and identify Mac-1 regulation of FcgammaRIIA-mediated neutrophil recr
124 ained with antibodies specific for IFNgamma, Mac-1 (CD11b), CD49b, F4/80, CD4, CD8, and CD11c.
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
127 ve leukocytes (P<0.01) and a 73% decrease in Mac-3-positive macrophages (P<0.05).
128 s and macrophages significantly decreased in Mac-1(-/-) compared with WT recipients.
129 te transfer rescues the thrombosis defect in Mac-1(-/-) mice, and Mac-1-dependent regulation of the t
130  mice and the phenotype in mice deficient in Mac-1 or neutrophil elastase was similar.
131 e, we demonstrate that P-Rex1 is involved in Mac-1-dependent intravascular crawling.
132 t not adhesion and migration, was reduced in Mac-1-deficient macrophages.
133 of Mac-1 because its activity was reduced in Mac-1-deficient mice and the phenotype in mice deficient
134 ost package is implemented to readily run in Mac or Linux environments.
135 ely twofold higher in wild-type mice than in Mac-1(-/-) mice.
136 emented using Perl and R, and can be used in Mac or Linux environments.
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
139                     Because of the increased Mac-1 adhesiveness, neutrophil crawling was impaired in
140                                The increased Mac-2 expression by MTZ astrocytes during glaucoma likel
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
143                       The leukocyte integrin Mac-1 (also known as integrin alphaMbeta2, or CD11b/CD18
144         Among beta2 family members, integrin Mac-1 (alphaMbeta2, CD11b/CD18) is abundantly expressed
145 ptor (IL-13R), as a novel ligand of integrin Mac-1, using a co-evolution-based algorithm.
146 s or lacking the leukocyte-specific integrin Mac-1, neutrophil recruitment, endothelial injury, glome
147 quired neutrophil expression of the integrin Mac-1 (alphaMbeta2).
148             Here, we identified the integrin Mac-1 (alphaMbeta2, CD11b/CD18) as the receptor mediatin
149 ts identify PTN as a ligand for the integrin Mac-1 on the surface of leukocytes and suggest that this
150          Recognition of BclA by the integrin Mac-1 promotes spore uptake by professional phagocytes,
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
154 he mice additionally lack the CD18 integrin, Mac-1.
155                         Therefore, integrins Mac-1 and alpha(4)beta(1) have a pivotal role in prevent
156    Neutrophil adhesion to both cell types is Mac-1-dependent and while ICAM-1 transduction of PCs inc
157 ctin-3-binding protein, also known as 90-kDa Mac-2-binding protein.
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
160                As observed with mice lacking Mac-1, CD14(-/-) mice are also more resistant than wild-
161 ncement of platelet P-selectin and leukocyte Mac-1 expression and oxidative activity.
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
166          Source code and binaries for Linux, Mac and Windows are available at http://www.infobiotics.
167 nd tutorials are freely available for Linux, Mac and Windows: http://go.usa.gov/QeH (Note shortened c
168 hensive R Archive Network (CRAN), for Linux, Mac OS and Windows platforms.
169          Source code and binaries for Linux, Mac OS X and Microsoft Windows are available.
170                 GeNN is available for Linux, Mac OS X and Windows platforms.
171 asyMIFs and SiteHound executables for Linux, Mac OS X, and MS Windows operating systems are freely av
172 any Unix-based operating system (e.g. Linux, Mac OSX).
173             The package can be run on Linux, Mac and Windows systems and also provides a graphical us
174                         It can run on Linux, Mac and Windows.
175 tware implemented using C# and run on Linux, Mac OS X & Windows operating systems.
176  implemented in Perl and supported on Linux, Mac OS X and MS Windows.
177 s implemented in C++ and supported on Linux, Mac OS X and other platforms supporting standard C++ com
178    OSA has been tested extensively on Linux, Mac OS X and Windows platforms.
179 s written in C++, and is supported on Linux, Mac OSX and MS Windows.
180 implemented in C/C++ and supported on Linux, Mac OSX and MS Windows.
181 sion of the proinflammatory marker CD14 in M-Mac relative to GM-Mac.
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
186             Our results indicate some of Mic-Mac-risk genes are involved in ASD.
187  addition, we prioritized 39 ASD-related Mic-Mac-risk genes, and showed their interaction and co-expr
188            This cytokine interplay modulates Mac differentiation, including generation of an intermed
189 o JAM-C via the neutrophil adhesion molecule Mac-1.
190 ed less inflammatory responses in human Mono Mac 6 and murine macrophage RAW264.7 cells in vitro.
191 oteins in the human monocytic cell line Mono Mac 6 (MM6).
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
194 man primary and immortalized monocytes (Mono Mac 6) were measured.
195 In human epithelial DLD-1 and monocytic Mono Mac 6 cells resveratrol decreased the expression of iNOS
196                Sample D stimulated only Mono-Mac 6 and HEK-human TLR4 (hTLR4) cells and was later ide
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
199                               Using multiple Mac activation markers, we further demonstrate that IL-4
200 s to cancer cells was mediated by neutrophil Mac-1/ICAM-1.
201              TEM, which increases neutrophil Mac-1 surface expression, concomitantly increases the ab
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
209                  mCLCA1-mediated adhesion of Mac-1- or LFA-1-expressing leukocytes to lymphatic vesse
210 nd LECs that were mediated by the binding of Mac-1 on DCs to ICAM-1 on LECs.
