ライフサイエンスコーパス: arginase

1 nfiltration of M2-type macrophages producing arginase.

2 , including PGE2, inducible NO synthase, and arginase.

3 enzyme of the polyamine production pathway, arginase.

4 d kidney activity of the Mn-dependent enzyme arginase.

5 Arginase 1 (40-fold) and IL-10 (265-fold) were higher in

6 A majority of OSM(+) neutrophils expressed arginase 1 (72.5% +/- 12%), suggesting an N2 phenotype.

7 these enzymes, a pegylated human recombinant arginase 1 (AEB1102), reduces plasma arginine in murine

8 Furthermore, by using microglia-specific arginase 1 (Arg1) ablation as well as overexpression in

9 n, such as stripes of macrophages expressing arginase 1 (ARG1) and mannose receptor, C type 1 (MRC1).

10 Arginase 1 (Arg1) and nitric oxide synthases compete for

11 Of the RAGs examined, only arginase 1 (Arg1) expression correlated with the increas

12 patients, the phenotypic characteristics and arginase 1 (ARG1) expression levels of these MDSCs remai

13 ginase deficiency is caused by deficiency of arginase 1 (ARG1), a urea cycle enzyme that converts arg

14 ficiency is caused by biallelic mutations in arginase 1 (ARG1), the final step of the urea cycle, and

15 Indoleamine 2,3 dioxygenase (IDO) and arginase 1 (ARG1), which catabolize Trp and Arg, respect

16 Arginase 1 (Arg1), which converts l-arginine into ornith

17 In contrast with PD-L1, arginase 1 (Arg1), which exerts T cell suppression at an

18 n markers, were specifically responsible for arginase 1 activity.

19 trained MSCs enhanced the anti-inflammatory (arginase 1 and CD206) marker expression, but decreased t

20 reduced inducible nitric oxide synthase and arginase 1 and displayed a reduced T-cell suppressive ac

21 ell proliferation and express high levels of Arginase 1 and iNOS.

22 arin increased the anti-inflammatory markers arginase 1 and interleukin-10 in murine BMDMs.

23 er cells stimulated with palmitate, enhanced arginase 1 and lower leukotriene B4 (LTB4) levels were d

24 m of l-Arginine (l-Arg), through the enzymes arginase 1 and NO synthase 2 (NOS2), is well documented

25 and decreased M2 macrophages that expressed Arginase 1 and were found in inflammatory zone protein (

26 More specifically, G-MDSCs producing arginase 1 are associated with a higher incidence of nos

27 MDSCs expressing arginase 1 are induced by PI.

28 show that the lactate-induced expression of arginase 1 by macrophages has an important role in tumou

29 erse physiological and anatomical markers of arginase 1 deficiency and therefore may be of therapeuti

30 Arginase 1 deficiency is a urea cycle disorder associate

31 Moreover, Nr4a2 transcriptionally activates arginase 1 expression by directly binding to its promote

32 naling while supporting IL-4-STAT6-activated arginase 1 expression by promoting chromatin remodeling.

33 We find that the loss of arginase 1 expression results in decreased dendritic com

34 eptors led to strikingly increased levels of arginase 1 gene expression and protein activity in infec

35 rophages induced NO synthase 2 and inhibited arginase 1 gene expression.

36 Hepatic arginase 1 gene therapy using adeno-associated virus res

37 alpha levels and the expression of M2 marker Arginase 1 in inflammatory-elicited macrophages.

38 e (iNOS), reactive oxygen species (ROS), and arginase 1 inhibitors.

39 omys and Mus lies in the macrophage-produced arginase 1 is found in Mus whereas arginase 2 is found i

40 9) had significantly higher mononuclear cell arginase 1 mRNA, protein, and enzyme activity; lower NOS

41 cells via a CD18-mediated contact-dependent arginase 1 release.

42 by adoptively transferring MDSC or injecting arginase 1 to noninjured mice.