211 egulated by spatial and temporal cleavage of Mac-1, which is triggered upon interaction with endothel
212 nzymes that control constitutive cleavage of Mac-1.
213                                  Deletion of Mac-COX-2 appeared to remove a restraint on COX-2 expres
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
216             We also found that expression of Mac-1 on the surface of human embryonic kidney (HEK) 293
217 ation, likely due to increased expression of Mac-1.
218 crophages showed that IL-4-induced fusion of Mac-1-deficient cells was strongly reduced compared with
219  conformational changes in the generation of Mac-1 outside-in signals.
220 eover, we found that genetic inactivation of Mac-1 promotes IL-13-induced JAK/STAT activation in macr
221 r impairment was seen with the inhibition of Mac-1, a receptor for ICAM-1.
222 uent thrombosis relied on the interaction of Mac-1 on recruited neutrophils with glycoprotein Ibalpha
223                                 The level of Mac-1 up-regulation peaked at an intermediate PF4 dose,
224  early as 12 hours pi, and the percentage of Mac-1(+) cells increased in the injected eye beginning a
225 I domain, the major ligand-binding region of Mac-1, and PTN.
226                  Consistent with the role of Mac-1 in crawling, Mac-1 block (compared with LFA-1) was
227                         However, the role of Mac-1 in macrophage fusion leading to the formation of m
228                         However, the role of Mac-1 in thrombosis is undefined.
229  may shed light on how the opposing roles of Mac-1 may be elicited.
230                     Moreover, stimulation of Mac-1 or FcgammaRI intensifies the constitutive Syk-medi
231     Antibody and small-molecule targeting of Mac-1:GPIbalpha inhibits thrombosis.
232  recognition specificity overlapping that of Mac-1, is unknown.
233 infection concurrently display both types of Mac polarization markers.
234               While binding to PTN, Mac-1 on Mac-1-expressing HEK293 cells appears to cooperate with
235 irculation into lungs, neutrophils depend on Mac-1 and alpha(4)beta(1), whereas the T cells are entir
236 BC in vitro, processes strictly dependent on Mac-1 and complement C3.
237               The toolkit can be executed on Mac OS X 10.5 and above or any Linux distribution.
238 iki.github.com/mz2/imotifs and can be run on Mac OS X Leopard (Intel/PowerPC).
239 sis framework is written in Perl and runs on Mac OS and Linux/Unix systems.
240  using an open-source R package that runs on Mac OS X, Linux and Windows systems.
241  has been implemented in Java for support on Mac OS X, Linux and MS Windows.
242 s available under a BSD license and works on Mac OS X and Linux systems.
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
245 ted nearly instantaneously on a modern PC or Mac computer.
246 s can be <1 h using a standard desktop PC or Mac.
247 or as a binary without MATLAB (on Windows or Mac).
248 le Vav- and Rac-independent pathways promote Mac-1/complement C3-dependent functions.
249                    Accordingly, PTN promoted Mac-1-dependent cell spreading and initiated intracellul
250 PrtS/ScpC and the integrin-like/IgG protease Mac/IdeS, findings that suggest a coordinated GAS virule
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 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
255 a models, MTZ astrocytes further up-regulate Mac-2 expression.
256       mCLCA1 also bound to the LFA-1-related Mac-1 integrin that is preferentially expressed on leuko
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
260 inds Mac-1 in a purified system and supports Mac-1-mediated cell adhesion.
261 s1143679, a single nucleotide non-synonymous Mac-1 polymorphism associated with SLE.
262   The predicted sequence of the cloned OA/TA(Mac) receptor consists of 1,579 base pairs (bp), with an
263                     We also mapped the OA/TA(Mac) receptor distribution by in-situ hybridization to t
264 ken together, these results demonstrate that Mac-1(+) cells are important IFNgamma-producing cells in
265                        Indeed, we found that Mac-1(-/-)LDLR(-/-) mice develop significantly more foam
266                  The prevailing view is that Mac-1 on macrophages is responsible for immune complex c
267                Importantly, we observed that Mac-1(-/-) macrophages exhibit increased expression of f
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
272                                          The Mac-1 integrin is expressed mainly on myeloid cells and
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
277          Overall, our data indicate that the Mac-1/BclA interaction may play a major role in B. anthr
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
281  in this pathway required for fMLF-triggered Mac-1 activation and neutrophil recruitment.
282                StochKit2 runs on Linux/Unix, Mac OS X and Windows.
283 g neutrophil shear resistant arrest, whereas Mac-1 was dominant over LFA-1 in mediating neutrophil po
284  impaired, and avidity was enhanced, whereas Mac-1 adhesiveness was increased.
285 he first time a molecular mechanism by which Mac-1 regulates the signaling activity of IL-13 in macro
286  system with R installed, including Windows, Mac OS and most Linux distributions.
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
290 ns of PathVisio 2.0.11 and later on Windows, Mac OS X and Linux.
291  compatible with R 3.2 and above on Windows, Mac OS X and Linux.
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
294 for execution on popular platforms (Windows, Mac and Linux).
295        PathVisio is compatible with Windows, Mac OS X and Linux.
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
298 -alpha production also fell in cultures with Mac-1(-/-) macrophages.
299 d alphaDbeta2 support macrophage fusion with Mac-1 playing a dominant role and suggest that Mac-1 may
300                Here we report that mice with Mac-1 deficiency (Mac-1(-/-)) or mutation of the Mac-1-b

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