43 MDSCs expressing arginase 1 were measured by flow cytometry.

44 ls of MDSC mediators S100A8/A9, S100A12, and arginase 1 were significantly increased.

45 ulating factor 1 receptor (CSF-1R)-dependent arginase 1(+) myeloid cells enhanced NO-dependent tumor

46 ation of (mannose receptor C type 1) MRC1+, (arginase 1) Arg+ macrophages in the tumor microenvironme

47 es express significantly increased levels of arginase 1, a biomarker of the alternatively activated M

48 n the peritoneum, which expressed functional arginase 1, and potently suppressed T cell proliferation

49 High initial levels of G-MDSCs, arginase 1, and S100A12 but not M-MDSCs were associated

50 Two L-arginine catalytic enzymes, iNOS and arginase 1, are well-characterized hallmark molecules of

51 Decompartmentalized hemoglobin, arginase 1, asymmetric dimethylarginine, and adenine nuc

52 ced expression of protumor type 2 molecules (arginase 1, Fizz 1, Mgl, and IDO), number of M2-type mac

53 pression of the pro-Th1 mediators Fizz-1 and arginase 1, indicating that it could promote proinflamma

54 ns of immunosuppressive molecules, including arginase 1, inducible nitric oxide synthase, signal tran

55 markers for alternative activation, such as Arginase 1, with concomitant downregulation of inducible

56 and mediated neuronal protection through an arginase 1-polyamine axis.

57 DSC and decreased expression of TGFbeta1 and arginase 1.

58 phenotype as determined by the expression of arginase 1.

59 nciding with an induction of MDSC expressing arginase 1.

60 r and expression of an M2 macrophage marker, arginase-1 (Arg 1) was lower in tumors from ogr1(-/-) mi

61 Arginase-1 (Arg-1) was found promote suppression because

62 nd involved complement, activating FcRs, and Arginase-1 (Arg1) activity.

63 Arginase-1 (Arg1) also metabolizes l-arginine but does n

64 alternative macrophage activation including arginase-1 (ARG1) and mannose receptor (CD206).

65 we demonstrate that expression of the enzyme arginase-1 (Arg1) during acute or chronic lung inflammat

66 chanisms responsible for immune suppression, arginase-1 (ARG1)-carrying small extracellular vesicles

67 expression of the anti-inflammatory mediator arginase-1 (P = 0.005), and a sustained reduction in ski

68 educing anti-inflammatory cytokine IL-10 and arginase-1 activities, suggesting a dominant classically

69 mouse population infected with Mtb, enhanced arginase-1 activity was associated with increased lung i

70 and expressed macrophage mannose receptors, arginase-1 activity, and IL-10.

71 Intravascular venous levels of arginase-1 and cell-free plasma hemoglobin increase imme

72 that aged stored blood has higher levels of arginase-1 and cell-free plasma hemoglobin.

73 nterleukin 6 (IL6) along with the M2 markers arginase-1 and chitinase-like 3 (Chil3 or YM1) were eval

74 eritoneal macrophages expressed an M2 marker arginase-1 and generated IL-31 when stimulated with a co

75 shown that the mRNA expression levels of the arginase-1 and inducible NO synthase genes, which charac

76 with higher circulatory suppressive factors arginase-1 and interleukin-10, and lower total antioxida

77 RHI correlated negatively with arginase-1 and positively with l-arginine (P = .001).

78 onditioned medium enhanced the expression of arginase-1 and YM1 in primary macrophages.

79 t inhibition of the anti-inflammatory factor arginase-1 by c-Jun.

80 Both iNOS and arginase-1 expression were reduced in peritoneal macroph

81 sion as evidenced by increased expression of arginase-1 in CD11b(+)Gr1(+) cells, diminished M1 functi

82 uctive effects could be further augmented by arginase-1 inhibition (indirectly increasing NO bioavail

83 l co-culture system, we show that macrophage arginase-1 is the only factor required by M2 macrophages

84 Accordingly, we found dramatically increased arginase-1 levels in post-cardiopulmonary bypass periphe

85 ic tumors of Bcl11b(F/F)/CD4-Cre mice, their arginase-1 levels were severely reduced.

86 fferentially regulating cyclooxygenase-2 and arginase-1 levels.

87 and correlates with hypoargininemia and high arginase-1 levels.

88 g luciferase expression to activation of the arginase-1 promoter.

89 3K27 trimethylation at IL-12, TNF-alpha, and arginase-1 promoters, respectively, whereas H3K4 trimeth

90 ophages migrated to the tumors and activated arginase-1 so that they could be detected by bioluminesc

91 vitamin D in skin homeostasis, and implicate arginase-1 upregulation as a previously unreported mecha

92 Here, we identify extrahepatic arginase-1(+) Id2(+) fetal ILC precursors that express a

93 macrophages and a concomitant enhancement in arginase-1(+) M2 macrophages.

94 Plg/Pla also increased M2 markers (CD206 and arginase-1) and secretory products (transforming growth

95 Pulmonary endothelial deletion of arginase-1, a downstream target of HIF-2alpha, likewise

96 t with the expression of IFN-gamma, but also Arginase-1, a functional antagonist of the iNOS pathway,

97 In addition, the expression of arginase-1, a marker for anti-inflammatory macrophages,

98 (EndoPAT), and plasma levels of l-arginine, arginase-1, and asymmetric dimethylarginine were measure

99 teins: vascular endothelial growth factor-A, Arginase-1, and CCL2, similarly shown in tumor-associate

100 including LIGHT, sphingosine kinase 1, CCL1, arginase-1, and costimulatory molecules, CD16/32, ICAM-1

101 ve Mvarphi activation markers, such as YM-1, arginase-1, and interleukin-10 by activation of mer rece

102 atory phenotype with reduced iNOS, increased Arginase-1, and lower wound tumor necrosis factor alpha

103 iated cells upregulated expression of IL-10, arginase-1, and PD-L1 and suppressed the proliferation o

104 y, as indicated by elevated levels of IL-10, arginase-1, and VEGF, and lowering of IL-1beta and TNF-a

105 immune regulatory factors, including IDO-1, arginase-1, Foxp3, TGF-beta, IL-10, and decreased levels

106 egulation of genes relevant to MDSCs such as arginase-1, IDO1, PDL1, and IL-10 at the injection site.

107 ny genes were similarly perturbed, including Arginase-1, IL-10, TREM1, and IFN signaling, revealing t

108 type counterparts due to lower expression of arginase-1, IL6, and phospho-Stat3.

109 Both subsets produced Arginase-1, inducible nitric oxide synthase (iNOS), and

110 d from S. aureus biofilms revealed increased arginase-1, inducible NO synthase, and IL-10 expression,

111 y elevated expression of mannose receptor-1, Arginase-1, interleukin-10 and transforming growth facto

112 companied by reduced expression of CD206 and arginase-1, markers for AAMs.

113 rleukin-10, transforming growth factor-beta, arginase-1, matrix metalloproteinase and vascular endoth

114 ione S-transferase alpha, alpha-fetoprotein, arginase-1, osteopontin (OPN), sorbitol dehydrogenase, f

115 oduction of the immune-suppressive cytokines arginase-1, TGF-beta, and IL-10 by MDSC, concomitant wit

116 correlated with increased serum activity of arginase-1, which was elevated in TB patients coinfected

117 ker iNOs and diminish that of the M2 markers Arginase-1, Ym-1, and FIZZ-1.

118 i infection resulted in accumulation of high arginase-1-expressing macrophages in the lung, which for

119 a indicate that helminth coinfection induces arginase-1-expressing type 2 granulomas, thereby increas

120 inflammatory macrophage mannose receptor and arginase-1.

121 expression of the arginine-degrading enzyme arginase-1.

122 Here we identify arginase 2 (Arg2) as a fasting-induced hepatocyte factor

123 We demonstrate here that arginase 2 (ARG2) drives neuroblastoma cell proliferatio

124 nity maturation of an inhibitory antibody to Arginase 2 (ARG2).

125 -produced arginase 1 is found in Mus whereas arginase 2 is found in Acomys.

126 our-necrosis factor-alpha production through arginase-2 activity.

127 atory mediators tumor necrosis factor-alpha, arginase-2, interleukin-1beta, interleukin-6, and interf

128 Helicobacter pylori arginase, a bimetallic enzyme, is crucial for pathogenes

129 el molecular mechanism drives OxLDL-mediated arginase activation, endothelial NOS uncoupling, endothe

130 by achieving near-normal ureagenesis; liver arginase activity achieved 54% of wild type.

131 We observed a lack of arginase activity also in several CHO cell strains (CHO-

132 Further, RM s inhibited AAM -promoted arginase activity and fibroblast proliferation in vitro.

133 MHC class II(+) macrophages with enhanced l-Arginase activity and IL-10 secretion at tumor beds.

134 iR-210 modulated MDSC function by increasing arginase activity and nitric oxide production, without a

135 Induction of arginase activity and parasite growth involved C-type le

136 Mechanistically, IND reduced arginase activity as well as NO and reactive oxygen spec

137 lation with IFN-gamma, we observed that MPhi arginase activity did not inhibit production of NO deriv

138 ively with lung function and positively with arginase activity in CF airway fluid.

139 The rapid increase in arginase activity in human aortic endothelial cells expo

140 ne together with inhibition of intracellular arginase activity increased cytosolic nitric oxide and e

141 ceptors, because mannose injection decreased arginase activity induction and parasite load in vitro a

142 Arginase activity induction in macrophages is an escape

143 Finally, we demonstrate that the arginase activity of neuroblastoma impairs NY-ESO-1-spec

144 eal macrophages with IL-33 failed to promote arginase activity or expression of YM-1 or Retnla, marke

145 Neuroblastoma arginase activity results in inhibition of myeloid cell

146 However, arginase activity was high in CF airway fluid and minima

147 CD11b(+)GR-1(+) myeloid cells with enhanced arginase activity, identified as myeloid-derived suppres

148 with tetrahydrobiopterin oxidation and high arginase activity, leading to endothelial nitric oxide s

149 ever, L-arginine supply can be restricted by arginase activity, resulting in inefficient NO output an

150 children cannot be fully explained by plasma arginase activity.

151 ed (13)C probe, [6-(13)C]-arginine, to image arginase activity.

152 press T-cell proliferation through increased arginase activity.

153 e signaling through inhibition of endogenous arginase activity.

154 hages, determined by cytokine production and arginase activity.

155 ine aortic intima with a concomitant rise in arginase activity.

156 applicable to mammalian cell lines that lack arginase activity.

157 hesis pathway, it relies mainly upon its own arginase-AdoMetDC/ODC pathway to acquire the polyamines

158 ach of targeting secreted arginine through l-arginase, along with targeting microenvironment-secreted

159 Under the same conditions, the enzymes arginase and agmatinase accelerate substrate hydrolysis

160 t (in contrast to the mechanisms employed by arginase and agmatinase) is believed to involve attack b

161 f a diverse set of enzymatic proteins (e.g., arginase and glutamine synthase).

162 rated recombinant CHO-K1 cells co-expressing arginase and human erythropoietin (hEPO), which also dis

163 Blocking arginase and inducible NO synthase did not restore B lym

164 bited Th2 ACT, consistent with a key role of arginase and M2 macrophages in myeloma elimination by Th

165 ough arginine depletion in the media using l-arginase and NOS inhibition in cancer cells using N(G)-n

166 inine utilization pathway by an inhibitor of arginase and ornithine decarboxylase protected the mice

167 h a bicistronic vector co-expressing GFP and arginase and selected cells in media devoid of l-ornithi

168 m-induced CD11b(+)Gr1(+) cells express Arg1 (arginase) and Nos2 (inducible NO synthase) and suppress

169 Arginase (Arg) 1 is expressed by hematopoietic (e.g., ma

170 g inducible nitric oxide synthase (iNOS) and arginase (ARG), are typical in asthmatic airway epitheli

171 However, the importance of arginase (ARG), the first enzyme of the polyamine pathwa

172 lism (IDO1, IDO2, Trp 2,3-dioxygenase [TDO], arginase [ARG] 1, ARG2, inducible NO synthetase) were ev

173 e cellular processes, is a substrate for two arginases-Arg1 and Arg2-having different expression patt

174 the expression of the mitochondrial form of arginase ARG2 in PDA and that ARG2 silencing or loss res

175 We find that the mitochondrial form of arginase (ARG2), which hydrolyzes arginine into ornithin

176 Arginase, arginine deiminase and arginine decarboxylase

177 s by upregulating the production of iNOS and arginase, as well as MMP-9 and VEGF.

178 f inducible nitric oxide synthase (iNOS) and arginase, as well as other suppressive mechanisms, allow

179 the basis of this phenotype, we developed an arginase-based selection system.

180 pletion of arginine by pegylated recombinant arginase BCT-100, significantly delayed tumor developmen

181 microglia was required for the induction of arginase by IL-4.

182 Plasma levels of arginine, arginase, cell-free hemoglobin, ADMA, symmetric-dimethyl

183 associated with an increase in intracellular arginase concentration detected using a spectrophotometr

184 -(13)C]-arginine is linearly correlated with arginase concentration in vitro.

185 Clinical features of arginase deficiency include elevated plasma arginine lev

186 Arginase deficiency is caused by biallelic mutations in

187 Arginase deficiency is caused by deficiency of arginase

188 % of plasma arginine levels in subjects with arginase deficiency were above the normal range despite

189 In neonatal and adult mice with arginase deficiency, AEB1102 reduced the plasma arginine

190 t the functional abnormalities that occur in arginase deficiency.

191 urea cycle disorders and the only to examine arginase deficiency.

192 an arginine-reducing agent in patients with arginase deficiency.

193 reduces plasma arginine in murine models of arginase deficiency.

194 gene-based therapeutic for the treatment of arginase deficiency.

195 to determine how single-copy and double-copy arginase deletion affects cortical circuits in mice.

196 the hypothesis that neuroblastoma creates an arginase-dependent immunosuppressive microenvironment in

197 Cs potently inhibited T cells in a partially arginase-dependent manner.

198 Knock out of Plasmodium arginase did not alter arginine depletion in infected mi

199 This indicates that the HKDM-encoded arginase enzyme produces the urea used by the E. ictalur

200 In persistent infection, arginase-expressing gMDSCs (and circulating arginase) in

201 se data demonstrate the capacity of expanded arginase-expressing gMDSCs to regulate liver immunopatho

202 Furthermore, we found that arginase-expressing MPhis preferred L-citrulline over L-

203 To gain insight on how loss of arginase expression affects the excitability and synapti

204 hypoxia, dietary nitrate suppressed cardiac arginase expression and activity and markedly elevated c

205 n with the IKKbeta inhibitor IKK16 decreased arginase expression and activity in azithromycin-treated

206 We report that arginase expression and activity were induced in macroph

207 HIF-2alpha stability, which causes increased arginase expression and dysregulates normal vascular NO

208 MAPK family members are involved in iNOS and arginase expression following LPS stimulation.

209 e derived based on an Interleukin-12beta and arginase expression ratio.

210 lic tracer analysis demonstrated that plasma arginase flux was unchanged by P. berghei infection.

211 crobial activity and the capacity to inhibit arginase from Leishmania were evaluated in spray-dried p

212 high inhibitory capacity against the enzyme arginase from Leishmania.

213 Plasmodium berghei ANKA with or without the arginase gene.

214 ombinant cellular assay overexpressing human arginase I (CHO cells).

215 of a pegylated form of the catabolic enzyme arginase I (peg-Arg I) has shown some promise as a thera

216 substituent (NED-3238), example 43, inhibits arginase I and II with IC(50) values of 1.3 and 8.1 nM,

217 elevation of cAMP results in upregulation of arginase I and increased polyamine synthesis.

218 the expression of immunosuppressive factors arginase I and iNOS.

219 suppressed T cell responses by expression of arginase I and production of reactive oxygen species and

220 , as associated with increased expression of arginase I and the cytokines IL10 and IL4.

221 analyses reinforced the association between arginase I expression and enzymes involved in prostaglan

222 Our findings also suggest that induction of arginase I expression is stochastic; that is, difference

223 ther they rapidly and synergistically induce arginase I mRNA, protein, and promoter activity in murin

224 eneic T cells and in the use of either IL-17/arginase I or IFN-gamma/inducible nitric oxide synthase

225 Inhibition of arginase I or ODC abrogates L. amazonensis replication i

226 increased protein and mRNA levels for iNOS, arginase I, and arginase II; although the induction of a

227 IL-4 and 8-bromo-cAMP individually induce arginase I, but together they rapidly and synergisticall

228 Immunohistochemistry confirmed that arginase I, ODC, and cyclooxygenase2 expression was high

229 Our data implicate arginase I, ODC, PGE2, and TGF-beta in the failure to mo

230 The plasma levels of arginase I, ornithine decarboxylase (ODC), transforming

231 of arginase II was more robust than that for arginase I.

232 ociated anti-inflammatory interleukin 10 and arginase I.

233 yl)hexanoic acid, compound 9, inhibits human arginases I and II with IC50s of 223 and 509 nM, respect

234 phenotype was characterized by a decrease in Arginase-I (ARG1) expression and an increase in iNOS, MH

235 and impede reparative response by decreasing Arginase-I (Arg1) expression through interaction with th

236 Finally, rescue of arginase-I activity after STAT3 blockade restored MDSC's

237 ssion of immunosuppressive molecules such as arginase-I and PD-L1 and alters their ability to suppres

238 phorylated STAT3 levels that correlated with arginase-I expression levels and activity.

239 ration and IFN-gamma production and had high arginase-I expression.

240 demonstrate that the suppressive function of arginase-I in both infiltrating and circulating MDSC is

241 lls were phenotyped as CD11b+, CD33+, CD34+, arginase-I+, and ROS+.

242 urea level correlating with increased renal Arginase II activity, hyperargininemia, and increased ki

243 reased following siRNA-mediated knockdown of arginase II and decreased when arginase II was overexpre

244 High arginase II expression correlates with poor survival for

245 inhibitor (ERK pathway) completely abolished arginase II expression while actually enhancing iNOS ind

246 while both the ERK and p38 pathways regulate arginase II induction in LPS-stimulated macrophages, iNO

247 ted iNOS expression while it only attenuated arginase II induction.

248 Arginase II is expressed and released from AML blasts an

249 Arginase II is the predominant isoform expressed and cre

250 Arginase II promoter activity was increased by approxima

251 Arginase II promoter activity was unaffected by a p38 in

252 vely active RAS mutant increased LPS-induced arginase II promoter activity, while transfection with a

253 t or a vector expressing MKP-3 inhibited the arginase II promoter activity.

254 , and arginase II; although the induction of arginase II was more robust than that for arginase I.

255 knockdown of arginase II and decreased when arginase II was overexpressed.

256 l and human cord blood CD71(+) cells express arginase II, and this enzymatic activity inhibits phagoc

257 ic data for selected examples bound to human arginase II.

258 in and mRNA levels for iNOS, arginase I, and arginase II; although the induction of arginase II was m

259 Arginase-II (Arg-II), the type-II L-arginine-ureahydrola

260 unique and previously unreported phenotype (arginase(+)/IL-1beta(+)) that augmented neurite growth a

261 en reduced IL-4Ralpha expression and reduced arginase, IL-1beta, and CCL2 expression was confirmed us

262 death by a mechanism involving activation of arginase in high inducible nitric oxide synthase-express

263 arginase-expressing gMDSCs (and circulating arginase) increased most in disease phases characterized

264 T. musculi excreted/secreted factor-mediated arginase induction.

265 Interestingly, arginine addition plus arginase inhibition also enhanced ORKAMBI-mediated incre

266 The protective effect of arginase inhibition was lost in the presence of a NOS in

267 A higher potency of arginase inhibition was observed with fisetin, which was

268 chol group on apigenin drastically decreased arginase inhibition.

269 Finally, combined treatment with arginase inhibitor and arginine rescued the suppression

270 Additionally, when the specific arginase inhibitor l-norvaline was used to treat E. icta

271 ion and increased infection were reversed by arginase inhibitor Nor-NOHA but were reproduced by adopt

272 th control RBCs (beta93C) pretreated with an arginase inhibitor to facilitate export of RBC NO bioact

273 tumor progression that can be blocked by an arginase inhibitor.

274 oxy-Nor-L-arginine (Nor-NOHA) was used as an arginase inhibitor.

275 Recent efforts to identify new highly potent arginase inhibitors have resulted in the discovery of a

276 gh adoptive transfer of MDSC or injection of arginase into noninjured mice.

277 xists based on the functional copy number of arginase: intrinsic excitability is altered, there is de

278 f arginine to ornithine by parasites or host arginase is a proposed mechanism of arginine depletion.

279 BCT-100, a pegylated human recombinant arginase, leads to a rapid depletion in extracellular an

280 acrophage cytokine profiles, leads to higher arginase level and activity, and decreased nitric oxide

281 lls, and increased M1 macrophages (iNOS(hi), arginase(lo), and IL10(lo)); the use of macrophage-deple

282 response in aged mice resulted in attenuated arginase (M2a associated), IL-1beta, and chemokine ligan

283 ulline was less effective as a substrate for arginase-mediated L-ornithine production compared with L

284 ponding recruitment of CCR2(+)/IL-4Ralpha(+)/arginase(+) myeloid cells in vivo.

285 e findings highlight for the first time that arginase of all Helicobacter gastric pathogens utilizes

286 resence of these two residues exclusively in arginase of other Helicobacter gastric pathogens, which

287 Using H. pylori arginase, our studies reveal that the interactions of Hi

288 is taken up is primarily metabolized by the arginase pathway to produce the polyamines required for

289 entified CD163-positive, CD206-positive, and arginase-positive cells, indicating a M2 macrophage phen

290 while the role of MAPKs in the regulation of arginase remains unclear.

291 ressive CD11c(+) microglia and extracellular arginase, resulting in arginine catabolism and reduced l

292 Inhibitors of arginase significantly improved postischemic functional

293 In vivo blockade of arginase strongly inhibited Th2 ACT, consistent with a k

294 conservation of the signature motifs in all arginases, the H. pylori homolog has a non-conserved mot

295 tration of adeno-associated virus expressing arginase, there is near-total recovery of the abnormalit

296 proliferation in vivo, whereas addition of L-arginase to cultured keratinocytes stimulated proliferat

297 kin (IL)10, transforming growth factor-beta, arginase type II, chemokine (C-C motif) ligand 22 (CCL22

298 g's effect on gene and protein expression of arginase was evaluated as a marker of alternative macrop

299 Plasma arginase was not elevated in those with malaria, and pla

300 plete arginine, MDSCs express high levels of arginase, which catalyzes the breakdown of arginine into